So in the case of this woman was it from the water or the tea? Did they rule out primary hyperparathyroidism?
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So in the case of this woman was it from the water or the tea? Did they rule out primary hyperparathyroidism?
There is no dispute that too much fluoride can damage bones. Fluoride is present in virtually all foods and beverages due to fluoride use in making them or fluoride-containing pesticide residues. Fluoride is found in tea in high doses. Boiling water condenses fluoride levels in water. So it's probably easier to determine fluoride in tea as a causation of skeletal fluorosis.
However, it can occur in people not drinking tea who consume large volumes of fluoride from all sources including toothpaste where fluoride gets absorbed into the bloodsteam. But those sources will be variable. So any study probably should determine fluoride content of urine, blood, hair, nails, etc and it's relation to skeletal effects to see if there is a correlation.
The EPA is now lowering accepted water fluoride levels because they are concerned that the present level 4mg/L consumed daily can lead to skeletal fluorosis.
for more info http://www.FluorideAciton.Net
However, it can occur in people not drinking tea who consume large volumes of fluoride from all sources including toothpaste where fluoride gets absorbed into the bloodsteam. But those sources will be variable. So any study probably should determine fluoride content of urine, blood, hair, nails, etc and it's relation to skeletal effects to see if there is a correlation.
The EPA is now lowering accepted water fluoride levels because they are concerned that the present level 4mg/L consumed daily can lead to skeletal fluorosis.
for more info http://www.FluorideAciton.Net
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Differential exercise recommendations for obese and non-obese.
Well - Tara Parker-Pope on Health
May 18, 2011, 12:01 am
The Body Weight-Muscle Mismatch
By GRETCHEN REYNOLDS
Jim ParkinPeople who are overweight complain that moving is difficult. It’s possible that their muscular strength is not keeping pace with their growing body size.
Recently scientists at Penn State sewed tiny weighted vests and slipped them around the middles of healthy laboratory rats, hoping to discover how animals’ muscles respond to changes in body size. The vests increased the animals’ weight by as much as 36 percent. After five days, the scientists found that the rats’ muscles contained increased amounts of certain proteins involved in the generation of muscle force. The muscles were redesigning themselves to be stronger.
In a separate group of obese rats, however, no such changes were evident. The rats were heavy, generally exceeding the weight of the animals wearing vests, and they continued to pack on ounces during the experiment. But their muscles did not show the same increases in the proteins that improve muscle power. The obese animals were not getting stronger as they became heavier. They were in danger of becoming too fat to move.
Related
More Phys Ed columns
Faster, Higher, Stronger
Fitness and Nutrition News
How muscles recognize changes in body weight — and why sometimes they don’t — are questions that are likely to have relevance for people, and not just lab rats. Studies have found that “individuals who are extremely overweight often complain that moving is difficult,” said James H. Marden, a professor of biology at Penn State and co-author of the rat study. It’s possible that their muscular strength is not keeping pace with their growing body size.
But why there should be such a mismatch between body weight and muscle strength is unknown. So Dr. Marden and his colleagues began, a few years ago, to study how different creatures deal with changes in their body size and what that might suggest about the human body. They began their work with moths. Flying creatures obviously must deal accurately with body mass or risk plummeting from the sky.
As it turned out, moths are quite good at gauging what they weigh. The bigger the moth, the more its muscles showed activity from one specific gene, the troponin T gene, that expresses various proteins that help muscles to contract. In general, the more of these proteins that a muscle contains, the more forcefully it contracts.
Even when the scientists artificially increased the insects’ body weight, using the simple expedient of gluing lead shot to the moths’ abdomens, the insects’ muscles responded quickly and appropriately. Within days, the troponin T gene in the moths’ wing muscles was pumping out more of the proper proteins to make the muscles stronger. The lead-laden insects had no trouble staying aloft.
But the situation was quite different when the scientists started looking at animals that were fat. Moths don’t become obese, but certain strains of lab rodents do. “We wondered whether there might be a relationship between obesity and the action” of the troponin T gene in muscles, said Rudolf J. Schilder, a postdoctoral fellow at Penn State and lead author of the rat study.
There was. When they biopsied the leg muscles of rats bred to be fat, they found that the chubby animals’ troponin T gene seemed to malfunction. Their muscles contained some of the proteins needed to increase muscle power, but not all of them — and none in as much profusion as in lean rats, even those of a comparable body weight. “The fat rats’ muscles seemed to think that the animals were much smaller than they actually were,” Dr. Schilder said. Their muscles hadn’t come to terms with how fat the animals had become.
Dr. Schilder emphasized that he and his colleagues do not think that troponin T activity, although it is an important marker of muscle function, explains everything about how muscles respond to changes in body weight. The process almost certainly involves a host of other genes and physiological reactions, he said.
It also is not known what mechanisms cause the troponin T gene to malfunction in fat animals, although fat itself is an obvious suspect. “Fat is a very physiologically active tissue,” Dr. Schilder said. “It produces hormones and biochemical messages” that might well disrupt how the troponin T gene functions. Through continuing experiments at his lab, Dr. Schilder hopes to discern more about the role that fat plays in muscle genetics and how much body fat must accumulate before troponin T activity is affected.
But perhaps the most pressing unanswered question about body weight and muscles is what this research means for people. “It’s impossible to know at the moment,” Dr. Marden said, since human studies have not been conducted. But his group’s findings are “suggestive,” he said. “It seems likely” that there are changes in troponin T activity in obese people’s muscles and that, as a result, “it really is physiologically hard for them to move,” he said.
If so, he continued, “we may need to rethink” some exercise programs and suggestions for obese people. “Maybe we should promote activities that require less muscular strain,” he said, like a swim instead of a walk.
“No one is trying to rationalize” remaining heavy, he added, but his group’s work does indicate that misapprehensions about the extent of one’s weight problem may run deep. At the cellular level, muscles and genes may be unable to “understand,” he said, or accept how much a person weighs, a delusion with which many of us, in our minds, can sympathize.
Copyright 2011 The New York Times Company
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Well - Tara Parker-Pope on Health
May 18, 2011, 12:01 am
The Body Weight-Muscle Mismatch
By GRETCHEN REYNOLDS
Jim ParkinPeople who are overweight complain that moving is difficult. It’s possible that their muscular strength is not keeping pace with their growing body size.
Recently scientists at Penn State sewed tiny weighted vests and slipped them around the middles of healthy laboratory rats, hoping to discover how animals’ muscles respond to changes in body size. The vests increased the animals’ weight by as much as 36 percent. After five days, the scientists found that the rats’ muscles contained increased amounts of certain proteins involved in the generation of muscle force. The muscles were redesigning themselves to be stronger.
In a separate group of obese rats, however, no such changes were evident. The rats were heavy, generally exceeding the weight of the animals wearing vests, and they continued to pack on ounces during the experiment. But their muscles did not show the same increases in the proteins that improve muscle power. The obese animals were not getting stronger as they became heavier. They were in danger of becoming too fat to move.
Related
More Phys Ed columns
Faster, Higher, Stronger
Fitness and Nutrition News
How muscles recognize changes in body weight — and why sometimes they don’t — are questions that are likely to have relevance for people, and not just lab rats. Studies have found that “individuals who are extremely overweight often complain that moving is difficult,” said James H. Marden, a professor of biology at Penn State and co-author of the rat study. It’s possible that their muscular strength is not keeping pace with their growing body size.
But why there should be such a mismatch between body weight and muscle strength is unknown. So Dr. Marden and his colleagues began, a few years ago, to study how different creatures deal with changes in their body size and what that might suggest about the human body. They began their work with moths. Flying creatures obviously must deal accurately with body mass or risk plummeting from the sky.
As it turned out, moths are quite good at gauging what they weigh. The bigger the moth, the more its muscles showed activity from one specific gene, the troponin T gene, that expresses various proteins that help muscles to contract. In general, the more of these proteins that a muscle contains, the more forcefully it contracts.
Even when the scientists artificially increased the insects’ body weight, using the simple expedient of gluing lead shot to the moths’ abdomens, the insects’ muscles responded quickly and appropriately. Within days, the troponin T gene in the moths’ wing muscles was pumping out more of the proper proteins to make the muscles stronger. The lead-laden insects had no trouble staying aloft.
But the situation was quite different when the scientists started looking at animals that were fat. Moths don’t become obese, but certain strains of lab rodents do. “We wondered whether there might be a relationship between obesity and the action” of the troponin T gene in muscles, said Rudolf J. Schilder, a postdoctoral fellow at Penn State and lead author of the rat study.
There was. When they biopsied the leg muscles of rats bred to be fat, they found that the chubby animals’ troponin T gene seemed to malfunction. Their muscles contained some of the proteins needed to increase muscle power, but not all of them — and none in as much profusion as in lean rats, even those of a comparable body weight. “The fat rats’ muscles seemed to think that the animals were much smaller than they actually were,” Dr. Schilder said. Their muscles hadn’t come to terms with how fat the animals had become.
Dr. Schilder emphasized that he and his colleagues do not think that troponin T activity, although it is an important marker of muscle function, explains everything about how muscles respond to changes in body weight. The process almost certainly involves a host of other genes and physiological reactions, he said.
It also is not known what mechanisms cause the troponin T gene to malfunction in fat animals, although fat itself is an obvious suspect. “Fat is a very physiologically active tissue,” Dr. Schilder said. “It produces hormones and biochemical messages” that might well disrupt how the troponin T gene functions. Through continuing experiments at his lab, Dr. Schilder hopes to discern more about the role that fat plays in muscle genetics and how much body fat must accumulate before troponin T activity is affected.
But perhaps the most pressing unanswered question about body weight and muscles is what this research means for people. “It’s impossible to know at the moment,” Dr. Marden said, since human studies have not been conducted. But his group’s findings are “suggestive,” he said. “It seems likely” that there are changes in troponin T activity in obese people’s muscles and that, as a result, “it really is physiologically hard for them to move,” he said.
If so, he continued, “we may need to rethink” some exercise programs and suggestions for obese people. “Maybe we should promote activities that require less muscular strain,” he said, like a swim instead of a walk.
“No one is trying to rationalize” remaining heavy, he added, but his group’s work does indicate that misapprehensions about the extent of one’s weight problem may run deep. At the cellular level, muscles and genes may be unable to “understand,” he said, or accept how much a person weighs, a delusion with which many of us, in our minds, can sympathize.
Copyright 2011 The New York Times Company
Privacy Policy
NYTimes.com 620 Eighth Avenue New York, NY 10018
Telomere Dysfunction Induces Metabolic And Mitochondrial Compromise
Multiple biological processes driven by diverse molecular factors conspire progressively to diminish organ function with advancing age. Molecular and cellular analyses of age-related conditions such as muscle atrophy, diabetes and cardiomyopathy implicate diminished mitochondrial function and telomere dysfunction in driving pathogenesis. Aged tissues show accumulation of mitochondrial DNA (mtDNA) mutations causing respiratory chain deficiency and increased reactive oxygen species (ROS), which may underlie declining mitochondrial energy production and progressive loss of vigour in the aged. The importance of mitochondrial integrity for healthy ageing is reinforced by premature ageing in mitochondrial polymerase (PolgA) mutant mice, which sustain increased mtDNA mutations. Whereas the instigating processes driving age-associated mitochondrial decline are not known, in the context of this study, it is notable that the activity of the master mitochondrial regulators PGC-1a and PGC-1b decreases across ageing tissues. The relevance of PGCs to age-related pathologies may stem from their regulation of mitochondrial biogenesis and control of metabolic processes (gluconeogenesis, fatty acid metabolism and b-oxidation), processes that relate to increased insulin resistance and diabetes in the aged.
Increasing evidence also implicated telomeres in the pathogenesis of age-related disorders. Telomeres are nucleoprotein complexes at chromosome ends that function to preserve chromosomal integrity and quell p53-dependent DNA damage and DNA repair activity at these free ends. In the absence of telomerase, continued cell division results in telomere shortening, loss of ‘capping’ function, and p53 activation. The prevailing view of how uncapped telomeres compromise organ function posits that p53 mediates cellular checkpoints of growth arrest, senescence and apoptosis in stem/progenitor cells. Correspondingly, p53 deficiency ameliorates these phenotypes, particularly in organs with high proliferative demands supported by resident stem cells. The relevance of p53 in ageing is evidenced by stem cell depletion and premature ageing in mice engineered with hyper-active p53 alleles. Whereas stem/progenitor cell failure due to p53-mediated cellular checkpoints may underlie compromise of highly proliferative organs, this mechanism seems inadequate to explain the profound physiological decline in more quiescent tissues, for example, heart (cardiomyopathy) and liver (reduced detoxification capacity, glucose intolerance). These pathologies indicate that telomere dysfunction elicits a degenerative state via additional mechanisms beyond the classical senescence and apoptosis checkpoints.
Sahin E, Colla S, Liesa M, et al. Telomere dysfunction induces metabolic and mitochondrial compromise. Nature 2011;470(7334):359-65. Telomere dysfunction induces metabolic and mitocho... [Nature. 2011] - PubMed result / http://www.jenage.de/assets/library/pdfs/sahin_et_al_NATURE_2011.pdf
Telomere dysfunction activates p53-mediated cellular growth arrest, senescence and apoptosis to drive progressive atrophy and functional decline in high-turnover tissues. The broader adverse impact of telomere dysfunction across many tissues including more quiescent systems prompted transcriptomic network analyses to identify common mechanisms operative in haematopoietic stem cells, heart and liver. These unbiased studies revealed profound repression of peroxisome proliferator-activated receptor gamma, coactivator 1 alpha and beta (PGC-1alpha and PGC-1beta, also known as Ppargc1a and Ppargc1b, respectively) and the downstream network in mice null for either telomerase reverse transcriptase (Tert) or telomerase RNA component (Terc) genes. Consistent with PGCs as master regulators of mitochondrial physiology and metabolism, telomere dysfunction is associated with impaired mitochondrial biogenesis and function, decreased gluconeogenesis, cardiomyopathy, and increased reactive oxygen species. In the setting of telomere dysfunction, enforced Tert or PGC-1alpha expression or germline deletion of p53 (also known as Trp53) substantially restores PGC network expression, mitochondrial respiration, cardiac function and gluconeogenesis. We demonstrate that telomere dysfunction activates p53 which in turn binds and represses PGC-1alpha and PGC-1beta promoters, thereby forging a direct link between telomere and mitochondrial biology. We propose that this telomere-p53-PGC axis contributes to organ and metabolic failure and to diminishing organismal fitness in the setting of telomere dysfunction.
________________________________________
A Blood Test Offers Clues to Longevity
http://www.nytimes.com/2011/05/19/business/19life.html
By ANDREW POLLACK
Published: May 18, 2011
Want to know how long you will live?
Blood tests that seek to tell people their biological age — possibly offering a clue to their longevity or how healthy they will remain — are now going on sale.
But contrary to various recent media reports, the tests cannot specify how many months or years someone can expect to live. Some experts say the tests will not provide any useful information.
The tests measure telomeres, which are structures on the tips of chromosomes that shorten as people age. Various studies have shown that people with shorter telomeres in their white blood cells are more likely to develop illnesses like cancer, heart disease and Alzheimer’s disease, or even to die earlier. Studies in mice have suggested that extending telomeres lengthens lives.
Seizing on that, laboratories are beginning to offer tests of telomere length, setting off a new debate over what genetic tests should be offered to the public and what would be the ethical implications if the results were used by employers or others.
Some of the laboratories offering the tests emphasize that the results are merely intended to raise a warning flag.
“We see it as a kind of wake-up call for the patient and the clinician to say, ‘You know, you’re on a rapidly aging path,’ ” said Otto Schaefer, vice president for sales and marketing at SpectraCell Laboratories in Houston, which offers a test for $290.
A company in Spain, provocatively named Life Length, has begun selling a test for 500 euros ($712), that says that it can tell people their biological age, which may not correspond to their chronologic age.
Another company, Telome Health of Menlo Park, Calif., plans to begin offering a test later this year for about $200. It was co-founded by Elizabeth H. Blackburn of the University of California, San Francisco, who shared a Nobel Prize in 2009 for discoveries related to telomeres.
Calvin B. Harley, the chief scientific officer at Telome Health, said the test would be akin to a car’s dashboard signal, a “check engine light.” He compared it with a cholesterol test, but more versatile since it can predict a risk of various illnesses, not just heart attacks.
But among the critics of such tests is Carol Greider, a molecular biologist at Johns Hopkins University, who was a co-winner of the Nobel Prize with Dr. Blackburn.
Dr. Greider acknowledged that solid evidence showed that the 1 percent of people with the shortest telomeres were at an increased risk of certain diseases, particularly bone marrow failure and pulmonary fibrosis, a fatal scarring of the lungs. But outside of that 1 percent, she said, “The science really isn’t there to tell us what the consequences are of your telomere length.”
Dr. Greider said that there was great variability in telomere length. “A given telomere length can be from a 20-year-old or a 70-year-old,” she said. “You could send me a DNA sample and I couldn’t tell you how old that person is.”
Dr. Peter Lansdorp, a telomere expert at the British Columbia Cancer Agency, also had doubts. “If telomeres are short for you or me, what does it mean?” he said. Dr. Lansdorp started a company, Repeat Diagnostics, which conducts telomere testing for medical researchers only.
Recent media reports speculated on the tests and their possible implications, including ethical problems.
“You could imagine insurance companies wanting this knowledge to set rates or deny coverage,” said Jerry W. Shay, a professor of cell biology at the University of Texas Southwestern Medical Center in Dallas, who is an adviser to Life Length.
Test vendors say the speculation is running wild.
“It doesn’t mean we will tell anyone how long they will live,” said María Blasco, a co-founder of Life Length and a molecular biologist at the Spanish National Cancer Research Center in Madrid. Even if a 50-year-old has the telomere length more typical of a 70-year-old, she said, “This doesn’t mean your whole body is like a 70-year-old person’s body.”
Still, she said, “We think it can be helpful to people who are especially keen on knowing how healthy they are.”
Generally tests offered by a single laboratory do not have to be approved by the Food and Drug Administration. But the F.D.A. has been cracking down recently on some tests offered to the public, saying they may need approval. The FDA said in a statement Wednesday that it was aware of the tests, and had not come to any conclusions.
Executives at both Telome Health and Life Length say they will require a doctor to be involved in ordering the test, though SpectraCell said it allowed individuals to order the test.
Telomeres are stretches of DNA linked to certain proteins that are at the ends of chromosomes. They are often likened to the caps at the end of shoelaces. Each time a cell divides, the telomeres get shorter. Eventually, the telomeres get so short that the cell can no longer divide. It enters a state of senescence or dies.
One study in Utah, using blood samples from 143 elderly people collected in the 1980s, found that those with shorter telomeres were almost twice as likely to die in the ensuing years as those with longer ones.
Another study, published in The Journal of the American Medical Association last July, followed 787 people in Italy, all initially free of cancer. Those with the shortest telomeres had three times the risk of developing cancers in the next 10 years as those with the longest telomeres.
Still, not all studies have found such strong correlations. In any case, correlations do not prove that the shorter telomeres are causing the problems, although experts say some animal and cell studies do suggest causality.
Some say that the telomere test might not tell people much that cannot be learned in other ways.
“You can pretty much look at people and determine their biological age,” said Michael West, who founded Geron, the biotechnology company that sponsored and conducted some important research on telomeres. He now runs BioTime, another biotechnology company.
It is also unclear what to do about short telomeres. At the moment, there is no drug that can lengthen telomeres, though researchers are working on drugs and stem cell therapies.
There is some evidence, however, that stress is associated with shorter telomeres and that stress relief, exercise or certain nutrients such as omega-3 fatty acids might at least slow the decline in telomere length. But healthy lifestyles are already recommended for people without having to know their telomere length.
There are also disputes about how to measure telomeres. Life Length says its technique, while more expensive, can detect not only average telomere length but the shortest telomeres in cells. The shortest telomeres cause the health problems, said Dr. Shay, the adviser to Life Length.
Telome Health and SpectraCell use a DNA amplification technique called polymerase chain reaction, or P.C.R., which is cheaper but provides only an average length. And there are some questions about the accuracy.
Dr. Harley of Telome said the P.C.R. test was more relevant because virtually all the studies correlating telomere length with disease had used that test.
For those wanting to know how long they might live, there are already some indexes that are used by geriatricians to estimate the chances of a patient dying in anywhere from six months to nine years. A patient with a short expected lifespan, for instance, might no longer need to undergo annual screening for cancer.
These estimates rely on factors such as person’s age, gender, smoking history, whether they have certain diseases and whether they can perform certain functions, like walking several blocks, pushing an armchair or managing their finances.
Dr. Sei Lee, an assistant professor at the University of California, San Francisco who developed a test that estimates the probability of dying within four years, said he was not sure how much telomere length testing would add. “The chance of any single factor being a great predictor is probably low,” he said.
Multiple biological processes driven by diverse molecular factors conspire progressively to diminish organ function with advancing age. Molecular and cellular analyses of age-related conditions such as muscle atrophy, diabetes and cardiomyopathy implicate diminished mitochondrial function and telomere dysfunction in driving pathogenesis. Aged tissues show accumulation of mitochondrial DNA (mtDNA) mutations causing respiratory chain deficiency and increased reactive oxygen species (ROS), which may underlie declining mitochondrial energy production and progressive loss of vigour in the aged. The importance of mitochondrial integrity for healthy ageing is reinforced by premature ageing in mitochondrial polymerase (PolgA) mutant mice, which sustain increased mtDNA mutations. Whereas the instigating processes driving age-associated mitochondrial decline are not known, in the context of this study, it is notable that the activity of the master mitochondrial regulators PGC-1a and PGC-1b decreases across ageing tissues. The relevance of PGCs to age-related pathologies may stem from their regulation of mitochondrial biogenesis and control of metabolic processes (gluconeogenesis, fatty acid metabolism and b-oxidation), processes that relate to increased insulin resistance and diabetes in the aged.
Increasing evidence also implicated telomeres in the pathogenesis of age-related disorders. Telomeres are nucleoprotein complexes at chromosome ends that function to preserve chromosomal integrity and quell p53-dependent DNA damage and DNA repair activity at these free ends. In the absence of telomerase, continued cell division results in telomere shortening, loss of ‘capping’ function, and p53 activation. The prevailing view of how uncapped telomeres compromise organ function posits that p53 mediates cellular checkpoints of growth arrest, senescence and apoptosis in stem/progenitor cells. Correspondingly, p53 deficiency ameliorates these phenotypes, particularly in organs with high proliferative demands supported by resident stem cells. The relevance of p53 in ageing is evidenced by stem cell depletion and premature ageing in mice engineered with hyper-active p53 alleles. Whereas stem/progenitor cell failure due to p53-mediated cellular checkpoints may underlie compromise of highly proliferative organs, this mechanism seems inadequate to explain the profound physiological decline in more quiescent tissues, for example, heart (cardiomyopathy) and liver (reduced detoxification capacity, glucose intolerance). These pathologies indicate that telomere dysfunction elicits a degenerative state via additional mechanisms beyond the classical senescence and apoptosis checkpoints.
Sahin E, Colla S, Liesa M, et al. Telomere dysfunction induces metabolic and mitochondrial compromise. Nature 2011;470(7334):359-65. Telomere dysfunction induces metabolic and mitocho... [Nature. 2011] - PubMed result / http://www.jenage.de/assets/library/pdfs/sahin_et_al_NATURE_2011.pdf
Telomere dysfunction activates p53-mediated cellular growth arrest, senescence and apoptosis to drive progressive atrophy and functional decline in high-turnover tissues. The broader adverse impact of telomere dysfunction across many tissues including more quiescent systems prompted transcriptomic network analyses to identify common mechanisms operative in haematopoietic stem cells, heart and liver. These unbiased studies revealed profound repression of peroxisome proliferator-activated receptor gamma, coactivator 1 alpha and beta (PGC-1alpha and PGC-1beta, also known as Ppargc1a and Ppargc1b, respectively) and the downstream network in mice null for either telomerase reverse transcriptase (Tert) or telomerase RNA component (Terc) genes. Consistent with PGCs as master regulators of mitochondrial physiology and metabolism, telomere dysfunction is associated with impaired mitochondrial biogenesis and function, decreased gluconeogenesis, cardiomyopathy, and increased reactive oxygen species. In the setting of telomere dysfunction, enforced Tert or PGC-1alpha expression or germline deletion of p53 (also known as Trp53) substantially restores PGC network expression, mitochondrial respiration, cardiac function and gluconeogenesis. We demonstrate that telomere dysfunction activates p53 which in turn binds and represses PGC-1alpha and PGC-1beta promoters, thereby forging a direct link between telomere and mitochondrial biology. We propose that this telomere-p53-PGC axis contributes to organ and metabolic failure and to diminishing organismal fitness in the setting of telomere dysfunction.
________________________________________
A Blood Test Offers Clues to Longevity
http://www.nytimes.com/2011/05/19/business/19life.html
By ANDREW POLLACK
Published: May 18, 2011
Want to know how long you will live?
Blood tests that seek to tell people their biological age — possibly offering a clue to their longevity or how healthy they will remain — are now going on sale.
But contrary to various recent media reports, the tests cannot specify how many months or years someone can expect to live. Some experts say the tests will not provide any useful information.
The tests measure telomeres, which are structures on the tips of chromosomes that shorten as people age. Various studies have shown that people with shorter telomeres in their white blood cells are more likely to develop illnesses like cancer, heart disease and Alzheimer’s disease, or even to die earlier. Studies in mice have suggested that extending telomeres lengthens lives.
Seizing on that, laboratories are beginning to offer tests of telomere length, setting off a new debate over what genetic tests should be offered to the public and what would be the ethical implications if the results were used by employers or others.
Some of the laboratories offering the tests emphasize that the results are merely intended to raise a warning flag.
“We see it as a kind of wake-up call for the patient and the clinician to say, ‘You know, you’re on a rapidly aging path,’ ” said Otto Schaefer, vice president for sales and marketing at SpectraCell Laboratories in Houston, which offers a test for $290.
A company in Spain, provocatively named Life Length, has begun selling a test for 500 euros ($712), that says that it can tell people their biological age, which may not correspond to their chronologic age.
Another company, Telome Health of Menlo Park, Calif., plans to begin offering a test later this year for about $200. It was co-founded by Elizabeth H. Blackburn of the University of California, San Francisco, who shared a Nobel Prize in 2009 for discoveries related to telomeres.
Calvin B. Harley, the chief scientific officer at Telome Health, said the test would be akin to a car’s dashboard signal, a “check engine light.” He compared it with a cholesterol test, but more versatile since it can predict a risk of various illnesses, not just heart attacks.
But among the critics of such tests is Carol Greider, a molecular biologist at Johns Hopkins University, who was a co-winner of the Nobel Prize with Dr. Blackburn.
Dr. Greider acknowledged that solid evidence showed that the 1 percent of people with the shortest telomeres were at an increased risk of certain diseases, particularly bone marrow failure and pulmonary fibrosis, a fatal scarring of the lungs. But outside of that 1 percent, she said, “The science really isn’t there to tell us what the consequences are of your telomere length.”
Dr. Greider said that there was great variability in telomere length. “A given telomere length can be from a 20-year-old or a 70-year-old,” she said. “You could send me a DNA sample and I couldn’t tell you how old that person is.”
Dr. Peter Lansdorp, a telomere expert at the British Columbia Cancer Agency, also had doubts. “If telomeres are short for you or me, what does it mean?” he said. Dr. Lansdorp started a company, Repeat Diagnostics, which conducts telomere testing for medical researchers only.
Recent media reports speculated on the tests and their possible implications, including ethical problems.
“You could imagine insurance companies wanting this knowledge to set rates or deny coverage,” said Jerry W. Shay, a professor of cell biology at the University of Texas Southwestern Medical Center in Dallas, who is an adviser to Life Length.
Test vendors say the speculation is running wild.
“It doesn’t mean we will tell anyone how long they will live,” said María Blasco, a co-founder of Life Length and a molecular biologist at the Spanish National Cancer Research Center in Madrid. Even if a 50-year-old has the telomere length more typical of a 70-year-old, she said, “This doesn’t mean your whole body is like a 70-year-old person’s body.”
Still, she said, “We think it can be helpful to people who are especially keen on knowing how healthy they are.”
Generally tests offered by a single laboratory do not have to be approved by the Food and Drug Administration. But the F.D.A. has been cracking down recently on some tests offered to the public, saying they may need approval. The FDA said in a statement Wednesday that it was aware of the tests, and had not come to any conclusions.
Executives at both Telome Health and Life Length say they will require a doctor to be involved in ordering the test, though SpectraCell said it allowed individuals to order the test.
Telomeres are stretches of DNA linked to certain proteins that are at the ends of chromosomes. They are often likened to the caps at the end of shoelaces. Each time a cell divides, the telomeres get shorter. Eventually, the telomeres get so short that the cell can no longer divide. It enters a state of senescence or dies.
One study in Utah, using blood samples from 143 elderly people collected in the 1980s, found that those with shorter telomeres were almost twice as likely to die in the ensuing years as those with longer ones.
Another study, published in The Journal of the American Medical Association last July, followed 787 people in Italy, all initially free of cancer. Those with the shortest telomeres had three times the risk of developing cancers in the next 10 years as those with the longest telomeres.
Still, not all studies have found such strong correlations. In any case, correlations do not prove that the shorter telomeres are causing the problems, although experts say some animal and cell studies do suggest causality.
Some say that the telomere test might not tell people much that cannot be learned in other ways.
“You can pretty much look at people and determine their biological age,” said Michael West, who founded Geron, the biotechnology company that sponsored and conducted some important research on telomeres. He now runs BioTime, another biotechnology company.
It is also unclear what to do about short telomeres. At the moment, there is no drug that can lengthen telomeres, though researchers are working on drugs and stem cell therapies.
There is some evidence, however, that stress is associated with shorter telomeres and that stress relief, exercise or certain nutrients such as omega-3 fatty acids might at least slow the decline in telomere length. But healthy lifestyles are already recommended for people without having to know their telomere length.
There are also disputes about how to measure telomeres. Life Length says its technique, while more expensive, can detect not only average telomere length but the shortest telomeres in cells. The shortest telomeres cause the health problems, said Dr. Shay, the adviser to Life Length.
Telome Health and SpectraCell use a DNA amplification technique called polymerase chain reaction, or P.C.R., which is cheaper but provides only an average length. And there are some questions about the accuracy.
Dr. Harley of Telome said the P.C.R. test was more relevant because virtually all the studies correlating telomere length with disease had used that test.
For those wanting to know how long they might live, there are already some indexes that are used by geriatricians to estimate the chances of a patient dying in anywhere from six months to nine years. A patient with a short expected lifespan, for instance, might no longer need to undergo annual screening for cancer.
These estimates rely on factors such as person’s age, gender, smoking history, whether they have certain diseases and whether they can perform certain functions, like walking several blocks, pushing an armchair or managing their finances.
Dr. Sei Lee, an assistant professor at the University of California, San Francisco who developed a test that estimates the probability of dying within four years, said he was not sure how much telomere length testing would add. “The chance of any single factor being a great predictor is probably low,” he said.
[Would this apply to TRT.]
Therapeutic Videoconferencing Interventions For The Treatment Of Long-Term Conditions
The present work was part of a larger study considering the evidence for the use of videoconferencing to provide therapy for adults with chronic fatigue syndrome. As only one study was found relating specifically to remote service provision for a chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ ME) population, the literature search strategy was broadened to include other chronic and/or long-term conditions. Two primary themes emerged from examination of systematic reviews relating to telerehabilitation: patient satisfaction and evidence of clinical effectiveness. Regarding patient satisfaction, the literature reviews agreed that although the quality of evidence was not high, patients were in general highly satisfied with telerehabilitation. There was no consensus about whether patients preferred remote to in-person treatment.
With regard to the clinical effectiveness, the literature reviews varied in their conclusions according to the type of telerehabilitation that was considered and how recently the review had been conducted. Two systematic reviews of high quality found mixed evidence for the clinical effectiveness of telemedicine, one reporting that studies producing evidence of clinical outcomes were of poor quality while the other concluded that telehealth positively affected clinical outcomes.
Seven further systematic reviews of moderate quality covering a variety of related applications also noted that the quality of evidence was compromised by design problems. However, despite identifying the small amount of available evidence on clinical effectiveness, a number of reviewers reached positive conclusions about videoconferencing, namely that it leads to improved clinical status and improved access to services in the UK particularly in rural areas with few negative effects on communication.
In summary, many reviews have stated that there is insufficient evidence to draw a conclusion about the clinical effectiveness of telerehabilitation, although there is some evidence of positive outcomes. The two most recent literature reviews state that there is no difference in clinical outcomes between distant delivery and in-person delivery. The difference in opinion between the earlier literature reviews (2000–2005) and the more recent literature (2006 onwards) suggests the rapid evolution of evidence in this area. Researchers therefore conducted a systematic review, specifically relating to the use of videoconferencing for chronic and/or long-term conditions.
Steel K, Cox D, Garry H. Therapeutic videoconferencing interventions for the treatment of long-term conditions. J Telemed Telecare 2011;17(3):109-17. http://jtt.rsmjournals.com/cgi/content/abstract/17/3/109?etoc (Therapeutic videoconferencing interventions for the treatment of long-term conditions -- Steel et al. 17 (3): 109 -- Journal of Telemedicine and Telecare)
We conducted a systematic review of literature relating to videoconferencing in therapeutic interventions for chronic conditions. Two hundred articles were reviewed in detail, 35 of which were relevant to the study. Of these, eight were randomized controlled trials (RCTs) and the remainder were service evaluations, pilot studies and case studies. Two major themes emerged, relating specifically to videoconferencing: clinical outcomes and patient satisfaction. There were 14 studies which measured clinical outcomes of interventions for chronic conditions delivered by videoconferencing. A range of evidence, including four RCTs of high quality, indicates that interventions for a variety of conditions, including psychological and physical, delivered by videoconferencing produce similar outcomes to treatment delivered in-person. Evidence suggests that levels of patient satisfaction with telerehabilitation are high and that the formation of a good therapeutic alliance is possible. Several papers reported that clinical staff showed lower levels of satisfaction in using telerehabilitation than patients. It is feasible to use videoconferencing as a means of delivering therapeutic interventions for people with chronic conditions in rural communities.
Therapeutic Videoconferencing Interventions For The Treatment Of Long-Term Conditions
The present work was part of a larger study considering the evidence for the use of videoconferencing to provide therapy for adults with chronic fatigue syndrome. As only one study was found relating specifically to remote service provision for a chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ ME) population, the literature search strategy was broadened to include other chronic and/or long-term conditions. Two primary themes emerged from examination of systematic reviews relating to telerehabilitation: patient satisfaction and evidence of clinical effectiveness. Regarding patient satisfaction, the literature reviews agreed that although the quality of evidence was not high, patients were in general highly satisfied with telerehabilitation. There was no consensus about whether patients preferred remote to in-person treatment.
With regard to the clinical effectiveness, the literature reviews varied in their conclusions according to the type of telerehabilitation that was considered and how recently the review had been conducted. Two systematic reviews of high quality found mixed evidence for the clinical effectiveness of telemedicine, one reporting that studies producing evidence of clinical outcomes were of poor quality while the other concluded that telehealth positively affected clinical outcomes.
Seven further systematic reviews of moderate quality covering a variety of related applications also noted that the quality of evidence was compromised by design problems. However, despite identifying the small amount of available evidence on clinical effectiveness, a number of reviewers reached positive conclusions about videoconferencing, namely that it leads to improved clinical status and improved access to services in the UK particularly in rural areas with few negative effects on communication.
In summary, many reviews have stated that there is insufficient evidence to draw a conclusion about the clinical effectiveness of telerehabilitation, although there is some evidence of positive outcomes. The two most recent literature reviews state that there is no difference in clinical outcomes between distant delivery and in-person delivery. The difference in opinion between the earlier literature reviews (2000–2005) and the more recent literature (2006 onwards) suggests the rapid evolution of evidence in this area. Researchers therefore conducted a systematic review, specifically relating to the use of videoconferencing for chronic and/or long-term conditions.
Steel K, Cox D, Garry H. Therapeutic videoconferencing interventions for the treatment of long-term conditions. J Telemed Telecare 2011;17(3):109-17. http://jtt.rsmjournals.com/cgi/content/abstract/17/3/109?etoc (Therapeutic videoconferencing interventions for the treatment of long-term conditions -- Steel et al. 17 (3): 109 -- Journal of Telemedicine and Telecare)
We conducted a systematic review of literature relating to videoconferencing in therapeutic interventions for chronic conditions. Two hundred articles were reviewed in detail, 35 of which were relevant to the study. Of these, eight were randomized controlled trials (RCTs) and the remainder were service evaluations, pilot studies and case studies. Two major themes emerged, relating specifically to videoconferencing: clinical outcomes and patient satisfaction. There were 14 studies which measured clinical outcomes of interventions for chronic conditions delivered by videoconferencing. A range of evidence, including four RCTs of high quality, indicates that interventions for a variety of conditions, including psychological and physical, delivered by videoconferencing produce similar outcomes to treatment delivered in-person. Evidence suggests that levels of patient satisfaction with telerehabilitation are high and that the formation of a good therapeutic alliance is possible. Several papers reported that clinical staff showed lower levels of satisfaction in using telerehabilitation than patients. It is feasible to use videoconferencing as a means of delivering therapeutic interventions for people with chronic conditions in rural communities.
Last edited:
Phosphodiesterase Type 5 Inhibitor Use and Hearing Impairment
[Add this concern with that for vision loss, there might be something to that age old adage about going deaf and blind!!! LOL]
Viagra 'could make you deaf'
Viagra could make you deaf, doctors have warned.
http://www.telegraph.co.uk/health/healthnews/8522746/Viagra-could-make-you-deaf.html
Viagra and similar impotence drugs have been linked to hundreds of cases of sudden hearing loss around the world, including some in the UK.
Doctors have begun to warn that the drugs could damage users' hearing after a spate of people in the US with auditory problems.
Experts, including some from Charing Cross, Stoke Mandeville and Royal Marsden hospitals, were so concerned by the claims that they demanded an investigation from official watchdogs across three continents.
Users in America, East Asia and Australia were questioned as to whether they suffered hearing loss shortly after taking the pills.
Forty-seven suspected cases of sensorineural hearing loss – a rapid loss of hearing in one or both ears – were linked to Viagra and related drugs Cialis and Levitra. Eight were from the UK.
However, another 223 reports made in the US had to be excluded due to a lack of detail.
The researchers are not sure how Viagra might affect hearing, but it may be that the chain of chemical reactions it triggers have knock-on effects in the inner ear.
The average age of those affected was 57, although two of the men involved were only 37, the study found.
Dr Afroze Shah Khan, of Charing Cross Hospital, said: "Medical practitioners involved in the prescription of these drugs need to be vigilant about this potential side-effect."
However, the Medicines and Healthcare Products Regulatory Agency, Britain’s drugs watchdog, said complaints of hearing loss linked to Viagra were "extremely rare".
A spokesman added that reports of an adverse reaction to a drug do not prove the medicine caused it.
Khan AS, Sheikh Z, Khan S, Dwivedi R, Benjamin E. Viagra deafness—Sensorineural hearing loss and phosphodiesterase-5 inhibitors. The Laryngoscope 2011;121(5):1049-54. Viagra deafness—Sensorineural hearing loss and phosphodiesterase-5 inhibitors - Khan - 2011 - The Laryngoscope - Wiley Online Library
Background: Viagra and PDE-5 inhibitors use has mushroomed since its launch over a decade ago. A growing body of evidence indicates significant morbidity associated with the side effect profile of this class of drug. Hearing loss associated with PDE-5 inhibitor use has recently been reported, but few studies have evaluated the causal link.
Aim: To review and scrutinise the current literature on the subject and propose possible physiologic mechanisms and to investigate the global reporting of this side effect.
Methods and Materials: Pharmacovigilance agencies around North America, Europe, and Australasia were contacted requesting reports of hearing loss associated with PDE-5 inhibitors. Reports were scrutinised to exclude those where others causes of hearing loss existed.
Results: Forty-seven cases of sensorineural hearing loss with a temporal association with PDE-5 inhibitor ingestion were obtained from both published literature and pharmacovigilance agencies. Cases had a mean age 56.6 years, male-to-female ratio of 7:1. Eighty-eight percent of reports were unilateral with an even left/right distribution. Hearing loss occurred within 24 hours of ingestion of PDE-5 inhibitor in 66.7% (n = 18) of cases. Sildenafil accounted for over 50% of cases.
Conclusion: There is increasing evidence that PDE-5 inhibitors may induce sensorineural hearing loss via plausible physiological mechanisms. There needs to be more awareness of this disabling side effect among healthcare professionals responsible for prescribing this drug.
[Add this concern with that for vision loss, there might be something to that age old adage about going deaf and blind!!! LOL]
Viagra 'could make you deaf'
Viagra could make you deaf, doctors have warned.
http://www.telegraph.co.uk/health/healthnews/8522746/Viagra-could-make-you-deaf.html
Viagra and similar impotence drugs have been linked to hundreds of cases of sudden hearing loss around the world, including some in the UK.
Doctors have begun to warn that the drugs could damage users' hearing after a spate of people in the US with auditory problems.
Experts, including some from Charing Cross, Stoke Mandeville and Royal Marsden hospitals, were so concerned by the claims that they demanded an investigation from official watchdogs across three continents.
Users in America, East Asia and Australia were questioned as to whether they suffered hearing loss shortly after taking the pills.
Forty-seven suspected cases of sensorineural hearing loss – a rapid loss of hearing in one or both ears – were linked to Viagra and related drugs Cialis and Levitra. Eight were from the UK.
However, another 223 reports made in the US had to be excluded due to a lack of detail.
The researchers are not sure how Viagra might affect hearing, but it may be that the chain of chemical reactions it triggers have knock-on effects in the inner ear.
The average age of those affected was 57, although two of the men involved were only 37, the study found.
Dr Afroze Shah Khan, of Charing Cross Hospital, said: "Medical practitioners involved in the prescription of these drugs need to be vigilant about this potential side-effect."
However, the Medicines and Healthcare Products Regulatory Agency, Britain’s drugs watchdog, said complaints of hearing loss linked to Viagra were "extremely rare".
A spokesman added that reports of an adverse reaction to a drug do not prove the medicine caused it.
Khan AS, Sheikh Z, Khan S, Dwivedi R, Benjamin E. Viagra deafness—Sensorineural hearing loss and phosphodiesterase-5 inhibitors. The Laryngoscope 2011;121(5):1049-54. Viagra deafness—Sensorineural hearing loss and phosphodiesterase-5 inhibitors - Khan - 2011 - The Laryngoscope - Wiley Online Library
Background: Viagra and PDE-5 inhibitors use has mushroomed since its launch over a decade ago. A growing body of evidence indicates significant morbidity associated with the side effect profile of this class of drug. Hearing loss associated with PDE-5 inhibitor use has recently been reported, but few studies have evaluated the causal link.
Aim: To review and scrutinise the current literature on the subject and propose possible physiologic mechanisms and to investigate the global reporting of this side effect.
Methods and Materials: Pharmacovigilance agencies around North America, Europe, and Australasia were contacted requesting reports of hearing loss associated with PDE-5 inhibitors. Reports were scrutinised to exclude those where others causes of hearing loss existed.
Results: Forty-seven cases of sensorineural hearing loss with a temporal association with PDE-5 inhibitor ingestion were obtained from both published literature and pharmacovigilance agencies. Cases had a mean age 56.6 years, male-to-female ratio of 7:1. Eighty-eight percent of reports were unilateral with an even left/right distribution. Hearing loss occurred within 24 hours of ingestion of PDE-5 inhibitor in 66.7% (n = 18) of cases. Sildenafil accounted for over 50% of cases.
Conclusion: There is increasing evidence that PDE-5 inhibitors may induce sensorineural hearing loss via plausible physiological mechanisms. There needs to be more awareness of this disabling side effect among healthcare professionals responsible for prescribing this drug.
The Visual Impact of Gossip
Psychology Professor Lisa Feldman Barrett of the Northeastern University in Boston and her colleagues used binocular rivalry, a technique in which different images are shown to the subjects' left and right eyes. The brain becomes conscious of one of the images before registering the other, and the time taken for the image to be registered is a measure of the importance the brain gives the image. The importance is also indicated by the length of time the image remains in the conscious awareness, as the brain alternates between consciously registering the images of the face and house.
The 66 volunteers, all university students, were shown photographs of faces and given some information about the people. Information was either positive (such as the person helped an elderly lady), neutral (such as they passed a man in the street) or negative gossip, such as the person had thrown a chair at a fellow student. The students saw the pictures of the faces with one eye, but the other eye was shown an image of a house. The students pressed a keyboard key when they were conscious of seeing the face and another when they saw the house. Some of the photographs of faces had not previously been seen by the students and they had received no information about them.
The results showed that it took the students the same length of time to register seeing the unknown faces and those about which they had been told neutral or positive information, but the picture of the person about whom they had heard negative information registered around half a second quicker. The face with negative associations also registered for substantially longer periods of time than the neutral, positive or unknown faces.
A second experiment backed up the findings and also showed that subjects saw the faces linked to negative gossip for longer periods than faces about whom they had heard about upsetting personal experiences.
The results suggest that if you have recently heard negative gossip about someone you are more likely to notice them in a crowd. The researchers said gossip gives people information about whether a person might be a friend or foe, and suggest that being able to spot the face of a person about whom they have heard negative stories could provide some social protection by focusing on people who could be a threat. This could protect us from “liars and cheaters” because the brain spends more time lingering on their image, giving time to gather more information on their potentially threatening behavior.
Anderson E, Siegel EH, Bliss-Moreau E, Barrett LF. The Visual Impact of Gossip. Science. The Visual Impact of Gossip
Gossip is a form of affective information about who is friend and who is foe. We show that gossip does not impact only how a face is evaluated—it affects whether a face is seen in the first place. In two experiments, neutral faces were paired with negative, positive, or neutral gossip and were then presented alone in a binocular rivalry paradigm (faces were presented to one eye, houses to the other). In both studies, faces previously paired with negative (but not positive or neutral) gossip dominated longer in visual consciousness. These findings demonstrate that gossip, as a potent form of social affective learning, can influence vision in a completely top-down manner, independent of the basic structural features of a face.
Psychology Professor Lisa Feldman Barrett of the Northeastern University in Boston and her colleagues used binocular rivalry, a technique in which different images are shown to the subjects' left and right eyes. The brain becomes conscious of one of the images before registering the other, and the time taken for the image to be registered is a measure of the importance the brain gives the image. The importance is also indicated by the length of time the image remains in the conscious awareness, as the brain alternates between consciously registering the images of the face and house.
The 66 volunteers, all university students, were shown photographs of faces and given some information about the people. Information was either positive (such as the person helped an elderly lady), neutral (such as they passed a man in the street) or negative gossip, such as the person had thrown a chair at a fellow student. The students saw the pictures of the faces with one eye, but the other eye was shown an image of a house. The students pressed a keyboard key when they were conscious of seeing the face and another when they saw the house. Some of the photographs of faces had not previously been seen by the students and they had received no information about them.
The results showed that it took the students the same length of time to register seeing the unknown faces and those about which they had been told neutral or positive information, but the picture of the person about whom they had heard negative information registered around half a second quicker. The face with negative associations also registered for substantially longer periods of time than the neutral, positive or unknown faces.
A second experiment backed up the findings and also showed that subjects saw the faces linked to negative gossip for longer periods than faces about whom they had heard about upsetting personal experiences.
The results suggest that if you have recently heard negative gossip about someone you are more likely to notice them in a crowd. The researchers said gossip gives people information about whether a person might be a friend or foe, and suggest that being able to spot the face of a person about whom they have heard negative stories could provide some social protection by focusing on people who could be a threat. This could protect us from “liars and cheaters” because the brain spends more time lingering on their image, giving time to gather more information on their potentially threatening behavior.
Anderson E, Siegel EH, Bliss-Moreau E, Barrett LF. The Visual Impact of Gossip. Science. The Visual Impact of Gossip
Gossip is a form of affective information about who is friend and who is foe. We show that gossip does not impact only how a face is evaluated—it affects whether a face is seen in the first place. In two experiments, neutral faces were paired with negative, positive, or neutral gossip and were then presented alone in a binocular rivalry paradigm (faces were presented to one eye, houses to the other). In both studies, faces previously paired with negative (but not positive or neutral) gossip dominated longer in visual consciousness. These findings demonstrate that gossip, as a potent form of social affective learning, can influence vision in a completely top-down manner, independent of the basic structural features of a face.
Breaking the Rules to Rise to Power
When people have power, they act the part. Powerful people smile less, interrupt others, and speak in a louder voice. When people do not respect the basic rules of social behavior, they lead others to believe that they have power, according to a study in the current Social Psychological and Personality Science.
People with power have a very different experience of the world than people without it. The powerful have fewer rules to follow, and they live in environments of money, knowledge and support. People without power live with threats of punishment and firm limits according to the research team lead by Gerben Van Kleef of the University of Amsterdam. Because the powerful are freer to break the rules—does breaking the rules seem more powerful?
People read about a visitor to an office who took a cup of employee coffee without asking or about a bookkeeper that bent accounting rules. The rule breakers were seen as more in control, and powerful compared to people who didn't steal the coffee, or didn't break bookkeeping rules.
Acting rudely also leads people to see power. People who saw a video of a man at a sidewalk café put his feet on another chair, drop cigarette ashes on the ground and order a meal brusquely thought the man was more likely to "get to make decisions" and able to "get people to listen to what he says" than the people who saw a video of the same man behaving politely.
What happens when people interact with a rule breaker? Van Kleef and colleagues had people come to the lab, and interact with a rule follower and a rule breaker. The rule follower was polite and acted normally, while the rule breaker arrived late, threw down his bag on a table and put up his feet. After the interaction, people thought the rule breaker had more power and was more likely to "get others to do what he wants."
"Norm violators are perceived as having the capacity to act as they please" write the researchers. Power may be corrupting, but showing the outward signs of corruption makes people think you're powerful.
Van Kleef GA, Homan AC, Finkenauer C, Gundemir S, Stamkou E. Breaking the Rules to Rise to Power: How Norm Violators Gain Power in the Eyes of Others. Social Psychological and Personality Science. http://spp.sagepub.com/content/early/2011/01/20/1948550611398416.full.pdf
Powerful people often act at will, even if the resulting behavior is inappropriate—hence the famous proverb “power corrupts.” Here, we introduce the reverse phenomenon—violating norms signals power. Violating a norm implies that one has the power to act according to one’s own volition in spite of situational constraints, which fuels perceptions of power. Four studies support this hypothesis. Individuals who took coffee from another person’s can (Study 1), violated rules of bookkeeping (Study 2), dropped cigarette ashes on the floor (Study 3), or put their feet on the table (Study 4) were perceived as more powerful than individuals who did not show such behaviors. The effect was mediated by inferences of volitional capacity, and it replicated across different methods (scenario, film clip, face-to-face interaction), different norm violations, and different indices of power (explicit measures, expected emotions, and approach/inhibition tendencies). Implications for power, morality, and social hierarchy are discussed.
When people have power, they act the part. Powerful people smile less, interrupt others, and speak in a louder voice. When people do not respect the basic rules of social behavior, they lead others to believe that they have power, according to a study in the current Social Psychological and Personality Science.
People with power have a very different experience of the world than people without it. The powerful have fewer rules to follow, and they live in environments of money, knowledge and support. People without power live with threats of punishment and firm limits according to the research team lead by Gerben Van Kleef of the University of Amsterdam. Because the powerful are freer to break the rules—does breaking the rules seem more powerful?
People read about a visitor to an office who took a cup of employee coffee without asking or about a bookkeeper that bent accounting rules. The rule breakers were seen as more in control, and powerful compared to people who didn't steal the coffee, or didn't break bookkeeping rules.
Acting rudely also leads people to see power. People who saw a video of a man at a sidewalk café put his feet on another chair, drop cigarette ashes on the ground and order a meal brusquely thought the man was more likely to "get to make decisions" and able to "get people to listen to what he says" than the people who saw a video of the same man behaving politely.
What happens when people interact with a rule breaker? Van Kleef and colleagues had people come to the lab, and interact with a rule follower and a rule breaker. The rule follower was polite and acted normally, while the rule breaker arrived late, threw down his bag on a table and put up his feet. After the interaction, people thought the rule breaker had more power and was more likely to "get others to do what he wants."
"Norm violators are perceived as having the capacity to act as they please" write the researchers. Power may be corrupting, but showing the outward signs of corruption makes people think you're powerful.
Van Kleef GA, Homan AC, Finkenauer C, Gundemir S, Stamkou E. Breaking the Rules to Rise to Power: How Norm Violators Gain Power in the Eyes of Others. Social Psychological and Personality Science. http://spp.sagepub.com/content/early/2011/01/20/1948550611398416.full.pdf
Powerful people often act at will, even if the resulting behavior is inappropriate—hence the famous proverb “power corrupts.” Here, we introduce the reverse phenomenon—violating norms signals power. Violating a norm implies that one has the power to act according to one’s own volition in spite of situational constraints, which fuels perceptions of power. Four studies support this hypothesis. Individuals who took coffee from another person’s can (Study 1), violated rules of bookkeeping (Study 2), dropped cigarette ashes on the floor (Study 3), or put their feet on the table (Study 4) were perceived as more powerful than individuals who did not show such behaviors. The effect was mediated by inferences of volitional capacity, and it replicated across different methods (scenario, film clip, face-to-face interaction), different norm violations, and different indices of power (explicit measures, expected emotions, and approach/inhibition tendencies). Implications for power, morality, and social hierarchy are discussed.
NSAIDs for Athletes
2009
Abstract:
Sports medicine physicians often treat athletes in pain with non-steroidal anti-inflammatory drugs (NSAIDs). However, there is a lack of high- quality evidence to guide NSAID use. Their adverse effects have clinical relevance, and their possible negative consequences on the long-term healing process are slowly becoming more obvious. This article provides some practical management guidelines for the use of NSAIDs, developed to help sports medicine physicians deal with frequent sports-related injuries. We do not recommend their use for muscle injuries, bone fractures (also stress fractures) or chronic tendinopathy. In all cases, if chosen, NSAID treatments should always be kept as short as possible and should take into account the specific type of injury, the level of dysfunction and pain.
2009
Abstract:
Sports medicine physicians often treat athletes in pain with non-steroidal anti-inflammatory drugs (NSAIDs). However, there is a lack of high- quality evidence to guide NSAID use. Their adverse effects have clinical relevance, and their possible negative consequences on the long-term healing process are slowly becoming more obvious. This article provides some practical management guidelines for the use of NSAIDs, developed to help sports medicine physicians deal with frequent sports-related injuries. We do not recommend their use for muscle injuries, bone fractures (also stress fractures) or chronic tendinopathy. In all cases, if chosen, NSAID treatments should always be kept as short as possible and should take into account the specific type of injury, the level of dysfunction and pain.
Cell Phone Use May Reduce Male Fertility, Austrian-Canadian Study Suggests
Cell phone use may reduce male fertility, Austrian-Canadian study suggests
ScienceDaily (May 19, 2011) — Men who have been diagnosed with poor sperm quality and who are trying to have children should limit their cell phone use, a new study suggests. Researchers in Austria and Canada have found that while cell phone use appears to increase the level of testosterone circulating in the body, it may also lead to low sperm quality and a decrease in fertility.
"Our findings were a little bit puzzling," says Rany Shamloul, a postdoctoral fellow in the Department of Pharmacology and Toxicology at Queen's University in Canada and a co-author of the study. "We were expecting to find different results, but the results we did find suggest that there could be some intriguing mechanisms at work."
The research team at Queen's and at the Medical University of Graz, Austria, discovered that men who reported cell phone use had higher levels of circulating testosterone but they also had lower levels of luteinizing hormone (LH), an important reproductive hormone that is secreted by the pituitary gland in the brain.
The researchers hypothesize that electromagnetic waves (EMW) emitted by cell phones may have a dual action on male hormone levels and fertility. EMW may increase the number of cells in the testes that produce testosterone; however, by lowering the levels of LH excreted by the pituitary gland, EMW may also block the conversion of this basic circulating type of testosterone to the more active, potent form of testosterone associated with sperm production and fertility.
More in-depth research is needed to determine the exact ways in which EMW affects male fertility.
Gutschi T, Mohamad Al-Ali B, Shamloul R, Pummer K, Trummer H. Impact of cell phone use on men’s semen parameters. Andrologia. Impact of cell phone use on men’s semen parameters - Gutschi - 2011 - Andrologia - Wiley Online Library
The objective of the present retrospective study was to report our experience concerning the effects of cell phone usage on semen parameters. We examined 2110 men attending our infertility clinic from 1993 to October 2007. Semen analysis was performed in all patients. Serum free testosterone (T), follicle stimulating hormone (FSH), luteinising hormone (LH) and prolactin (PRL) were collected from all patients. The information on cell phone use of the patients was recorded and the subjects were divided into two groups according to their cell phone use: group A: cell phone use (n = 991); group B: no use (n = 1119).
Significant difference was observed in sperm morphology between the two groups. In the patients of group A, 68.0% of the spermatozoa featured a pathological morphology compared to only 58.1% in the subjects of group B. Patients with cell phone usage showed significantly higher T and lower LH levels than those who did not use cell phone. No significant difference between the two groups was observed regarding FSH and PRL values. Our results showed that cell phone use negatively affects sperm quality in men. Further studies with a careful design are needed to determine the effect of cell phone use on male fertility.
Cell phone use may reduce male fertility, Austrian-Canadian study suggests
ScienceDaily (May 19, 2011) — Men who have been diagnosed with poor sperm quality and who are trying to have children should limit their cell phone use, a new study suggests. Researchers in Austria and Canada have found that while cell phone use appears to increase the level of testosterone circulating in the body, it may also lead to low sperm quality and a decrease in fertility.
"Our findings were a little bit puzzling," says Rany Shamloul, a postdoctoral fellow in the Department of Pharmacology and Toxicology at Queen's University in Canada and a co-author of the study. "We were expecting to find different results, but the results we did find suggest that there could be some intriguing mechanisms at work."
The research team at Queen's and at the Medical University of Graz, Austria, discovered that men who reported cell phone use had higher levels of circulating testosterone but they also had lower levels of luteinizing hormone (LH), an important reproductive hormone that is secreted by the pituitary gland in the brain.
The researchers hypothesize that electromagnetic waves (EMW) emitted by cell phones may have a dual action on male hormone levels and fertility. EMW may increase the number of cells in the testes that produce testosterone; however, by lowering the levels of LH excreted by the pituitary gland, EMW may also block the conversion of this basic circulating type of testosterone to the more active, potent form of testosterone associated with sperm production and fertility.
More in-depth research is needed to determine the exact ways in which EMW affects male fertility.
Gutschi T, Mohamad Al-Ali B, Shamloul R, Pummer K, Trummer H. Impact of cell phone use on men’s semen parameters. Andrologia. Impact of cell phone use on men’s semen parameters - Gutschi - 2011 - Andrologia - Wiley Online Library
The objective of the present retrospective study was to report our experience concerning the effects of cell phone usage on semen parameters. We examined 2110 men attending our infertility clinic from 1993 to October 2007. Semen analysis was performed in all patients. Serum free testosterone (T), follicle stimulating hormone (FSH), luteinising hormone (LH) and prolactin (PRL) were collected from all patients. The information on cell phone use of the patients was recorded and the subjects were divided into two groups according to their cell phone use: group A: cell phone use (n = 991); group B: no use (n = 1119).
Significant difference was observed in sperm morphology between the two groups. In the patients of group A, 68.0% of the spermatozoa featured a pathological morphology compared to only 58.1% in the subjects of group B. Patients with cell phone usage showed significantly higher T and lower LH levels than those who did not use cell phone. No significant difference between the two groups was observed regarding FSH and PRL values. Our results showed that cell phone use negatively affects sperm quality in men. Further studies with a careful design are needed to determine the effect of cell phone use on male fertility.
The aim of this study was to evaluate in detail circulating Estradiol (E2) levels in a series of young men with Congenital Hypogonadotropic Hypogonadism (CHH) to identify a possible E2 deficiency. They also compared the effects of T enanthate, combined gonadotropin treatment, and dihydrotestosterone (DHT) administration on these patients’ E2 levels.
Trabado Sv, Maione L, Salenave S, et al. Estradiol levels in men with congenital hypogonadotropic hypogonadism and the effects of different modalities of hormonal treatment. Fertility and sterility 2011;95(7):2324-9.e3. http://www.fertstert.org/article/S0015-0282(11)00521-8/abstract (Elsevier)
Objective - To evaluate the degree of E2 deficiency in male congenital hypogonadotropic hypogonadism (CHH), and its response to different hormonal treatments.
Design - Retrospective and prospective studies.
Setting - Academic institution.
Patient(s) - Untreated or treated CHH, healthy men, untreated men with Klinefelter syndrome (KS).
Intervention(s) - Serum sex hormone-binding globulin (SHBG) and total E2 (TE2) as well as bioavailable (BE2) and free (FE2) levels were measured and determined.
Main Outcome Measure(s) - Total, bioavailable, and free testosterone, TE2, BE2, FE2 were compared in normal men, untreated and treated CHH and in untreated KS.
Result(s) - TE2, BE2, and FE2 levels were very significantly lower in untreated patients with CHH (n = 91) than in controls (n = 63) and in patients with KS (n = 45). The TE2 correlated positively with serum total T in patients with CHH. The TE2 also correlated very positively with serum LH in the combined population of patients with CHH and healthy men, suggesting that low E2 levels in CHH are due to severe LH-driven T deficiency. All fractions of circulating E2 were very significantly higher in patients with CHH receiving T enanthate (n = 101) or the FSH–hCG combination (n = 88) than in untreated patients with CHH. Contrary to dihydrotestosterone (DHT), both T enanthate and combined FSH-hCG therapy significantly and prospectively increased TE2 levels in patients with CHH.
Conclusion(s) - Contrary to KS, the male hypogonadism observed in CHH is associated with profound E2 deficiency, which can be overcome by aromatizable androgen or combined gonadotropin therapy.
Trabado Sv, Maione L, Salenave S, et al. Estradiol levels in men with congenital hypogonadotropic hypogonadism and the effects of different modalities of hormonal treatment. Fertility and sterility 2011;95(7):2324-9.e3. http://www.fertstert.org/article/S0015-0282(11)00521-8/abstract (Elsevier)
Objective - To evaluate the degree of E2 deficiency in male congenital hypogonadotropic hypogonadism (CHH), and its response to different hormonal treatments.
Design - Retrospective and prospective studies.
Setting - Academic institution.
Patient(s) - Untreated or treated CHH, healthy men, untreated men with Klinefelter syndrome (KS).
Intervention(s) - Serum sex hormone-binding globulin (SHBG) and total E2 (TE2) as well as bioavailable (BE2) and free (FE2) levels were measured and determined.
Main Outcome Measure(s) - Total, bioavailable, and free testosterone, TE2, BE2, FE2 were compared in normal men, untreated and treated CHH and in untreated KS.
Result(s) - TE2, BE2, and FE2 levels were very significantly lower in untreated patients with CHH (n = 91) than in controls (n = 63) and in patients with KS (n = 45). The TE2 correlated positively with serum total T in patients with CHH. The TE2 also correlated very positively with serum LH in the combined population of patients with CHH and healthy men, suggesting that low E2 levels in CHH are due to severe LH-driven T deficiency. All fractions of circulating E2 were very significantly higher in patients with CHH receiving T enanthate (n = 101) or the FSH–hCG combination (n = 88) than in untreated patients with CHH. Contrary to dihydrotestosterone (DHT), both T enanthate and combined FSH-hCG therapy significantly and prospectively increased TE2 levels in patients with CHH.
Conclusion(s) - Contrary to KS, the male hypogonadism observed in CHH is associated with profound E2 deficiency, which can be overcome by aromatizable androgen or combined gonadotropin therapy.
An Analysis Of Legal Highs
Researchers report here the analysis of legal highs purchased in the second half of 2010 from several Internet sites using a standard approach of Fourier Transform Infrared (FTIR) and gas chromatography-mass spectrometry (GC-MS) of methanol extracts. They were interested in the chemical composition of these products to test the previous findings that legal-high products are not always what they are advertised to be. They were also interested in seeing if these products are in fact illegal as reported in previous investigations; if so, suppliers and users would be committing an offence even if they were ignorant of this fact.
Seven samples were purchased online as legal highs and characterized by FTIR and GC-MS. The FTIR study revealed that 6 out of 7 samples did not contain the claimed drug but large quantities of caffeine. The presence of large amounts of caffeine was confirmed by GC-MS. Moreover, it was found that only one of the purchased samples contained MDAI as claimed. Five samples were a mixture of the controlled substances BZP and 3-TFMPP combined with caffeine. As BZP and 3-TFMPP are both controlled substances, users of these Internet products are in possession of illegal substances having purchased them assuming them to be legal. Another issue of concern, previously highlighted by others, is the lack of consistency between products of the same name. If purchasers use different suppliers for the same-named product, it is also highly likely that they could be using products with different active ingredients.
Baron M, Elie M, Elie L. An analysis of legal highs—do they contain what it says on the tin? Drug Testing and Analysis. An analysis of legal highs—do they contain what it says on the tin? - Baron - 2011 - Drug Testing and Analysis - Wiley Online Library
In recent years the availability of so-called legal highs over the Internet has hugely increased. Numerous online legal-high retailers market a broad variety of products which are advertised as research chemicals, bath salts, or plant food although clearly intended for human consumption as recreational drug replacements. No guidelines exist as to what is sold and in what purity. Consumers are led to believe that purchased goods are entirely legal.
In this study, several legal-high products were purchased and analyzed for their content. The powdered products were screened with attenuated total reflectance—Fourier Transform Infrared (ATR-FTIR) followed by gas chromatography-mass spectrometry (GC-MS) analysis of methanol extracts. Spectra were compared to reference standards and the NIST library.
Results showed that 6 out of 7 products did not contain the advertised active ingredient. Moreover, five samples contained the controlled substances benzylpiperazine and 1-[3-(trifluoromethyl)phenyl] piperazine combined with caffeine.
Researchers report here the analysis of legal highs purchased in the second half of 2010 from several Internet sites using a standard approach of Fourier Transform Infrared (FTIR) and gas chromatography-mass spectrometry (GC-MS) of methanol extracts. They were interested in the chemical composition of these products to test the previous findings that legal-high products are not always what they are advertised to be. They were also interested in seeing if these products are in fact illegal as reported in previous investigations; if so, suppliers and users would be committing an offence even if they were ignorant of this fact.
Seven samples were purchased online as legal highs and characterized by FTIR and GC-MS. The FTIR study revealed that 6 out of 7 samples did not contain the claimed drug but large quantities of caffeine. The presence of large amounts of caffeine was confirmed by GC-MS. Moreover, it was found that only one of the purchased samples contained MDAI as claimed. Five samples were a mixture of the controlled substances BZP and 3-TFMPP combined with caffeine. As BZP and 3-TFMPP are both controlled substances, users of these Internet products are in possession of illegal substances having purchased them assuming them to be legal. Another issue of concern, previously highlighted by others, is the lack of consistency between products of the same name. If purchasers use different suppliers for the same-named product, it is also highly likely that they could be using products with different active ingredients.
Baron M, Elie M, Elie L. An analysis of legal highs—do they contain what it says on the tin? Drug Testing and Analysis. An analysis of legal highs—do they contain what it says on the tin? - Baron - 2011 - Drug Testing and Analysis - Wiley Online Library
In recent years the availability of so-called legal highs over the Internet has hugely increased. Numerous online legal-high retailers market a broad variety of products which are advertised as research chemicals, bath salts, or plant food although clearly intended for human consumption as recreational drug replacements. No guidelines exist as to what is sold and in what purity. Consumers are led to believe that purchased goods are entirely legal.
In this study, several legal-high products were purchased and analyzed for their content. The powdered products were screened with attenuated total reflectance—Fourier Transform Infrared (ATR-FTIR) followed by gas chromatography-mass spectrometry (GC-MS) analysis of methanol extracts. Spectra were compared to reference standards and the NIST library.
Results showed that 6 out of 7 products did not contain the advertised active ingredient. Moreover, five samples contained the controlled substances benzylpiperazine and 1-[3-(trifluoromethyl)phenyl] piperazine combined with caffeine.
Over the Counter Supplements for the Treatment of Male Infertility
The purpose of this manuscript is to review OTC supplements readily available in the United States and the current Pub Med and Medline literature on their effects upon male fertility over the last 3 decades. They begin with a discussion on oxidative stress and antioxidants which appears to be the common pathway for the majority of OTC interventions. The supplements reviewed include Arginine, Carnitines, Co-Enzyme Q-10, Folic Acid, Glutathione, Lycopene, N-Acetylcysteine, Vitamins A, C, & E, Selenium, and Zinc.
Ko EY, Sabanegh ES, Jr. The Role of Over the Counter Supplements for the Treatment of Male Infertility - Fact or Fiction? J Androl. The Role of Over the Counter Supplements for the Treatment of Male Infertility - Fact or Fiction? -- Ko and Sabanegh, 10.2164/jandrol.111.013730 -- Journal of Andrology / The Role of Over the Counter Supplements for the Treatment of Male Infertility - Fact or Fiction? -- Ko and Sabanegh, 10.2164/jandrol.111.013730 -- Journal of Andrology
Introduction: Many over-the-counter (OTC) vitamins and supplements have been utilized for improving male fertility. The purpose of this study is to review the effects of these OTC supplements on male fertility.
Methods: A Pub Med and Medline review of the randomized controlled studies utilizing OTC vitamins and supplements readily available in the United States over the last 3 decades was performed.
Results: Many studies demonstrate the positive effects of OTC supplementation on semen parameters and pregnancy outcomes. Conversely, there are also many studies demonstrating a lack of improvement and potential complications with supplementation. Confounding factors include lack of standard dosing regimens, duration of treatment, and control for dietary intake.
Conclusion: There remains no standard to which OTC supplement and vitamin studies have been conducted or the medications dosed. Definitive conclusions as to their true effects on male subfertility and dosing regimen could not be identified.
The purpose of this manuscript is to review OTC supplements readily available in the United States and the current Pub Med and Medline literature on their effects upon male fertility over the last 3 decades. They begin with a discussion on oxidative stress and antioxidants which appears to be the common pathway for the majority of OTC interventions. The supplements reviewed include Arginine, Carnitines, Co-Enzyme Q-10, Folic Acid, Glutathione, Lycopene, N-Acetylcysteine, Vitamins A, C, & E, Selenium, and Zinc.
Ko EY, Sabanegh ES, Jr. The Role of Over the Counter Supplements for the Treatment of Male Infertility - Fact or Fiction? J Androl. The Role of Over the Counter Supplements for the Treatment of Male Infertility - Fact or Fiction? -- Ko and Sabanegh, 10.2164/jandrol.111.013730 -- Journal of Andrology / The Role of Over the Counter Supplements for the Treatment of Male Infertility - Fact or Fiction? -- Ko and Sabanegh, 10.2164/jandrol.111.013730 -- Journal of Andrology
Introduction: Many over-the-counter (OTC) vitamins and supplements have been utilized for improving male fertility. The purpose of this study is to review the effects of these OTC supplements on male fertility.
Methods: A Pub Med and Medline review of the randomized controlled studies utilizing OTC vitamins and supplements readily available in the United States over the last 3 decades was performed.
Results: Many studies demonstrate the positive effects of OTC supplementation on semen parameters and pregnancy outcomes. Conversely, there are also many studies demonstrating a lack of improvement and potential complications with supplementation. Confounding factors include lack of standard dosing regimens, duration of treatment, and control for dietary intake.
Conclusion: There remains no standard to which OTC supplement and vitamin studies have been conducted or the medications dosed. Definitive conclusions as to their true effects on male subfertility and dosing regimen could not be identified.
Physical Activity And Erectile Dysfunction In Middle-Aged Men: A Brief Review
Physical inactivity negatively impacts on erectile function, and experimental and clinical exercise interventions have been shown to improve sexual responses and overall cardiovascular health. Mediterranean-style diets and a reduction in caloric intake have been found to improve erectile function in men with the aspects of the metabolic syndrome. In addition, several studies have confirmed that combining the two interventions provides additional benefit to erectile function, likely via reduced metabolic disturbances (e.g., inflammatory markers, insulin resistance), decreased visceral adipose tissue, and improvement in vascular function (e.g., increased endothelial function).
There is now a wealth of sophisticated epidemiological evidence to demonstrate that physical activity (PhA) is associated with reduced risk of coronary heart disease, obesity, type 2 diabetes, and other chronic diseases and conditions. Causal relationships between PhA and cardiovascular disease, type 2 diabetes, colon cancer, and all-cause mortality have been recognized for some time. More recently, the pertinent issue has been the dose–response relationship between PhA and health: What is the minimum dose of activity associated with health and well-being? What doses of activity offer greater health benefits ?
A multidisciplinary approach might be relevant for the treatment of erectile dysfunction, in this context an adequate program of physical activity, especially when there are cardiovascular risk factors, could be very important; to this end, this review summarizes the major findings of the literature about a direct impact of the physical activity on the quality of erection and two of the main factors involved in erectile dysfunction: the endothelial dysfunction and androgen status. Another aim is to stimulate the reader to standardize effective and reproducible protocols of physical activity for clinical practice in this area, to combine with drugs and/or psychological treatment.
La Vignera S, Condorelli R, Vicari E, D'Agata R, Calogero A. Physical activity and erectile dysfunction in middle-aged men : a brief review. J Androl:jandrol.111.013649. Physical activity and erectile dysfunction in middle-aged men : a brief review -- La Vignera et al., 10.2164/jandrol.111.013649 -- Journal of Andrology / Physical activity and erectile dysfunction in middle-aged men : a brief review -- La Vignera et al., 10.2164/jandrol.111.013649 -- Journal of Andrology
The prevalence of erectile dysfunction is high in men of all ages and increases greatly in the elderly. In particular severity and prevalence both increase with aging. Since erectile dysfunction is a symptom, physicians should diagnose underlying pathologies that might lead to it instead of focusing only on finding a viable treatment. Physical inactivity negatively impacts on erectile function; experimental and clinical exercise interventions have been shown to improve sexual responses and overall cardiovascular health. Several studies have confirmed that combining the two interventions (mediterranean diet and physical activity) provides additional benefit to erectile function, likely via reduced metabolic disturbances (e.g., inflammatory markers, insulin resistance), decreased visceral adipose tissue, and improvement in vascular function (e.g., increased endothelial function).
This brief review shows the main clinical evidences on benefits induced by physical activity on erectile and endothelial dysfunction. The literature shows that erectile dysfunction in middle-aged men is often an early event in endothelial damage, and physical activity is able to improve both erectile and endothelial dysfunction. Conflicting data regarding the effects of exercise on the androgen status. In clinical practice would be recommended to add regular physical activity to balanced diet and drugs to achieve better therapeutic results.
Physical inactivity negatively impacts on erectile function, and experimental and clinical exercise interventions have been shown to improve sexual responses and overall cardiovascular health. Mediterranean-style diets and a reduction in caloric intake have been found to improve erectile function in men with the aspects of the metabolic syndrome. In addition, several studies have confirmed that combining the two interventions provides additional benefit to erectile function, likely via reduced metabolic disturbances (e.g., inflammatory markers, insulin resistance), decreased visceral adipose tissue, and improvement in vascular function (e.g., increased endothelial function).
There is now a wealth of sophisticated epidemiological evidence to demonstrate that physical activity (PhA) is associated with reduced risk of coronary heart disease, obesity, type 2 diabetes, and other chronic diseases and conditions. Causal relationships between PhA and cardiovascular disease, type 2 diabetes, colon cancer, and all-cause mortality have been recognized for some time. More recently, the pertinent issue has been the dose–response relationship between PhA and health: What is the minimum dose of activity associated with health and well-being? What doses of activity offer greater health benefits ?
A multidisciplinary approach might be relevant for the treatment of erectile dysfunction, in this context an adequate program of physical activity, especially when there are cardiovascular risk factors, could be very important; to this end, this review summarizes the major findings of the literature about a direct impact of the physical activity on the quality of erection and two of the main factors involved in erectile dysfunction: the endothelial dysfunction and androgen status. Another aim is to stimulate the reader to standardize effective and reproducible protocols of physical activity for clinical practice in this area, to combine with drugs and/or psychological treatment.
La Vignera S, Condorelli R, Vicari E, D'Agata R, Calogero A. Physical activity and erectile dysfunction in middle-aged men : a brief review. J Androl:jandrol.111.013649. Physical activity and erectile dysfunction in middle-aged men : a brief review -- La Vignera et al., 10.2164/jandrol.111.013649 -- Journal of Andrology / Physical activity and erectile dysfunction in middle-aged men : a brief review -- La Vignera et al., 10.2164/jandrol.111.013649 -- Journal of Andrology
The prevalence of erectile dysfunction is high in men of all ages and increases greatly in the elderly. In particular severity and prevalence both increase with aging. Since erectile dysfunction is a symptom, physicians should diagnose underlying pathologies that might lead to it instead of focusing only on finding a viable treatment. Physical inactivity negatively impacts on erectile function; experimental and clinical exercise interventions have been shown to improve sexual responses and overall cardiovascular health. Several studies have confirmed that combining the two interventions (mediterranean diet and physical activity) provides additional benefit to erectile function, likely via reduced metabolic disturbances (e.g., inflammatory markers, insulin resistance), decreased visceral adipose tissue, and improvement in vascular function (e.g., increased endothelial function).
This brief review shows the main clinical evidences on benefits induced by physical activity on erectile and endothelial dysfunction. The literature shows that erectile dysfunction in middle-aged men is often an early event in endothelial damage, and physical activity is able to improve both erectile and endothelial dysfunction. Conflicting data regarding the effects of exercise on the androgen status. In clinical practice would be recommended to add regular physical activity to balanced diet and drugs to achieve better therapeutic results.
Ethnic Variation In Allele Distribution of the Androgen Receptor (AR) (CAG)n Repeat
[This is one step towards an assay system that tests for bioactivity rather than a static hormone level.]
The human androgen receptor (AR) gene is located on chromosome Xq11.2-q12 and codes for a protein with three major functional domains: the N-terminal transactivation domain, DNA-binding domain, and androgen-binding domain. The protein functions as a steroid hormone activated transcription factor, which signals through classical and nonclassical signaling pathways. The AR gene contains a highly polymorphic (CAG)n repeat in exon 1 encoding a glutamine tract in the N-terminal transactivation domain of the protein, which becomes active only after AR binds to its ligand. The polyglutamine tract length is inversely correlated to the transcriptional competence of the receptor, with longer tracts being associated with lower levels of AR-mediated transcription in both normal and disease states.
AR (CAG)n repeats within the normal range (10-36 repeats) are associated with numerous endocrine cancers, male and female infertility, and many other neurological and endocrine conditions. There is a continuous relationship between AR (CAG)n repeat length and metabolic traits in Caucasian men, where repeat number correlates negatively with AR sensitivity and positively with body fat, insulin levels, and leptin in healthy and diabetic men. Additionally, testosterone and LH levels are higher in diabetic men with >24 repeats, reflecting reduced negative feedback through a less sensitive receptor. In women with Polycystic Ovary Syndrome (PCOS), a disorder diagnosed by hyperandrogenism, association between testosterone and insulin resistance may be modified by the (CAG)n repeat polymorphism. Therefore, ethnic differences in allele distributions of this marker could have far-reaching impact on diverse conditions in men and women.
Here, researchers report the allelic distribution of the (CAG)n polymorphism in Caucasian, Afro-Caribbean, Hispanic, and Thai populations from the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) cohort. To examine this they genotyped 14,833 mothers and neonates of these four ethnicities and tested for differences in allele distributions of the AR (CAG)n repeat.
Ackerman CM, Lowe LP, Lee H, et al. Ethnic Variation in Allele Distribution of the Androgen Receptor (AR) (CAG)n Repeat. J Androl:jandrol.111.013391. Ethnic Variation in Allele Distribution of the Androgen Receptor (AR) (CAG)n Repeat -- Ackerman et al., 10.2164/jandrol.111.013391 -- Journal of Andrology / Ethnic Variation in Allele Distribution of the Androgen Receptor (AR) (CAG)n Repeat -- Ackerman et al., 10.2164/jandrol.111.013391 -- Journal of Andrology
The androgen receptor (AR) is important in reproductive organ development, as well as tissue homeostasis of the pancreas, liver and skeletal muscle in adulthood. The trinucleotide (CAG)n repeat polymorphism in exon 1 of the AR gene is thought to regulate AR activity, with longer alleles conferring reduced receptor activity. Therefore, the evaluation of the allelic distribution of the AR (CAG)n repeat in various ethnic groups is crucial in understanding the interindividual variability in AR activity.
We evaluated ethnic variation of this AR polymorphism by genotyping individuals from the multi-ethnic Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study cohort. We genotyped 4421 Caucasian mothers and 3365 offspring of European ancestry, 1494 Thai mothers and 1742 offspring, 1119 Afro-Caribbean mothers and 1142 offspring; and 780 Hispanic mothers and 770 offspring of Mexican ancestry from Bellflower, CA, USA.
The distributions of (CAG)n alleles among all four ethnic groups are significantly different (p < 0.0001). Pairwise tests confirmed significant differences between each pair of ethnicities tested (p < 10-28). The relative AR (CAG)n repeat length in the different groups was as follows: Afro-Caribbean (shortest repeat lengths and greatest predicted AR activity) < Caucasian < Hispanic < Thai (longest repeat length and lowest predicted AR activity). Significant interethnic differences in the allele frequencies of the AR exon 1 (CAG)n polymorphism exist.
Our results suggest that there may be potential ethnic differences in androgenic pathway activity and androgen sensitivity.
[This is one step towards an assay system that tests for bioactivity rather than a static hormone level.]
The human androgen receptor (AR) gene is located on chromosome Xq11.2-q12 and codes for a protein with three major functional domains: the N-terminal transactivation domain, DNA-binding domain, and androgen-binding domain. The protein functions as a steroid hormone activated transcription factor, which signals through classical and nonclassical signaling pathways. The AR gene contains a highly polymorphic (CAG)n repeat in exon 1 encoding a glutamine tract in the N-terminal transactivation domain of the protein, which becomes active only after AR binds to its ligand. The polyglutamine tract length is inversely correlated to the transcriptional competence of the receptor, with longer tracts being associated with lower levels of AR-mediated transcription in both normal and disease states.
AR (CAG)n repeats within the normal range (10-36 repeats) are associated with numerous endocrine cancers, male and female infertility, and many other neurological and endocrine conditions. There is a continuous relationship between AR (CAG)n repeat length and metabolic traits in Caucasian men, where repeat number correlates negatively with AR sensitivity and positively with body fat, insulin levels, and leptin in healthy and diabetic men. Additionally, testosterone and LH levels are higher in diabetic men with >24 repeats, reflecting reduced negative feedback through a less sensitive receptor. In women with Polycystic Ovary Syndrome (PCOS), a disorder diagnosed by hyperandrogenism, association between testosterone and insulin resistance may be modified by the (CAG)n repeat polymorphism. Therefore, ethnic differences in allele distributions of this marker could have far-reaching impact on diverse conditions in men and women.
Here, researchers report the allelic distribution of the (CAG)n polymorphism in Caucasian, Afro-Caribbean, Hispanic, and Thai populations from the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) cohort. To examine this they genotyped 14,833 mothers and neonates of these four ethnicities and tested for differences in allele distributions of the AR (CAG)n repeat.
Ackerman CM, Lowe LP, Lee H, et al. Ethnic Variation in Allele Distribution of the Androgen Receptor (AR) (CAG)n Repeat. J Androl:jandrol.111.013391. Ethnic Variation in Allele Distribution of the Androgen Receptor (AR) (CAG)n Repeat -- Ackerman et al., 10.2164/jandrol.111.013391 -- Journal of Andrology / Ethnic Variation in Allele Distribution of the Androgen Receptor (AR) (CAG)n Repeat -- Ackerman et al., 10.2164/jandrol.111.013391 -- Journal of Andrology
The androgen receptor (AR) is important in reproductive organ development, as well as tissue homeostasis of the pancreas, liver and skeletal muscle in adulthood. The trinucleotide (CAG)n repeat polymorphism in exon 1 of the AR gene is thought to regulate AR activity, with longer alleles conferring reduced receptor activity. Therefore, the evaluation of the allelic distribution of the AR (CAG)n repeat in various ethnic groups is crucial in understanding the interindividual variability in AR activity.
We evaluated ethnic variation of this AR polymorphism by genotyping individuals from the multi-ethnic Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study cohort. We genotyped 4421 Caucasian mothers and 3365 offspring of European ancestry, 1494 Thai mothers and 1742 offspring, 1119 Afro-Caribbean mothers and 1142 offspring; and 780 Hispanic mothers and 770 offspring of Mexican ancestry from Bellflower, CA, USA.
The distributions of (CAG)n alleles among all four ethnic groups are significantly different (p < 0.0001). Pairwise tests confirmed significant differences between each pair of ethnicities tested (p < 10-28). The relative AR (CAG)n repeat length in the different groups was as follows: Afro-Caribbean (shortest repeat lengths and greatest predicted AR activity) < Caucasian < Hispanic < Thai (longest repeat length and lowest predicted AR activity). Significant interethnic differences in the allele frequencies of the AR exon 1 (CAG)n polymorphism exist.
Our results suggest that there may be potential ethnic differences in androgenic pathway activity and androgen sensitivity.
International Web Survey Shows High Prevalence Of Symptomatic Testosterone Deficiency
There is increasing recognition among doctors that testosterone deficiency is a common and important condition. As well as the key symptoms of loss of energy, drive, libido and impaired erectile function, there is often depression, memory loss and increased irritability which can impair work, home and social life.
An even more important point is that not only are there strong theoretical and epidemiological links to these disorders, but testosterone treatment has also been shown to be effective in the prevention and treatment of many of them, especially diseases linked with the recent epidemic of obesity such as metabolic syndrome, Type 2 diabetes and coronary heart disease. Also many of the conditions seen in aging populations world-wide which lead to frailty and disability can be prevented by such treatment, making it an effective form of preventive medicine. In view of these benefits, it was decided to undertake a web-based survey of the prevalence of symptomatic testosterone deficiency.
Trinick TR, Feneley MR, Welford H, Carruthers M. International web survey shows high prevalence of symptomatic testosterone deficiency in men. Aging Male 2011;14(1):10-5. International web survey shows high prevalence of symptomatic testosterone deficiency in men
INTRODUCTION: Though the clinical significance of testosterone deficiency is becoming increasingly apparent, its prevalence in the general population remains unrecognised. A large web-based survey was undertaken over 3 years to study the scale of this missed diagnosis.
METHODS: An online questionnaire giving the symptoms characterising testosterone deficiency syndrome (Aging Male Symptoms-AMS-scale) was set up on three web sites, together with questions about possible contributory factors.
RESULTS: Of over 10,000 men, mainly from the UK and USA, who responded, 80% had moderate or severe scores likely to benefit from testosterone replacement therapy (TRT). The average age was 52, but with many in their 40s when the diagnosis of 'late onset hypogonadism' is not generally considered. Other possible contributory factors to the high testosterone deficiency scores reported were obesity (29%), alcohol (17.3%), testicular problems such as mumps orchitis (11.4%), prostate problems (5.6%), urinary infection (5.2%) and diabetes 5.7%.
CONCLUSIONS: In this self-selected large international sample of men, there was a very high prevalence of scores which if clinically relevant would warrant a therapeutic trial of testosterone treatment. This study suggests that there are large numbers of men in the community whose testosterone deficiency is neither being diagnosed nor treated.
There is increasing recognition among doctors that testosterone deficiency is a common and important condition. As well as the key symptoms of loss of energy, drive, libido and impaired erectile function, there is often depression, memory loss and increased irritability which can impair work, home and social life.
An even more important point is that not only are there strong theoretical and epidemiological links to these disorders, but testosterone treatment has also been shown to be effective in the prevention and treatment of many of them, especially diseases linked with the recent epidemic of obesity such as metabolic syndrome, Type 2 diabetes and coronary heart disease. Also many of the conditions seen in aging populations world-wide which lead to frailty and disability can be prevented by such treatment, making it an effective form of preventive medicine. In view of these benefits, it was decided to undertake a web-based survey of the prevalence of symptomatic testosterone deficiency.
Trinick TR, Feneley MR, Welford H, Carruthers M. International web survey shows high prevalence of symptomatic testosterone deficiency in men. Aging Male 2011;14(1):10-5. International web survey shows high prevalence of symptomatic testosterone deficiency in men
INTRODUCTION: Though the clinical significance of testosterone deficiency is becoming increasingly apparent, its prevalence in the general population remains unrecognised. A large web-based survey was undertaken over 3 years to study the scale of this missed diagnosis.
METHODS: An online questionnaire giving the symptoms characterising testosterone deficiency syndrome (Aging Male Symptoms-AMS-scale) was set up on three web sites, together with questions about possible contributory factors.
RESULTS: Of over 10,000 men, mainly from the UK and USA, who responded, 80% had moderate or severe scores likely to benefit from testosterone replacement therapy (TRT). The average age was 52, but with many in their 40s when the diagnosis of 'late onset hypogonadism' is not generally considered. Other possible contributory factors to the high testosterone deficiency scores reported were obesity (29%), alcohol (17.3%), testicular problems such as mumps orchitis (11.4%), prostate problems (5.6%), urinary infection (5.2%) and diabetes 5.7%.
CONCLUSIONS: In this self-selected large international sample of men, there was a very high prevalence of scores which if clinically relevant would warrant a therapeutic trial of testosterone treatment. This study suggests that there are large numbers of men in the community whose testosterone deficiency is neither being diagnosed nor treated.
The Endocrine Effects Of Oral Opioid Therapy
[OPioid-Induced Androgen Deficiency (OPIAD)]
With the increased use of opioids for the management of chronic pain, there is growing need to recognize and treat associated sex hormone deficiencies. Perhaps, increased vigilance on the part of physicians and the early initiation of treatment for opioid-related hypogonadism may lead to decreased associated adverse consequences of long-term opioid use such as osteoporosis and depression. Patients should be educated about the symptoms of hypogonadism, and appropriate evaluation of these symptoms by the physician should be routinely undertaken. Management of opioid associated hypogonadism may involve testosterone replacement therapy, and follow-up for potentially serious side effects of these treatments is necessary. When opioid-associated hypogonadism is identified and properly managed, complications such as depression and osteoporosis may be minimized, with the additional potential benefits of enhanced analgesia and reduced opioid requirements. Additional prospective trials in this area are required to further establish opioid dosing thresholds that may predispose patients to hypogonadism. Studies to evaluate the effect of androgen replacement on opioid consumption in chronic pain patients suffering from hypogonadism during opioid therapy are also needed.
Elliott JA, Horton E, Fibuch EE. The endocrine effects of long-term oral opioid therapy: a case report and review of the literature. J Opioid Manag 2011;7(2):145-54. The endocrine effects of long-term oral opioid the... [J Opioid Manag. 2011 Mar-Apr] - PubMed result
The negative effects of long-term opioid administration on the body's endocrine system have been known for decades. These effects have been observed and studied with the use of intrathecal opioids and in heroin addicts. However, they have also been noted to occur with the use of oral opioids, especially in those patients who require chronic opioids for the management of nonmalignant and cancer-associated pain. Epidemiologic data in recent years suggest that up to five million men with chronic nonmalignant pain suffer from opioid-induced androgen deficiency (OPIAD) in the United States. Therefore, it is important to understand the physiologic impact of chronic opioid administration in patients. In view of the increasing use of opioids for chronic pain, we must anticipate the potential occurrence of hypogonadism during chronic opioid therapy and monitor patients accordingly. If symptoms of endocrine dysfunction are recognized during chronic opioid therapy, appropriate evaluation, treatment, and follow-up should be instituted. This article describes a case report of a patient who suffered from a clinically significant testosterone deficiency and osteoporosis related to the use of long-term oral opioids for chronic nonmalignant pain. It also includes a review of the existing literature regarding OPIAD and provides recommendations regarding the evaluation and management of OPIAD.
[OPioid-Induced Androgen Deficiency (OPIAD)]
With the increased use of opioids for the management of chronic pain, there is growing need to recognize and treat associated sex hormone deficiencies. Perhaps, increased vigilance on the part of physicians and the early initiation of treatment for opioid-related hypogonadism may lead to decreased associated adverse consequences of long-term opioid use such as osteoporosis and depression. Patients should be educated about the symptoms of hypogonadism, and appropriate evaluation of these symptoms by the physician should be routinely undertaken. Management of opioid associated hypogonadism may involve testosterone replacement therapy, and follow-up for potentially serious side effects of these treatments is necessary. When opioid-associated hypogonadism is identified and properly managed, complications such as depression and osteoporosis may be minimized, with the additional potential benefits of enhanced analgesia and reduced opioid requirements. Additional prospective trials in this area are required to further establish opioid dosing thresholds that may predispose patients to hypogonadism. Studies to evaluate the effect of androgen replacement on opioid consumption in chronic pain patients suffering from hypogonadism during opioid therapy are also needed.
Elliott JA, Horton E, Fibuch EE. The endocrine effects of long-term oral opioid therapy: a case report and review of the literature. J Opioid Manag 2011;7(2):145-54. The endocrine effects of long-term oral opioid the... [J Opioid Manag. 2011 Mar-Apr] - PubMed result
The negative effects of long-term opioid administration on the body's endocrine system have been known for decades. These effects have been observed and studied with the use of intrathecal opioids and in heroin addicts. However, they have also been noted to occur with the use of oral opioids, especially in those patients who require chronic opioids for the management of nonmalignant and cancer-associated pain. Epidemiologic data in recent years suggest that up to five million men with chronic nonmalignant pain suffer from opioid-induced androgen deficiency (OPIAD) in the United States. Therefore, it is important to understand the physiologic impact of chronic opioid administration in patients. In view of the increasing use of opioids for chronic pain, we must anticipate the potential occurrence of hypogonadism during chronic opioid therapy and monitor patients accordingly. If symptoms of endocrine dysfunction are recognized during chronic opioid therapy, appropriate evaluation, treatment, and follow-up should be instituted. This article describes a case report of a patient who suffered from a clinically significant testosterone deficiency and osteoporosis related to the use of long-term oral opioids for chronic nonmalignant pain. It also includes a review of the existing literature regarding OPIAD and provides recommendations regarding the evaluation and management of OPIAD.
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This is Your Brain on Violent Video Games
Violent Video Games Reduce Brain Response to Violence and Increase Aggressive Behavior, Study Suggests
Violent video games reduce brain response to violence and increase aggressive behavior, study suggests
ScienceDaily (May 25, 2011) — Scientists have known for years that playing violent video games causes players to become more aggressive. The findings of a new University of Missouri (MU) study provide one explanation for why this occurs: the brains of violent video game players become less responsive to violence, and this diminished brain response predicts an increase in aggression.
"Many researchers have believed that becoming desensitized to violence leads to increased human aggression. Until our study, however, this causal association had never been demonstrated experimentally," said Bruce Bartholow, associate professor of psychology in the MU College of Arts and Science.
During the study, 70 young adult participants were randomly assigned to play either a nonviolent or a violent video game for 25 minutes. Immediately afterwards, the researchers measured brain responses as participants viewed a series of neutral photos, such as a man on a bike, and violent photos, such as a man holding a gun in another man's mouth. Finally, participants competed against an opponent in a task that allowed them to give their opponent a controllable blast of loud noise. The level of noise blast the participants set for their opponent was the measure of aggression.
The researchers found that participants who played one of several popular violent games, such as "Call of Duty," "Hitman," "Killzone" and "Grand Theft Auto," set louder noise blasts for their opponents during the competitive task -- that is, they were more aggressive -- than participants who played a nonviolent game. In addition, for participants that had not played many violent video games before completing the study, playing a violent game in the lab caused a reduced brain response to the photos of violence -- an indicator of desensitization. Moreover, this reduced brain response predicted participants' aggression levels: the smaller the brain response to violent photos, the more aggressive participants were. Participants who had already spent a lot of time playing violent video games before the study showed small brain response to the violent photos, regardless of which type of game they played in the lab.
"The fact that video game exposure did not affect the brain activity of participants who already had been highly exposed to violent games is interesting and suggests a number of possibilities," Bartholow said. "It could be that those individuals are already so desensitized to violence from habitually playing violent video games that an additional exposure in the lab has very little effect on their brain responses. There also could be an unmeasured factor that causes both a preference for violent video games and a smaller brain response to violence. In either case, there are additional measures to consider."
Bartholow said that future research should focus on ways to moderate media violence effects, especially among individuals who are habitually exposed. He cites surveys that indicate that the average elementary school child spends more than 40 hours a week playing video games -- more than any other activity besides sleeping. As young children spend more time with video games than any other forms of media, the researchers say children could become accustomed to violent behavior as their brains are forming.
"More than any other media, these video games encourage active participation in violence," said Bartholow. "From a psychological perspective, video games are excellent teaching tools because they reward players for engaging in certain types of behavior. Unfortunately, in many popular video games, the behavior is violence."
Engelhardt CR, Bartholow BD, Kerr GT, Bushman BJ. This is your brain on violent video games: Neural desensitization to violence predicts increased aggression following violent video game exposure. Journal of Experimental Social Psychology;In Press, Corrected Proof. http://socialcogneurolab.missouri.edu/pdfs/CRE_BDB_GTK_BJB_inpress_JESP.pdf
Previous research has shown that media violence exposure can cause desensitization to violence, which in theory can increase aggression. However, no study to date has demonstrated this association. In the present experiment, participants played a violent or nonviolent video game, viewed violent and nonviolent photos while their brain activity was measured, and then gave an ostensible opponent unpleasant noise blasts. Participants low in previous exposure to video game violence who played a violent (relative to a nonviolent) game showed a reduction in the P3 component of the event-related brain potential (ERP) to violent images (indicating physiological desensitization), and this brain response mediated the effect of video game content on subsequent aggressive behavior. These data provide the first experimental evidence linking violence desensitization with increased aggression, and show that a neural marker of this process can at least partially account for the causal link between violent game exposure and aggression.
Violent Video Games Reduce Brain Response to Violence and Increase Aggressive Behavior, Study Suggests
Violent video games reduce brain response to violence and increase aggressive behavior, study suggests
ScienceDaily (May 25, 2011) — Scientists have known for years that playing violent video games causes players to become more aggressive. The findings of a new University of Missouri (MU) study provide one explanation for why this occurs: the brains of violent video game players become less responsive to violence, and this diminished brain response predicts an increase in aggression.
"Many researchers have believed that becoming desensitized to violence leads to increased human aggression. Until our study, however, this causal association had never been demonstrated experimentally," said Bruce Bartholow, associate professor of psychology in the MU College of Arts and Science.
During the study, 70 young adult participants were randomly assigned to play either a nonviolent or a violent video game for 25 minutes. Immediately afterwards, the researchers measured brain responses as participants viewed a series of neutral photos, such as a man on a bike, and violent photos, such as a man holding a gun in another man's mouth. Finally, participants competed against an opponent in a task that allowed them to give their opponent a controllable blast of loud noise. The level of noise blast the participants set for their opponent was the measure of aggression.
The researchers found that participants who played one of several popular violent games, such as "Call of Duty," "Hitman," "Killzone" and "Grand Theft Auto," set louder noise blasts for their opponents during the competitive task -- that is, they were more aggressive -- than participants who played a nonviolent game. In addition, for participants that had not played many violent video games before completing the study, playing a violent game in the lab caused a reduced brain response to the photos of violence -- an indicator of desensitization. Moreover, this reduced brain response predicted participants' aggression levels: the smaller the brain response to violent photos, the more aggressive participants were. Participants who had already spent a lot of time playing violent video games before the study showed small brain response to the violent photos, regardless of which type of game they played in the lab.
"The fact that video game exposure did not affect the brain activity of participants who already had been highly exposed to violent games is interesting and suggests a number of possibilities," Bartholow said. "It could be that those individuals are already so desensitized to violence from habitually playing violent video games that an additional exposure in the lab has very little effect on their brain responses. There also could be an unmeasured factor that causes both a preference for violent video games and a smaller brain response to violence. In either case, there are additional measures to consider."
Bartholow said that future research should focus on ways to moderate media violence effects, especially among individuals who are habitually exposed. He cites surveys that indicate that the average elementary school child spends more than 40 hours a week playing video games -- more than any other activity besides sleeping. As young children spend more time with video games than any other forms of media, the researchers say children could become accustomed to violent behavior as their brains are forming.
"More than any other media, these video games encourage active participation in violence," said Bartholow. "From a psychological perspective, video games are excellent teaching tools because they reward players for engaging in certain types of behavior. Unfortunately, in many popular video games, the behavior is violence."
Engelhardt CR, Bartholow BD, Kerr GT, Bushman BJ. This is your brain on violent video games: Neural desensitization to violence predicts increased aggression following violent video game exposure. Journal of Experimental Social Psychology;In Press, Corrected Proof. http://socialcogneurolab.missouri.edu/pdfs/CRE_BDB_GTK_BJB_inpress_JESP.pdf
Previous research has shown that media violence exposure can cause desensitization to violence, which in theory can increase aggression. However, no study to date has demonstrated this association. In the present experiment, participants played a violent or nonviolent video game, viewed violent and nonviolent photos while their brain activity was measured, and then gave an ostensible opponent unpleasant noise blasts. Participants low in previous exposure to video game violence who played a violent (relative to a nonviolent) game showed a reduction in the P3 component of the event-related brain potential (ERP) to violent images (indicating physiological desensitization), and this brain response mediated the effect of video game content on subsequent aggressive behavior. These data provide the first experimental evidence linking violence desensitization with increased aggression, and show that a neural marker of this process can at least partially account for the causal link between violent game exposure and aggression.
Growth Hormone Induced Insulin Resistance Is Rapidly Reversible
The first evidence that GH has insulin-antagonistic effects was published in 1936, when B. A. Houssay reported that hypophysectomized dogs become hypoglycemic, whereas an excess of anterior pituitary lobe increased insulin resistance. Subsequent studies with human pituitary GH extracts showed that injection of large amounts of GH in human subjects stimulates lipolysis and causes hyperglycemia. Additionally, studies where GH was perfused locally via the brachial artery demonstrated that GH acutely inhibits insulin-stimulated muscle glucose uptake in normal postabsorptive subjects. During physiological conditions, insulin is activated in response to a meal and becomes suppressed with fasting, whereas the reciprocal pattern is observed regarding GH.
By contrast, patients with active acromegaly exhibit sustained elevations in GH levels including the postprandial period, which causes pronounced insulin resistance. This phenomenon may also apply to GH treatment in patients with GH deficiency (GHD). The standard regimen is daily sc injections at bedtime, which to some extent imitates the nocturnal secretion of GH, but a small sustained elevation in GH prevails during the subsequent daytime period. Indeed, this mode of GH administration induces significant insulin resistance in skeletal muscle in normal subjects as well as in GHD adults. It is, however, noteworthy that insulin sensitivity in these studies was assessed in the morning approximately 12 h after the last sc GH injection when serum GH levels have not returned to baseline level. Experimental studies in healthy subjects exposed to iv GH infusion for 1 hour in different doses demonstrate that insulin resistance assessed by the hyperinsulinemic glucose clamp peaks after 2 h and subsides 4–7 h after termination of the GH infusion. A comparable temporal pattern was observed as regards the suppressive effect of a GH pulse on forearm glucose uptake after an overnight fast.
It remains to be investigated whether GH-induced insulin resistance depends on the timing of GH exposure relative to the time point where insulin sensitivity is assessed. Such data are clinically important and will provide insight into the physiological effects of GH.
In the present study, researchers tested the hypothesis that insulin resistance in skeletal muscle induced by exogenous GH in GHD adults is rapidly reversible. They observed significant insulin resistance when GH infusion was continued into the first part of the clamp and increased insulin sensitivity when GH was not administered, whereas discontinuation of GH infusion 5 h before the clamp resulted in identical insulin sensitivity to healthy untreated control subjects. These differences in insulin sensitivity were preceded by distinctive differences in the patterns of circulating FFA reflecting the acute lipolytic effects of GH.
Krusenstjerna-Hafstrom T, Clasen BF, Moller N, et al. Growth Hormone (GH)-Induced Insulin Resistance Is Rapidly Reversible: An Experimental Study in GH-Deficient Adults. Journal of Clinical Endocrinology & Metabolism. http://jcem.endojournals.org/content/early/2011/05/19/jc.2011-0273.abstract (Growth Hormone (GH)-Induced Insulin Resistance Is Rapidly Reversible: An Experimental Study in GH-Deficient Adults)
Context: It is clinically relevant and of physiological interest to investigate whether GH-induced insulin resistance depends on the timing of GH exposure relative to when insulin sensitivity is assessed.
Hypothesis: GH-induced insulin resistance is rapidly reversible.
Design and Participants: Eight male GH-deficient patients underwent a 6-h euglycemic-hyperinsulinemic glucose clamp thrice in a randomized crossover design receiving either no GH (study 0), a 7-h GH infusion (0.2–0.3 mg in total) that terminated 5 h before the clamp (study 1), or a similar GH infusion timed to continue during the first hour of the clamp (study 2). A muscle biopsy was obtained 30 min into the clamp. The patients were compared with eight healthy untreated control subjects (study c).
Main Outcome Measures: The glucose infusion rate, indirect calorimetry, and free fatty acid metabolism were assessed. In muscle biopsies, protein phosphorylation of signal transducer and activator of transcription 5, Akt, and Akt substrate 160 (phospho-Akt substrate signal) and gene expression of IGF-I and SOCS1-3 were assessed.
Results: Insulin sensitivity differed significantly between the GH-deficiency studies (P = 0.005) with distinct insulin resistance in study 2 and increased insulin sensitivity in study 0 [area under the glucose infusion rate curve (mg/kg • min): 1663 ± 151 (study 0) vs. 1482 ± 166 (study 1) vs.1123 ± 136 (study 2) vs. 1492 ± 229 (control group)]. Free fatty acid levels and lipid oxidation were elevated in response to GH exposure but became suppressed during the clamp. IGF-I andSOCS3 gene expression was increased in study 2.
Conclusions: Very-low-dose GH exposure evokes acute insulin resistance that subsides after 5 h. This time-dependent reversibility should be considered when assessing the impact of GH on glucose homeostasis.
The first evidence that GH has insulin-antagonistic effects was published in 1936, when B. A. Houssay reported that hypophysectomized dogs become hypoglycemic, whereas an excess of anterior pituitary lobe increased insulin resistance. Subsequent studies with human pituitary GH extracts showed that injection of large amounts of GH in human subjects stimulates lipolysis and causes hyperglycemia. Additionally, studies where GH was perfused locally via the brachial artery demonstrated that GH acutely inhibits insulin-stimulated muscle glucose uptake in normal postabsorptive subjects. During physiological conditions, insulin is activated in response to a meal and becomes suppressed with fasting, whereas the reciprocal pattern is observed regarding GH.
By contrast, patients with active acromegaly exhibit sustained elevations in GH levels including the postprandial period, which causes pronounced insulin resistance. This phenomenon may also apply to GH treatment in patients with GH deficiency (GHD). The standard regimen is daily sc injections at bedtime, which to some extent imitates the nocturnal secretion of GH, but a small sustained elevation in GH prevails during the subsequent daytime period. Indeed, this mode of GH administration induces significant insulin resistance in skeletal muscle in normal subjects as well as in GHD adults. It is, however, noteworthy that insulin sensitivity in these studies was assessed in the morning approximately 12 h after the last sc GH injection when serum GH levels have not returned to baseline level. Experimental studies in healthy subjects exposed to iv GH infusion for 1 hour in different doses demonstrate that insulin resistance assessed by the hyperinsulinemic glucose clamp peaks after 2 h and subsides 4–7 h after termination of the GH infusion. A comparable temporal pattern was observed as regards the suppressive effect of a GH pulse on forearm glucose uptake after an overnight fast.
It remains to be investigated whether GH-induced insulin resistance depends on the timing of GH exposure relative to the time point where insulin sensitivity is assessed. Such data are clinically important and will provide insight into the physiological effects of GH.
In the present study, researchers tested the hypothesis that insulin resistance in skeletal muscle induced by exogenous GH in GHD adults is rapidly reversible. They observed significant insulin resistance when GH infusion was continued into the first part of the clamp and increased insulin sensitivity when GH was not administered, whereas discontinuation of GH infusion 5 h before the clamp resulted in identical insulin sensitivity to healthy untreated control subjects. These differences in insulin sensitivity were preceded by distinctive differences in the patterns of circulating FFA reflecting the acute lipolytic effects of GH.
Krusenstjerna-Hafstrom T, Clasen BF, Moller N, et al. Growth Hormone (GH)-Induced Insulin Resistance Is Rapidly Reversible: An Experimental Study in GH-Deficient Adults. Journal of Clinical Endocrinology & Metabolism. http://jcem.endojournals.org/content/early/2011/05/19/jc.2011-0273.abstract (Growth Hormone (GH)-Induced Insulin Resistance Is Rapidly Reversible: An Experimental Study in GH-Deficient Adults)
Context: It is clinically relevant and of physiological interest to investigate whether GH-induced insulin resistance depends on the timing of GH exposure relative to when insulin sensitivity is assessed.
Hypothesis: GH-induced insulin resistance is rapidly reversible.
Design and Participants: Eight male GH-deficient patients underwent a 6-h euglycemic-hyperinsulinemic glucose clamp thrice in a randomized crossover design receiving either no GH (study 0), a 7-h GH infusion (0.2–0.3 mg in total) that terminated 5 h before the clamp (study 1), or a similar GH infusion timed to continue during the first hour of the clamp (study 2). A muscle biopsy was obtained 30 min into the clamp. The patients were compared with eight healthy untreated control subjects (study c).
Main Outcome Measures: The glucose infusion rate, indirect calorimetry, and free fatty acid metabolism were assessed. In muscle biopsies, protein phosphorylation of signal transducer and activator of transcription 5, Akt, and Akt substrate 160 (phospho-Akt substrate signal) and gene expression of IGF-I and SOCS1-3 were assessed.
Results: Insulin sensitivity differed significantly between the GH-deficiency studies (P = 0.005) with distinct insulin resistance in study 2 and increased insulin sensitivity in study 0 [area under the glucose infusion rate curve (mg/kg • min): 1663 ± 151 (study 0) vs. 1482 ± 166 (study 1) vs.1123 ± 136 (study 2) vs. 1492 ± 229 (control group)]. Free fatty acid levels and lipid oxidation were elevated in response to GH exposure but became suppressed during the clamp. IGF-I andSOCS3 gene expression was increased in study 2.
Conclusions: Very-low-dose GH exposure evokes acute insulin resistance that subsides after 5 h. This time-dependent reversibility should be considered when assessing the impact of GH on glucose homeostasis.
Sleep Apnea, Reproductive Hormones, and Quality of Sexual Life in Severely Obese Men
Obesity is associated with multiple negative health outcomes including increased risk for diabetes, cardiovascular disorders, and reduced life expectancy. Obesity in men is also shown to be associated with reduced reproductive potential. Obese men have lower total and free testosterone levels and report diminished sexual quality of life. Multiple and interacting mechanisms are responsible for the alteration in reproductive hormones and sexual function in men. Among these is increased aromatization of the C19 androgens to estradiol, increased central opioid tone that suppresses the hypothalamic pituitary axis and hyperinsulinemia that lowers sex hormone binding protein levels. In addition, anatomic features of obesity result in increased scrotal temperature and sleep apnea that can independently affect reproductive physiology. Male sex and obesity are known risk factors for sleep apnea. Some studies suggest that sleep apnea may have an independent association with reduced testosterone, sexual dysfunction, and impotence. However, these studies either had small number of participants or studied the hormonal or sexual response separately. Other studies show weak or lack of association between sleep apnea and reproductive hormone levels and sexual function after correction for BMI, or showed correlation with some but not all sleep apnea parameters.
The independent effect of sleep apnea on testosterone levels and male sexual function needs further clarification. The objective of this study is to describe the relation between sleep apnea, testosterone levels, and male sexual quality of life in 89 severely obese men. An adequate understanding of this relation, independent of weight, can help the conceptualization and validation of the results of studies that would look at the effect of correction of sleep apnea on serum testosterone and sexual function in men.
This study showed that increased severity of sleep apnea is associated with lower free testosterone levels independent of age and BMI. Correcting for BMI allowed us to control for other obesity-associated factors that can result in low testosterone levels such as estradiol levels, hyperinsulinemia, central hypothalamic suppression, and increased scrotal temperature. Moreover, the study showed that all measures of sleep apnea showed a negative correlation with free testosterone including RDI, mean SpO2, percent time below a SpO2 of 90%, and percent time below a SpO2 of 80%. In this population of severely obese men, the quality of sexual life was severely reduced in correlation with BMI and coronary artery disease. Sleep apnea was also associated with reduced quality of sexual life. However, the severity of sleep apnea did not seem to reduce an already low quality of sexual life.
In this study, arterial blood gases were not part of patients’ evaluation. This did not allow the assessment of the prevalence of the obesity hypoventilation syndrome. This syndrome has been associated with more advanced metabolic abnormalities when present in association with obstructive sleep apnea. The effect of obesity hypoventilation syndrome on hormonal parameters and quality of sexual life scores could not be evaluated.
Hammoud AO, Walker JM, Gibson M, et al. Sleep Apnea, Reproductive Hormones and Quality of Sexual Life in Severely Obese Men. Obesity 2011;19(6):1118-23. Obesity - Abstract of article: Sleep Apnea, Reproductive Hormones and Quality of Sexual Life in Severely Obese Men
The effect of sleep apnea on the reproductive function of obese men is not entirely elucidated. The objective of this study was to define the effect of sleep apnea on the reproductive hormones and sexual function in obese men. This study included 89 severely obese men with BMI ?35 kg/m2 considering gastric bypass surgery. Anthropometrics (weight, and BMI), reproductive hormones, and sleep studies were measured. The sexual quality of life was assessed using the Impact of Weight on Quality of Life-Lite questionnaire (IWQOL-Lite). The mean age of our patients was 46.9 ± 11.0 years, the mean BMI was 47.8 ± 8.7 kg/m2 and the mean weight was 337.7 ± 62.4 lb.
After correction for age and BMI, means of free testosterone per severity group of sleep apnea were as follows: no or mild sleep apnea 74.4 ± 3.8 pg/ml, moderate sleep apnea 68.6 ± 4.2 pg/ml, and severe sleep apnea 60.2 ± 2.92 pg/ml, P = 0.014. All other parameters of sleep apnea including hypopnea index, percent time below a SpO2 of 90%, and percent time below a SpO2 of 80% were also negatively correlated with testosterone levels after correction for age and BMI. BMI and presence of coronary artery disease decreased the sexual quality of life. Sleep apnea was associated with reduced sexual quality of life.
In summary, sleep apnea negatively affects testosterone levels independent of BMI. Severely obese men had decreased sexual quality of life.
Obesity is associated with multiple negative health outcomes including increased risk for diabetes, cardiovascular disorders, and reduced life expectancy. Obesity in men is also shown to be associated with reduced reproductive potential. Obese men have lower total and free testosterone levels and report diminished sexual quality of life. Multiple and interacting mechanisms are responsible for the alteration in reproductive hormones and sexual function in men. Among these is increased aromatization of the C19 androgens to estradiol, increased central opioid tone that suppresses the hypothalamic pituitary axis and hyperinsulinemia that lowers sex hormone binding protein levels. In addition, anatomic features of obesity result in increased scrotal temperature and sleep apnea that can independently affect reproductive physiology. Male sex and obesity are known risk factors for sleep apnea. Some studies suggest that sleep apnea may have an independent association with reduced testosterone, sexual dysfunction, and impotence. However, these studies either had small number of participants or studied the hormonal or sexual response separately. Other studies show weak or lack of association between sleep apnea and reproductive hormone levels and sexual function after correction for BMI, or showed correlation with some but not all sleep apnea parameters.
The independent effect of sleep apnea on testosterone levels and male sexual function needs further clarification. The objective of this study is to describe the relation between sleep apnea, testosterone levels, and male sexual quality of life in 89 severely obese men. An adequate understanding of this relation, independent of weight, can help the conceptualization and validation of the results of studies that would look at the effect of correction of sleep apnea on serum testosterone and sexual function in men.
This study showed that increased severity of sleep apnea is associated with lower free testosterone levels independent of age and BMI. Correcting for BMI allowed us to control for other obesity-associated factors that can result in low testosterone levels such as estradiol levels, hyperinsulinemia, central hypothalamic suppression, and increased scrotal temperature. Moreover, the study showed that all measures of sleep apnea showed a negative correlation with free testosterone including RDI, mean SpO2, percent time below a SpO2 of 90%, and percent time below a SpO2 of 80%. In this population of severely obese men, the quality of sexual life was severely reduced in correlation with BMI and coronary artery disease. Sleep apnea was also associated with reduced quality of sexual life. However, the severity of sleep apnea did not seem to reduce an already low quality of sexual life.
In this study, arterial blood gases were not part of patients’ evaluation. This did not allow the assessment of the prevalence of the obesity hypoventilation syndrome. This syndrome has been associated with more advanced metabolic abnormalities when present in association with obstructive sleep apnea. The effect of obesity hypoventilation syndrome on hormonal parameters and quality of sexual life scores could not be evaluated.
Hammoud AO, Walker JM, Gibson M, et al. Sleep Apnea, Reproductive Hormones and Quality of Sexual Life in Severely Obese Men. Obesity 2011;19(6):1118-23. Obesity - Abstract of article: Sleep Apnea, Reproductive Hormones and Quality of Sexual Life in Severely Obese Men
The effect of sleep apnea on the reproductive function of obese men is not entirely elucidated. The objective of this study was to define the effect of sleep apnea on the reproductive hormones and sexual function in obese men. This study included 89 severely obese men with BMI ?35 kg/m2 considering gastric bypass surgery. Anthropometrics (weight, and BMI), reproductive hormones, and sleep studies were measured. The sexual quality of life was assessed using the Impact of Weight on Quality of Life-Lite questionnaire (IWQOL-Lite). The mean age of our patients was 46.9 ± 11.0 years, the mean BMI was 47.8 ± 8.7 kg/m2 and the mean weight was 337.7 ± 62.4 lb.
After correction for age and BMI, means of free testosterone per severity group of sleep apnea were as follows: no or mild sleep apnea 74.4 ± 3.8 pg/ml, moderate sleep apnea 68.6 ± 4.2 pg/ml, and severe sleep apnea 60.2 ± 2.92 pg/ml, P = 0.014. All other parameters of sleep apnea including hypopnea index, percent time below a SpO2 of 90%, and percent time below a SpO2 of 80% were also negatively correlated with testosterone levels after correction for age and BMI. BMI and presence of coronary artery disease decreased the sexual quality of life. Sleep apnea was associated with reduced sexual quality of life.
In summary, sleep apnea negatively affects testosterone levels independent of BMI. Severely obese men had decreased sexual quality of life.
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