As a number of as 20% of adolescents from 11 to 17 years of age smoke. This was the result of the nationwide German Health Interview and Examination Survey for Children and Adolescents (KiGGS), performed by the Robert Koch Institute and presented by the sociologist Thomas Lampert in the current edition of Deutsches rzteblatt International (Dtsch Arztebl Int 2008; 105[15]: 265-71).
The analysis of tobacco consumption by children and adolescents covered almost 7,000 girls and boys aged 11 to 17. Data on the current smoking status and on exposure to passive smoking were collected for the years 2003 to 2006. Possible factors influencing the findings were examined, including the social status of the family, the type of school attended by the adolescents, and the smoking status of parents and friends.
Thomas Lampert's study shows that friends and the type of school have greater influence on smoking behavior than the parents do. The probability that an adolescent starts smoking is markedly greater when his or her friends smoke. The risk is hardly increased if the parents smoke. Conversely, students at general secondary schools (Hauptschule), intermediate schools (Realschule) or comprehensive schools (Gesamtschule) smoke much more frequently than do pupils at high school (Gymnasium).
Sunday, June 15, 2008
Thursday, May 15, 2008
Vitamin D Deficiency Makes Breast Cancer More Deadly
Women with low levels of vitamin D when they’re diagnosed with breast cancer are more likely to die from the disease than those who have higher levels of the vitamin, doctors are reporting.
The finding — part of a growing body of evidence that connects vitamin D to several types of cancer — was just published, ahead of the upcoming American Society of Clinical Oncology conference. It was based on a University of Toronto study of 512 women diagnosed with breast cancer between 1989 and 1995. Researchers kept track of the women’s health through 2006.
Vitamin D levels were broken into three categories: “deficient” (192 of the women were in this group) “insufficient” (197 women) and “sufficient” (124 women). (Even among healthy women, high rates of vitamin D deficiency are common.)
Those with deficient levels were 73% more likely to die than those with sufficient levels. Cancer was also significantly more likely to spread to other parts of the body in women with vitamin D deficiency, the researchers found.
Previous studies have connected low vitamin D levels with higher risk of colon, prostate and breast cancer, as well as higher mortality from the cancers, according to this NEJM article.
The link is still poorly understood, but vitamin D may bind with cancer cells and slow the growth of cells or cause them to die.
Sunlight is an important source of vitamin D. Some foods, such oily fish, are also sources, as are dietary supplements. For more on vitamin D in foods and supplements, along with info on recommended daily intake by age and gender, see this page from the NIH.
The finding — part of a growing body of evidence that connects vitamin D to several types of cancer — was just published, ahead of the upcoming American Society of Clinical Oncology conference. It was based on a University of Toronto study of 512 women diagnosed with breast cancer between 1989 and 1995. Researchers kept track of the women’s health through 2006.
Vitamin D levels were broken into three categories: “deficient” (192 of the women were in this group) “insufficient” (197 women) and “sufficient” (124 women). (Even among healthy women, high rates of vitamin D deficiency are common.)
Those with deficient levels were 73% more likely to die than those with sufficient levels. Cancer was also significantly more likely to spread to other parts of the body in women with vitamin D deficiency, the researchers found.
Previous studies have connected low vitamin D levels with higher risk of colon, prostate and breast cancer, as well as higher mortality from the cancers, according to this NEJM article.
The link is still poorly understood, but vitamin D may bind with cancer cells and slow the growth of cells or cause them to die.
Sunlight is an important source of vitamin D. Some foods, such oily fish, are also sources, as are dietary supplements. For more on vitamin D in foods and supplements, along with info on recommended daily intake by age and gender, see this page from the NIH.
Sunday, May 11, 2008
How body size is regulated?
Researchers are beginning to unravel the question why people distinctly vary in size. In cooperation with researchers of the Helmholtz Zentrum Muenchen, an international genome-wide study has discovered ten new genes that influence body height and thus provides new insights into biological pathways that are important for human growth.
This meta-analysis, reported in the latest issue of Nature Genetics, is based on data from more than 26,000 study participants. It verifies two already known genes, but also discovered ten new genes. Altogether they explain a difference in body size of about 3.5 centimeters.
The analysis produced some biologically insightful findings. Several of the identified genes are targeted by the microRNA let-7, which affects the regulation of other genes. This connection was completely unknown until now. Several other SNPs may affect the structure of chromatin, the chromosome-surrounding proteins. Moreover, the results could have relevance for patients with inherited growth problems, or with problems in bone development, because some of the newly discovered genes have rare mutations, known to be linked to anomalous skeletal growth. Further functional studies are necessary to completely elucidate the biological mechanisms behind this growing list of genes correlation to height.
As German contribution to the meta-analysis, data from about 5,600 participants of the KORA study were analyzed by the HelmholtzZentrum scientists, Dr. Christian Gieger, Dr. Susana Eyheramendy, PD Dr. Thomas Illig, Dr. Iris M. Heid and Prof. Dr. Dr. H.-Erich Wichmann. In order to genotype 500,000 of the most frequent variants in the human genome, DNA chips were analyzed at the Institute for Human Genetics and the Institute of Epidemiology of the Helmholtz Zentrum Muenchen under the direction of Prof. Dr. Thomas Meitinger. The coordinator of the study was Dr. Guillaume Lettre; Prof. Joel Hirschhorn acted as the principal investigator. Both researchers work at the Broad Institute of the MIT and the Harvard University, Cambridge. All researchers are part of the recently formed international consortium to study height and obesity-related traits (GIANT, Genetic Investigation of ANthropometric Traits).
Along with the results of a British study that was published simultaneously in Nature Genetics, the total number of known "height genes" now amounts to 26.
Source.
This meta-analysis, reported in the latest issue of Nature Genetics, is based on data from more than 26,000 study participants. It verifies two already known genes, but also discovered ten new genes. Altogether they explain a difference in body size of about 3.5 centimeters.
The analysis produced some biologically insightful findings. Several of the identified genes are targeted by the microRNA let-7, which affects the regulation of other genes. This connection was completely unknown until now. Several other SNPs may affect the structure of chromatin, the chromosome-surrounding proteins. Moreover, the results could have relevance for patients with inherited growth problems, or with problems in bone development, because some of the newly discovered genes have rare mutations, known to be linked to anomalous skeletal growth. Further functional studies are necessary to completely elucidate the biological mechanisms behind this growing list of genes correlation to height.
As German contribution to the meta-analysis, data from about 5,600 participants of the KORA study were analyzed by the HelmholtzZentrum scientists, Dr. Christian Gieger, Dr. Susana Eyheramendy, PD Dr. Thomas Illig, Dr. Iris M. Heid and Prof. Dr. Dr. H.-Erich Wichmann. In order to genotype 500,000 of the most frequent variants in the human genome, DNA chips were analyzed at the Institute for Human Genetics and the Institute of Epidemiology of the Helmholtz Zentrum Muenchen under the direction of Prof. Dr. Thomas Meitinger. The coordinator of the study was Dr. Guillaume Lettre; Prof. Joel Hirschhorn acted as the principal investigator. Both researchers work at the Broad Institute of the MIT and the Harvard University, Cambridge. All researchers are part of the recently formed international consortium to study height and obesity-related traits (GIANT, Genetic Investigation of ANthropometric Traits).
Along with the results of a British study that was published simultaneously in Nature Genetics, the total number of known "height genes" now amounts to 26.
Source.
Tuesday, April 29, 2008
How Neurons Generate Movement
When the eye tracks a bird's flight across the sky, the visual experience is normally smooth, without interruption. But underlying this behavior is a complex coordination of neurons that has remained mysterious to scientists. Now, UCSF scientists have broken ground in understanding how the brain generates this tracking motion, a finding that offers a window, they say, into how neurons orchestrate all of the body's movements.
The study, published in the April 24 issue of Neuron, reveals that individual neurons do not fire independently across the entire duration of a motor function as traditionally thought. Rather, they coordinate their activity with other neurons, each firing at a particular moment in time.
"Researchers have known that neurons that connect to muscles initiate movement in a coordinated fashion. But they have not known how the neurons we are studying - which coordinate these front-line neurons -- commit the brain to move the eyes,"says co-lead author David Schoppik, PhD, who conducted the study while a doctoral candidate in the laboratory of senior author Stephen Lisberger, PhD, at the University of California, San Francisco.
"For decades, researchers have been asking, 'Do the signals involve a handful of neurons or thousands? What is the nature of the commands?' The classical understanding has been that one class of neuron is responsible for one movement, such as generating eye movement to the left, and that it remains active across the entire duration of a behavior," he says.
"The new findings suggest a totally different way of looking at how movement is controlled across time," says Lisberger, a Howard Hughes Medical Institute Investigator at UCSF, where he is professor of physiology, director of the W.M. Keck Foundation Center for Integrative Neuroscience, and co-director of the Sloan Center for Theoretical Neurobiology.
The findings, the scientists say, could inform efforts to develop neural prosthetics to treat paralysis and motor dysfunctions, such as those resulting from stroke. "The brain's messages don't reach the muscles in these conditions," says Schoppik, "so it's critical that the drive to these prosthetics reflect what the brain is trying to do to move muscles. Understanding how multiple neurons work together could influence the type of software created to drive these devices".
The investigation of how neurons give rise to motor behaviorshas been stymied until now, says Schoppik, by the difficulties inherent in studying more than one neuron in action at a time during the course of a behavior. In the current study, the researchers overcame this obstacle in a study of macaque monkeys that had been trained to track a moving object with their eyes.
Basing their approach on two key pieces of information -- first, that when a neuron responds to a stimulus there is always a slight variation in its performance, a phenomenon that neuroresearchers traditionally refer to as "noise," and, second, that each attempt of the eye to pursue a moving target is also unique - they proposed that some aspects of neural variation may reflect behavioral variation.
They used this inherent variability as a probe. Using a formula from financial securities market analysis that looks at how individual stocks behave at a given time within the context of fluctuations in the larger financial market, they explored how individual neurons would behave relative to their neighbors.
They compared the deviations from the average spiking activity of single neurons and simultaneous deviations from the mean eye velocity. They also measured the degree to which variation shared across two pairs of concurrently active neurons.
The data demonstrated that individual neurons encode different aspects of behavior, controlling eye velocity fluctuations at particular moments during the course of eye movement, while the population of neurons collectively tiles the entire duration of the movement.
The analysis also revealed the strength of correlations in the eye movement predictions derived from pairs of simultaneously recorded neurons, and suggests, the researcher say, either that a small number of neurons are sufficient to drive the behavior at any given time or that a number of neurons operate collectively at each moment.
The finding, says Lisberger, underscores the importance of recording for more than one neuron at a time. "There is a lot that we can learn from how multiple neurons interact."
Source
The study, published in the April 24 issue of Neuron, reveals that individual neurons do not fire independently across the entire duration of a motor function as traditionally thought. Rather, they coordinate their activity with other neurons, each firing at a particular moment in time.
"Researchers have known that neurons that connect to muscles initiate movement in a coordinated fashion. But they have not known how the neurons we are studying - which coordinate these front-line neurons -- commit the brain to move the eyes,"says co-lead author David Schoppik, PhD, who conducted the study while a doctoral candidate in the laboratory of senior author Stephen Lisberger, PhD, at the University of California, San Francisco.
"For decades, researchers have been asking, 'Do the signals involve a handful of neurons or thousands? What is the nature of the commands?' The classical understanding has been that one class of neuron is responsible for one movement, such as generating eye movement to the left, and that it remains active across the entire duration of a behavior," he says.
"The new findings suggest a totally different way of looking at how movement is controlled across time," says Lisberger, a Howard Hughes Medical Institute Investigator at UCSF, where he is professor of physiology, director of the W.M. Keck Foundation Center for Integrative Neuroscience, and co-director of the Sloan Center for Theoretical Neurobiology.
The findings, the scientists say, could inform efforts to develop neural prosthetics to treat paralysis and motor dysfunctions, such as those resulting from stroke. "The brain's messages don't reach the muscles in these conditions," says Schoppik, "so it's critical that the drive to these prosthetics reflect what the brain is trying to do to move muscles. Understanding how multiple neurons work together could influence the type of software created to drive these devices".
The investigation of how neurons give rise to motor behaviorshas been stymied until now, says Schoppik, by the difficulties inherent in studying more than one neuron in action at a time during the course of a behavior. In the current study, the researchers overcame this obstacle in a study of macaque monkeys that had been trained to track a moving object with their eyes.
Basing their approach on two key pieces of information -- first, that when a neuron responds to a stimulus there is always a slight variation in its performance, a phenomenon that neuroresearchers traditionally refer to as "noise," and, second, that each attempt of the eye to pursue a moving target is also unique - they proposed that some aspects of neural variation may reflect behavioral variation.
They used this inherent variability as a probe. Using a formula from financial securities market analysis that looks at how individual stocks behave at a given time within the context of fluctuations in the larger financial market, they explored how individual neurons would behave relative to their neighbors.
They compared the deviations from the average spiking activity of single neurons and simultaneous deviations from the mean eye velocity. They also measured the degree to which variation shared across two pairs of concurrently active neurons.
The data demonstrated that individual neurons encode different aspects of behavior, controlling eye velocity fluctuations at particular moments during the course of eye movement, while the population of neurons collectively tiles the entire duration of the movement.
The analysis also revealed the strength of correlations in the eye movement predictions derived from pairs of simultaneously recorded neurons, and suggests, the researcher say, either that a small number of neurons are sufficient to drive the behavior at any given time or that a number of neurons operate collectively at each moment.
The finding, says Lisberger, underscores the importance of recording for more than one neuron at a time. "There is a lot that we can learn from how multiple neurons interact."
Source
Thursday, January 31, 2008
New Treatment Target for Asthma
An enzyme released by mast cells in the lungs appears to play a key role in the tightening of airways that is a hallmark of asthma - pointing to a potential new target for therapy against the illness.
Reporting in the online edition of Proceedings of the National Academy of Sciences, a team at Weill Cornell Medical College explains that during an immune response, mast cells release the enzyme - called renin - which in turn produces angiotensin, a potent constrictor of the smooth muscle that lines airways.
Mast cells are normally present in small numbers in all organs, and are best known for their role in allergy, shock, wound healing and defense against pathogens.
"Back in 2005, our team was the first to discover that mast cells in the heart released renin locally, which elicited heart arrhythmias by triggering angiotensin production within the heart," explained co-senior author Dr. Roberto Levi, professor of pharmacology at Weill Cornell Medical College.
"Now, we've expanded those findings to the lungs, where similar mechanisms appear to work locally to help trigger constriction in the airway," he says.
Renin is no stranger to medical research - for decades, doctors have known that the enzyme is produced by the kidney in relatively large quantities for systemic use throughout the body. But the Weill Cornell team was the first to discover that mast cells also produced their own "local" supply of the enzyme, at a variety of body sites.
"In the heart and now the lungs, this localized production of renin appears to have a profound effect on nearby tissues," says co-senior author Dr. Randi Silver, associate professor of physiology and biophysics at Weill Cornell.
"More study is needed, of course, but our finding suggests that drugs that target renin might prove effective agents in dampening asthma or other respiratory diseases," she says. "These types of 'renin inhibitors' are, in fact, currently being developed by the pharmaceutical industry right now".
The genesis of the new study came through the efforts of the study's lead author, Arul Veerappan, now a postdoctoral researcher in Dr. Silver's laboratory. He looked closely at rings of bronchial tissue from rodents, discovering that mast cells in these rings released renin along with other substances.
"You ended up getting the same biochemical cascade that we had seen elsewhere - newly produced renin bringing about a local rise in angiotensin in tissues," Veerappan says.
Research led by co-author Alicia Reid, also a postdoctoral associate in Dr. Silver's lab, led to another first. Using a technology Reid developed, the scientists confirmed for the first time that mast cells from human lung tissue release a form of renin that is nearly identical to renin found in human mast cells grown in culture or human kidney renin.
"That's a big achievement, because it supports the notion that the mechanism we have discovered is not just a laboratory phenomenon - it's actually occurring in the living human lung," Dr. Levi notes.
New research suggests that local renin production may also be crucial in diseases marked by tissue fibrosis (stiffening). In fact, Dr. Silver's lab is now looking at the role locally produced renin might play in a rare, deadly illness called idiopathic pulmonary fibrosis (IPF), where lung tissue becomes increasingly inflexible over time.
"We're interested in any disease in which we can also detect local renin/angiotensin production because it appears to be associated with fibrosis, vasoconstriction, and now bronchoconstriction," Dr. Silver explains.
The goal of all this research: new therapy targets for a range of illnesses.
"Of course, we already have antihypertensive medicines - such as ACE inhibitors and angiotensin receptor blockers -- that focus on curbing angiotensin in a more systemic way," says Dr. Levi. "But if we could find agents that dampen this renin-angiotensin cascade locally - in the heart or the lung, for example - that could prove to be a formidable new weapon against disease".
This work was funded by grants from the U.S. National Institutes of Health.
Source.
Reporting in the online edition of Proceedings of the National Academy of Sciences, a team at Weill Cornell Medical College explains that during an immune response, mast cells release the enzyme - called renin - which in turn produces angiotensin, a potent constrictor of the smooth muscle that lines airways.
Mast cells are normally present in small numbers in all organs, and are best known for their role in allergy, shock, wound healing and defense against pathogens.
"Back in 2005, our team was the first to discover that mast cells in the heart released renin locally, which elicited heart arrhythmias by triggering angiotensin production within the heart," explained co-senior author Dr. Roberto Levi, professor of pharmacology at Weill Cornell Medical College.
"Now, we've expanded those findings to the lungs, where similar mechanisms appear to work locally to help trigger constriction in the airway," he says.
Renin is no stranger to medical research - for decades, doctors have known that the enzyme is produced by the kidney in relatively large quantities for systemic use throughout the body. But the Weill Cornell team was the first to discover that mast cells also produced their own "local" supply of the enzyme, at a variety of body sites.
"In the heart and now the lungs, this localized production of renin appears to have a profound effect on nearby tissues," says co-senior author Dr. Randi Silver, associate professor of physiology and biophysics at Weill Cornell.
"More study is needed, of course, but our finding suggests that drugs that target renin might prove effective agents in dampening asthma or other respiratory diseases," she says. "These types of 'renin inhibitors' are, in fact, currently being developed by the pharmaceutical industry right now".
The genesis of the new study came through the efforts of the study's lead author, Arul Veerappan, now a postdoctoral researcher in Dr. Silver's laboratory. He looked closely at rings of bronchial tissue from rodents, discovering that mast cells in these rings released renin along with other substances.
"You ended up getting the same biochemical cascade that we had seen elsewhere - newly produced renin bringing about a local rise in angiotensin in tissues," Veerappan says.
Research led by co-author Alicia Reid, also a postdoctoral associate in Dr. Silver's lab, led to another first. Using a technology Reid developed, the scientists confirmed for the first time that mast cells from human lung tissue release a form of renin that is nearly identical to renin found in human mast cells grown in culture or human kidney renin.
"That's a big achievement, because it supports the notion that the mechanism we have discovered is not just a laboratory phenomenon - it's actually occurring in the living human lung," Dr. Levi notes.
New research suggests that local renin production may also be crucial in diseases marked by tissue fibrosis (stiffening). In fact, Dr. Silver's lab is now looking at the role locally produced renin might play in a rare, deadly illness called idiopathic pulmonary fibrosis (IPF), where lung tissue becomes increasingly inflexible over time.
"We're interested in any disease in which we can also detect local renin/angiotensin production because it appears to be associated with fibrosis, vasoconstriction, and now bronchoconstriction," Dr. Silver explains.
The goal of all this research: new therapy targets for a range of illnesses.
"Of course, we already have antihypertensive medicines - such as ACE inhibitors and angiotensin receptor blockers -- that focus on curbing angiotensin in a more systemic way," says Dr. Levi. "But if we could find agents that dampen this renin-angiotensin cascade locally - in the heart or the lung, for example - that could prove to be a formidable new weapon against disease".
This work was funded by grants from the U.S. National Institutes of Health.
Source.
Monday, December 31, 2007
LASIK works well in highly myopic patients
Laser surgery to correct vision problems has been in use since the early part of 1990s. Photorefractive Keratotomy (PRK) is typically used to correct low to moderate myopia, while laser in-situ keratomileusis (LASIK) is preferred for high myopia corrections. Eventhough over 18 million LASIK procedures have been performed worldwide, there is still some controversy regarding the maximum correction possible and efficacy with this technique. In an article reported in the January 2008 issue of the American Journal of Ophthalmology, scientists from Miguel Hernandez University, Medical School, Alicante, Spain; and Ankara University School of Medicine, Ankara, Turkey; report on a study of high myopia patients ten years after LASIK surgery. The findings show that LASIK for myopia over -10 D is a safe and effective procedure in the long-term.
196 high myopic eyes of 118 patients, preoperatively needing at least 10 diopter (10 D) corrections to achieve 20/20 vision, were reviewed ten years following surgery. Uncorrected vision was 77% of best-corrected vision (BSCVA) before surgery. BSCVA improved 1 line. Only 5% of eyes lost more than 2 lines of BSCVA and 40% avoided the use of glasses. 119 (61 %) of eyes were within 2.00 Diopters at 10 years. Only 2 eyes (1%) developed corneal ectasia. The retreatment rate was 27%.
As per lead investigator Jorge L. Ali, These results are extremely encouraging considering that this refractive correction implies the maximum limit of application of this technique. This study has allowed us to demonstrate that, in spite of the prejudices about the limits of LASIK technique, the results regarding predictability, efficacy and safety for high myopic patients are very good in the long term. The optimum limit of predictability for this technique is around 10 D of myopia. This reference study, with a long time perspective, allows us to know the safety, precision and limits of LASIK in highly myopic eyes.
Source from:Medicine World.
196 high myopic eyes of 118 patients, preoperatively needing at least 10 diopter (10 D) corrections to achieve 20/20 vision, were reviewed ten years following surgery. Uncorrected vision was 77% of best-corrected vision (BSCVA) before surgery. BSCVA improved 1 line. Only 5% of eyes lost more than 2 lines of BSCVA and 40% avoided the use of glasses. 119 (61 %) of eyes were within 2.00 Diopters at 10 years. Only 2 eyes (1%) developed corneal ectasia. The retreatment rate was 27%.
As per lead investigator Jorge L. Ali, These results are extremely encouraging considering that this refractive correction implies the maximum limit of application of this technique. This study has allowed us to demonstrate that, in spite of the prejudices about the limits of LASIK technique, the results regarding predictability, efficacy and safety for high myopic patients are very good in the long term. The optimum limit of predictability for this technique is around 10 D of myopia. This reference study, with a long time perspective, allows us to know the safety, precision and limits of LASIK in highly myopic eyes.
Source from:Medicine World.
Thursday, July 26, 2007
Why are doctors so unhappy?
Doctors are unhappy. They are not all unhappy all the time, but when doctors gather, their conversation turns to misery and talk of early retirement. The unhappiness has been illustrated in a plethora of surveys and manifests itself in talk of a mass resignation by general practitioners from the NHS.The British government is rattled by the unhappiness of doctors, recognising that a health service staffed by demoralised doctors cannot flourish. It has responded by trying to hand more control of the service to frontline staff.2 3 But is this the right treatment? Treatment must, of course, follow diagnosis, and the causes of doctors' unhappiness may be many and deep. The most obvious cause of doctors' unhappiness is that they feel overworked and undersupported. They hear politicians make extravagant promises but then must explain to patients why the health service cannot deliver what is promised. Endless initiatives are announced, but on the ground doctors find that operating lists are cancelled, they cannot admit or discharge patients, and community services are disappearing. They struggle to respond, but they feel as though they are battling the system rather than being supported by it. Those in the NHS are the last survivors of a socialist inspired system. In a society that pays a businessman £500 000 a year and many public servants £10 000, they try to patch up the social and health damage that accompanies such divisions. It's difficult, if not impossible, work. And, worse, it is undertaken against a backcloth of negative media coverage. Dr Kildare has been replaced by Dr Shipman, and stories of errors outnumber tales of triumph. Government ministers look down on the health service and don't quite understand. Resources are being increased in real terms. General practitioners have more time with patients than they had 20 years ago. Doctors are more and more involved in running the service—as czars, medical or clinical directors, or members of primary care groups. Dozens of initiatives—national service frameworks and health action zones—are being developed to counter problems that doctors have been highlighting for years. And the ministers work harder than anybody—criss crossing the country, chairing task forces, doing their ministerial work in the morning, answering parliamentary questions in the afternoon, and conducting surgeries on Saturday mornings. Ministers are thus likely to diagnose doctors'unhappiness in terms of diminished control, more change, and increased accountability. It's impossible to reverse the increasing accountability. This is a
worldwide phenomenon that affects not only doctors. Similarly, ministers cannot imagine slowing the pace of change. They live in a world where escalation of promises is routine. Ministers thus fall back on “sweeping away bureaucracy and giving more control to frontline staff,” not least because nobody wants more bureaucracy. Health workers might, however, want better management of the service, and they themselves might not be the best people to do this. And here we come to something deeper—the mismatch between what doctors were trained for and what they are required to do. Julian Tudor Hart, a general practitioner who retired recently, observed that what he learnt at medical school didn't serve him well for hospital medicine, which in turn didn't serve him well for general practice. In other words, he started three times as a doctor. But maybe now it's more extreme.
Trained in pathophysiology, diagnosis, and treatment, doctors find themselves spending more time thinking about issues like management, improvement, finance, law, ethics, and communication. Luke Filde's 19th century painting of a contemplative doctor alone with a sick child might now be replaced by a harassed doctor trying to park his car to get to a meeting on time. The gratification that comes from curing a sick child is different from that which comes from being part of the meeting that agrees to take an abused child into care. Christian Koeck—a doctor, professor of health policy, and member of the BMJ editorial board—thinks the problem goes deeper. He thinks the intellectual model of medicine is wrong and that instead of being trained simply to apply the natural sciences to peoples' health problems doctors should also be trained as change managers. That way they can help people adjust to the sickness, pain, and death that are central to being human. Another way to think about doctors' unhappiness is to think of the change in the contract between doctors and patients. We hear much about doctors changing from being authorities to being partners with patients, and some find this transition unsettling. But perhaps the change is deeper still. Maybe we are changing from what has become a bogus contract between doctors and patients to something more real. Doctors are often acutely aware of the limitations of what they can do, whereas patients—partly through the exaggeration of doctors—have inflated ideas of the power of medicine. Negative media coverage might represent the world's waking up to the limitations of doctors and medicine, and—though it's uncomfortable now—it may lead to a much more honest, adult, and comfortable, relationship.
Written by Richard Smith from:BMJ.
worldwide phenomenon that affects not only doctors. Similarly, ministers cannot imagine slowing the pace of change. They live in a world where escalation of promises is routine. Ministers thus fall back on “sweeping away bureaucracy and giving more control to frontline staff,” not least because nobody wants more bureaucracy. Health workers might, however, want better management of the service, and they themselves might not be the best people to do this. And here we come to something deeper—the mismatch between what doctors were trained for and what they are required to do. Julian Tudor Hart, a general practitioner who retired recently, observed that what he learnt at medical school didn't serve him well for hospital medicine, which in turn didn't serve him well for general practice. In other words, he started three times as a doctor. But maybe now it's more extreme.
Trained in pathophysiology, diagnosis, and treatment, doctors find themselves spending more time thinking about issues like management, improvement, finance, law, ethics, and communication. Luke Filde's 19th century painting of a contemplative doctor alone with a sick child might now be replaced by a harassed doctor trying to park his car to get to a meeting on time. The gratification that comes from curing a sick child is different from that which comes from being part of the meeting that agrees to take an abused child into care. Christian Koeck—a doctor, professor of health policy, and member of the BMJ editorial board—thinks the problem goes deeper. He thinks the intellectual model of medicine is wrong and that instead of being trained simply to apply the natural sciences to peoples' health problems doctors should also be trained as change managers. That way they can help people adjust to the sickness, pain, and death that are central to being human. Another way to think about doctors' unhappiness is to think of the change in the contract between doctors and patients. We hear much about doctors changing from being authorities to being partners with patients, and some find this transition unsettling. But perhaps the change is deeper still. Maybe we are changing from what has become a bogus contract between doctors and patients to something more real. Doctors are often acutely aware of the limitations of what they can do, whereas patients—partly through the exaggeration of doctors—have inflated ideas of the power of medicine. Negative media coverage might represent the world's waking up to the limitations of doctors and medicine, and—though it's uncomfortable now—it may lead to a much more honest, adult, and comfortable, relationship.
Written by Richard Smith from:BMJ.
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