Experts say U.S. doctors overtesting, overtreating

Too much cancer screening, too many heart tests, too many cesarean sections. A spate of recent reports suggest that too many Americans — maybe even President Obama — are being overtreated.

Is it doctors practicing defensive medicine? Or are patients so accustomed to a culture of medical technology that they insist on extensive tests and treatments?

A combination of both is at work, but now new evidence and guidelines are recommending a step back and more thorough doctor-patient conversations about risks and benefits.

As a medical journal editorial said this week about Obama's recent checkup, Americans including the commander in chief need to realize that "more care is not necessarily better care."

Obama's exam included prostate-cancer screening and a virtual colonoscopy. The PSA test for prostate cancer is not routinely recommended for any age and colon screening is not routinely recommended for patients younger than 50. Obama is 48. (PSA stands for prostate-specific antigen screening).

Earlier colon-cancer screening is sometimes recommended for high-risk groups — which a White House spokesman noted includes blacks. Doctors disagree on whether a virtual colonoscopy is the best method. But it's less invasive than traditional colonoscopies and doesn't require sedation — or the possible temporary transfer of presidential power, the White House said.

The colon exam exposed him to radiation "while likely providing no benefit to his care," Dr. Rita Redberg, editor of Archives of Internal Medicine, wrote in an online editorial. "People have come to equate tests with good care and prevention," Redberg, a cardiologist with the University of California, San Francisco, said in an interview Thursday. "Prevention is all the things your mother told you — eat right, exercise, get enough sleep, don't smoke — and we've made it into getting a new test."

This week alone, a New England Journal of Medicine study suggested that too many patients are getting angiograms — invasive imaging tests for heart disease — who don't really need them; and specialists convened by the National Institutes of Health said doctors are too often demanding repeat cesarean deliveries for pregnant women after a first C-section.

Experts dispute how much routine cancer screening saves lives.

Not all doctors and advocacy groups agree with the criticism of screening. Many argue that it can improve survival chances and that saving even a few lives is worth the cost of routinely testing tens of thousands of people.

While some patients clearly do benefit from screening, others clearly do not, said Dr. Richard Wender, former president of the American Cancer Society.

These include very old patients, who may unrealistically fear cancer and demand a screening test, when their risks are far higher of dying from something else, Wender said.

Doctors also often order tests or procedures to protect themselves against lawsuits — so-called defensive medicine — and also because the fee-for-service system compensates them for it, said Dr. Gilbert Welch, a Dartmouth University internist and health-outcomes researcher.

While many patients also demand routine tests, they're often bolstered by advertisements, medical information online — and by doctors, too, Welch said.

The new guidance from the cancer society last week on PSA testing, echoing others' advice on mammograms, is for doctors and patients to thoroughly discuss testing, including a patient's individual disease risks, general pros and cons of testing and possible harms it may cause.

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Medical Identity Theft

     The latest addition to the world of fraud , medical identity theft. You might be wondering what really is " Medical Identity Theft" . It is in simple words , usage of ones health cards by some other person without the knowledge of its real owner. The owner of the card may come to the realization of the fraud only when his service provoder sent him bills for thousands of dollars for some surgeries that he never underwent.
                                     The irony is that most of the fraud are done by family members or close family friends. So the number of cases reported will be very rare. The hospital authorities also didn't check much details once they are provided with health cards , that also is a reason for this fraud to develop.

             To read a detailed report on Medical Identity Theft Read from here  :: Medical Identity Theft

Genetic Variant Offers Protection Against Tuberculosis and Leprosy

When people get exposed to the mycobacterium responsible for tuberculosis (TB), some will become sick with a disease that is a major cause of mortality around the world while others simply don't. Now, researchers reporting in the March 5th issue of the journal Cell, a Cell Press publication, can point to one important reason for this variation in susceptibility or resistance: genetic differences among individuals in levels of an immune enzyme (LTA4H) that is involved in the production of leukotriene B, a pro-inflammatory fatty acid immune signaling molecule.
It turns out individuals who are heterozygous for LTA4H, meaning they carry two versions of the enzyme-encoding gene and produce an average amount of the enzyme (not too little or too much), are less likely to succumb to tuberculosis. They also appear to gain protection against leprosy, a disease which is also caused by mycobacterial infection.
"TB is obviously a big problem," said Lalita Ramakrishnan of the University of Washington. "There isn't a good vaccine, notwithstanding the fact that the TB vaccine has been administered to more people than any other. On top of that, it requires long-term treatment for cure and there is an epidemic of drug-resistant TB. Increasingly, people are becoming infected with strains that are resistant to every antibiotic. On this backdrop, it made sense to go back to the drawing board and try to understand the pathogenesis of the disease."
In the new study, Ramakrishnan and her colleague David Tobin did just that, in an unbiased screen for TB susceptibility genes in the zebrafish. They then collaborated with University of Washington human geneticists Jay Vary, Thomas Hawn and Mary-Claire King and others in Vietnam and Nepal to validate their findings in human populations.
A second study in the same issue of Cell approached the question in another way. Kanury Rao and his colleagues at the International Centre for Genetic Engineering and Biotechnology in India used a genome-wide analysis to produce what now becomes a resource for TB researchers everywhere. They uncovered all of the "cellular machinery" within human macrophages -- the cells primarily targeted by TB -- that interact with the infectious mycobacteria and allow the infection to stably persist.
Rao's team uncovered 275 players within host cells that interact with each other to form a dense network. That picture allowed the researchers to make a detailed molecular-level description of what he refers to as "functional modules" within host cells that are engaged and perturbed by TB infection. Interestingly, they showed that the shape of that interaction varies depending on which isolated strain of TB one considers, suggesting that the different strains rely on somewhat different tactics for successful infection.
Rao's findings offer new leads in the fight against TB, he says. "We identify a core set of molecules which can be targeted through drug development efforts to treat both drug sensitive and multiple drug resistant forms of TB infection. Rather than targeting the pathogen itself, our studies highlight an alternate strategy wherein the host factors required to support pathogen survival can be used as targets for TB therapy."
The discovery of LTA4H as a TB susceptibility gene may have clinical implications too, even if it doesn't offer a direct path to a better vaccine, Ramakrishnan says. For one thing, the finding that medium activity of the immune enzyme is best when it comes to TB might help to explain something that has been known but not well understood in clinical circles: people with hard-to-treat TB sometimes improve when they are given anti-inflammatory, immunosuppressive therapies along with more standard drug treatments alone.
Ramakrishnan also notes that the same polymorphisms in LTA4H they uncovered were earlier linked to heart disease. That suggests that drugs that target this pathway in heart disease might be useful in the context of TB, she says.
The connection between infectious disease and heart disease also has implications for understanding the evolution of the immune system's inflammatory responses. "In general, people have thought that inflammation is a positive when it comes to fighting infection, but then it can cause modern-day disease," Ramakrishnan says. The finding that it is heterozygotes -- with intermediate activity of the immunity enzyme -- who fare best in the context of TB and leprosy suggests that in these infections also, inflammation has to be finely tuned for optimal protection.
The researchers include David M. Tobin, University of Washington, Seattle, WA; Jay C. Vary, Jr., University of Washington, Seattle, WA; John P. Ray, University of Washington, Seattle, WA; Gregory S. Walsh, Howard Hughes Medical Institute and Division of Basic Science, Fred Hutchinson Cancer Research Center, Seattle, WA; Sarah J. Dunstan, Oxford University Clinical Research Unit, Hospital for Tropical Diseases, Ho Chi Minh City, Vietnam, Oxford University, Oxford, UK; Nguyen D. Bang, Pham Ngoc Thach Hospital for Tuberculosis and Lung Disease, Ho Chi Minh City, Vietnam; Deanna A. Hagge, Mycobacterial Research Laboratory, Anandaban Hospital, Kathmandu, Nepal; Saraswoti Khadge, Mycobacterial Research Laboratory, Anandaban Hospital, Kathmandu, Nepal; Mary-Claire King, University of Washington, Seattle, WA; Thomas R. Hawn, University of Washington, Seattle, WA; Cecilia B. Moens, Howard Hughes Medical Institute and Division of Basic Science, Fred Hutchinson Cancer Research Center, Seattle, WA; and Lalita Ramakrishnan, University of Washington, Seattle, WA.

Vitamin D Crucial to Activating Immune Defenses

Scientists at the University of Copenhagen have discovered that Vitamin D is crucial to activating our immune defenses and that without sufficient intake of the vitamin, the killer cells of the immune system -- T cells -- will not be able to react to and fight off serious infections in the body.
For T cells to detect and kill foreign pathogens such as clumps of bacteria or viruses, the cells must first be 'triggered' into action and 'transform' from inactive and harmless immune cells into killer cells that are primed to seek out and destroy all traces of a foreign pathogen.
The researchers found that the T cells rely on vitamin D in order to activate and they would remain dormant, 'naïve' to the possibility of threat if vitamin D is lacking in the blood.
Chemical Reaction that Enables Activation
In order for the specialized immune cells (T cells) to protect the body from dangerous viruses or bacteria, the T cells must first be exposed to traces of the foreign pathogen. This occurs when they are presented by other immune cells in the body (known as macrophages) with suspicious 'cell fragments' or 'traces' of the pathogen. The T cells then bind to the fragment and divide and multiply into hundreds of identical cells that are all focused on the same pathogen type. The sequence of chemical changes that the T cells undergo enables them to both be 'sensitized to' and able to deliver a targeted immune response.
Professor Carsten Geisler from the Department of International Health, Immunology and Microbiology explains that "when a T cell is exposed to a foreign pathogen, it extends a signaling device or 'antenna' known as a vitamin D receptor, with which it searches for vitamin D. This means that the T cell must have vitamin D or activation of the cell will cease. If the T cells cannot find enough vitamin D in the blood, they won't even begin to mobilize. "
T cells that are successfully activated transform into one of two types of immune cell. They either become killer cells that will attack and destroy all cells carrying traces of a foreign pathogen or they become helper cells that assist the immune system in acquiring "memory." The helper cells send messages to the immune system, passing on knowledge about the pathogen so that the immune system can recognize and remember it at their next encounter. T cells form part of the adaptive immune system, which means that they function by teaching the immune system to recognize and adapt to constantly changing threats.
Activating and Deactivating the Immune System
For the research team, identifying the role of vitamin D in the activation of T cells has been a major breakthrough. "Scientists have known for a long time that vitamin D is important for calcium absorption and the vitamin has also been implicated in diseases such as cancer and multiple sclerosis, but what we didn't realize is how crucial vitamin D is for actually activating the immune system -- which we know now. "
The discovery, the scientists believe, provides much needed information about the immune system and will help them regulate the immune response. This is important not only in fighting disease but also in dealing with anti-immune reactions of the body and the rejection of transplanted organs. Active T cells multiply at an explosive rate and can create an inflammatory environment with serious consequences for the body. After organ transplants, e.g. T cells can attack the donor organ as a "foreign invader." In autoimmune disease, hypersensitive T cells mistake fragments of the body's own cells for foreign pathogens, leading to the body launching an attack upon itself.
The research team was also able to track the biochemical sequence of the transformation of an inactive T cell to an active cell, and thus would be able to intervene at several points to modulate the immune response. Inactive or 'naïve' T cells crucially contain neither the vitamin D receptor nor a specific molecule (PLC-gamma1) that would enable the cell to deliver an antigen specific response.
The findings, continues Professor Geisler "could help us to combat infectious diseases and global epidemics. They will be of particular use when developing new vaccines, which work precisely on the basis of both training our immune systems to react and suppressing the body's natural defenses in situations where this is important -- as is the case with organ transplants and autoimmune disease."
Most Vitamin D is produced as a natural byproduct of the skin's exposure to sunlight. It can also be found in fish liver oil, eggs and fatty fish such as salmon, herring and mackerel or taken as a dietary supplement. No definitive studies have been carried out for the optimal daily dosage of vitamin D but as a large proportion of the population have very low concentrations of vitamin D in the blood, a number of experts recommend between 25-50mg micrograms a day

Viruses Helped Shape Human Genetic Variability

Viruses have played a role in shaping human genetic variability, according to a study published February 19 in the open-access journal PLoS Genetics. The researchers, from the Don C. Gnocchi and Eugenio Medea Scientific Institutes, the University of Milan and the Politecnico di Milano, Italy, used population genetics approaches to identify gene variants that augment susceptibility to viral infections or protect from such infections.
Viruses have represented a threat to human populations throughout history and still account for a large proportion of disease and death worldwide. The identification of gene variants that modulate the susceptibility to viral infections is thus central to the development of novel therapeutic approaches and vaccines. Due to the long relationship between humans and viruses, gene variants conferring increased resistance to these pathogens have likely been targeted by natural selection. This concept was exploited to identify variants in the human genome that modulate susceptibility to infection or the severity of the ensuing disease.
In particular, the authors based their study on the idea that populations living in different geographic areas have been exposed to different viral loads and therefore have been subjected to a variable virus-driven selective pressure. By analysing genetic data for 52 populations distributed worldwide, the authors identified variants that display higher frequency where the viral load is also high. Using this approach, they found 139 human genes that modulate susceptibility to viral infections; the protein products of several of these genes interact with one another and often with viral components.
The study relied on predictions generated in computer simulations; therefore, experimental validation of these results will be required. The authors conclude that approaches similar to the one they applied might be used to identify susceptibility variants for infections transmitted by pathogens other than viruses.

Genetic Link Between Misery and Death Discovered; Novel Strategy Probes 'Genetic Haystack'

Interaction between nerves (red) and tumor cells (blue) in an ovary provides one way by which stress biochemistry signals can be distributed to sites of disease in the body

In ongoing work to identify how genes interact with social environments to impact human health, UCLA researchers have discovered what they describe as a biochemical link between misery and death. In addition, they found a specific genetic variation in some individuals that seems to disconnect that link, rendering them more biologically resilient in the face of adversity.
Perhaps most important to science in the long term, Steven Cole, a member of the UCLA Cousins Center for Psychoneuroimmunology and an associate professor of medicine in the division of hematology-oncology, and his colleagues have developed a unique strategy for finding and confirming gene-environment interactions to more efficiently probe what he calls the "genetic haystack."
The research appears in the current online edition of Proceedings of the National Academy of Sciences.
Using an approach that blends computational, in vivo and epidemiological studies to focus their genetic search, Cole and his colleagues looked at specific groups of proteins known as transcription factors, which regulate gene activity and mediate environmental influences on gene expression by binding to specific DNA sequences. These sequences differ within the population and may affect a gene's sensitivity to environmental activation.
Specifically, Cole analyzed transcription factor binding sequences in a gene called IL6, a molecule that is known to cause inflammation in the body and that contributes to cardiovascular disease, neurodegeneration and some types of cancer.
"The IL6 gene controls immune responses but can also serve as 'fertilizer' for cardiovascular disease and certain kinds of cancer," said Cole, who is also a member of UCLA's Jonsson Comprehensive Cancer Center and UCLA's Molecular Biology Institute. "Our studies were able to trace a biochemical pathway through which adverse life circumstances -- fight-or-flight stress responses -- can activate the IL6 gene.
"We also identified the specific genetic sequence in this gene that serves as a target of that signaling pathway, and we discovered that a well-known variation in that sequence can block that path and disconnect IL6 responses from the effects of stress."
To confirm the biochemical link between misery and death, and the genetic variation that breaks it, the researchers turned to epidemiological studies to prove that carriers of that specific genetic variation were less susceptible to death due to inflammation-related mortality causes under adverse social-environmental conditions.
They found that people with the most common type of the IL6 gene showed an increased risk of death for approximately 11 years after they had been exposed to adverse life events that were strong enough to trigger depression. However, people with the rarer variant of the IL6 gene appeared to be immune to those effects and showed no increase in mortality risk in the aftermath of significant life adversity.
This novel method of discovery -- using computer modeling and then confirming genetic relationships using test-tube biochemistry, experimental stress studies and human genetic epidemiology -- could speed the discovery of such gene and environmental relationships, the researchers say.
"Right now, we have to hunt down genetic influences on health through blind searches of huge databases, and the results from that approach have not yielded as much as expected," Cole said. "This study suggests that we can use computer modeling to discover gene-environment interactions, then confirm them, in order to focus our search more efficiently and hopefully speed the discovery process.
"This opens a new era in which we can begin to understand the influence of adversity on physical health by modeling the basic biology that allows the world outside us to influence the molecular processes going on inside our cells."
Other authors on the study were Jesusa M. G. Arevalo, Rie Takahashi, Erica K. Sloan and Teresa E. Seeman, of UCLA; Susan K. Lutgendorf, of the University of Iowa; Anil K. Sood, of the University of Texas; and John F. Sheridan, of Ohio State University. Funding was provided by the National Institutes of Health, the UCLA Norman Cousins Center and the James L. Pendleton Charitable Trust. The authors report no conflict of interest.