It's true that we get too much radiation, but not from the sources we fret about—airport scanners, power lines, cell phones, even microwaves. It's from too many medical tests.
Some researchers have suggested a 'radiation medical record' that would track patients' radiation exposure from tests such as CT scans.
Americans get the most medical radiation in the world—even more than folks in other rich countries—and the average American's dose has grown sixfold over the last couple of decades.
Too much radiation raises the risk of cancer. The risk is growing as people in everyday situations get imaging tests far too often. A New Hampshire teen was about to get a CT scan to check for kidney stones until a radiologist, Dr. Steven Birnbaum, discovered he'd already had 14 of these powerful X-rays for previous episodes. Adding up the total dose, "I was horrified'' at the cancer risk it posed, Dr. Birnbaum says.
After his daughter, Molly, was given too many scans after a car accident, Dr. Birnbaum took action. He asked the two hospitals where he works to watch for patients who had had 10 or more CT scans, or patients under 40 who' had had five—clearly dangerous amounts. They found 50 people over a three-year period, including a young woman with 31 abdominal scans.
When other radiologists tell him they've never found such a case, Dr. Birnbaum replies, "That tells me you haven't looked."
The U.S. accounts for half of the most advanced procedures that use radiation, and CT scans—"super X-rays'' that give fast, extremely detailed images—have soared in use over the past decade, often replacing ultrasound and MRI (magnetic resonance imaging), tests that don't require radiation.
Radiation is a hidden danger: You don't feel it when you get it, and any damage usually doesn't show up for years. Taken individually, tests that use radiation pose little risk. Over time, though, the dose accumulates.
Doctors don't keep track of radiation given their patients. They order a test, not a dose. Except for mammograms, there are no federal rules on radiation dose. Children and young women, who are most vulnerable to radiation harm, sometimes get too much at busy imaging centers that don't adjust doses for each patient's size.
The U.S. Food and Drug Administration is pushing industry and doctors to set standard doses for common tests such as CT scans. Another possibility is requiring device makers to print the radiation dose on each X-ray or other image, so patients and doctors can see how much was given.
"We are considering requirements and guidelines for record-keeping of dose and other technical parameters of the imaging exam,'' says Sean Boyd, chief of the FDA's diagnostic devices branch. A near-term goal is developing a "radiation medical record" to track dose from cradle to grave,
"One of the ways we could improve care is if we had a running sort of Geiger counter'' that a doctor checked before ordering a test, says Dr. Prashant Kaul of Duke University. Dr. Kaul led a study that found that U.S. heart attack patients get the radiation equivalent of 850 chest X-rays over the first few days they are in the hospital—much of it for repeat tests that may not have been needed.
How much radiation is risky? It's hard to say. The best guess is based on the 1986 Chernobyl nuclear power plant accident and studies of Japanese atomic bomb survivors who had excess cancer risk after exposures of 50 to 150 millisieverts (a measure of dose) of radiation.
A chest or abdominal CT scan involves 10 to 20 millisieverts, versus 0.01 to 0.1 for an ordinary chest X-ray, less than 1 for a mammogram, and as little as 0.005 for a dental X-ray. Natural radiation from the sun and soil accounts for about 2 millisieverts a year.
A study by Columbia University researchers, published in 2007, estimated that in a few decades, as many as 2% of all cancers in the U.S. might be due to radiation from CT scans given now.
Because previous studies suggest that a third of all tests are unnecessary, the researchers concluded that 20 million adults and more than 1 million children are being put needlessly at risk.
Which tests are overused? A scientific group, the International Commission on Radiological Protection, cites routine chest X-rays when people are admitted to a hospital or before surgery; imaging tests on car- crash victims who don't show signs of head or abdominal injuries; and low-back X-rays in older people with degenerative, but stable, spine conditions.
Even when tests are justified, they often include more views than needed and too much radiation. Top offender: chest CT scans looking for clogged arteries and heart problems.
A Columbia University study on dummies by Dr. Andrew Jeffrey Einstein found two dose-modifying techniques could lower the needed radiation dose by 90% without harming image quality.
Another cardiologist and radiation-safety expert, Dr. Gilbert Raff, led a study of nearly 5,000 patients at 15 imaging centers in Michigan. It found the radiation dose could be cut by two-thirds with no loss of quality.
What should patients do? "You should question everything—what's the dose, why am I getting it? You should be an informed consumer,'' says Dr. Fred Mettler, radiology chief in the New Mexico Veterans Administration health-care system. He led a study of health effects after the Chernobyl accident and is a U.S. representative to the United Nations on radiation safety.
Dr. Mettler advises challenging "big ticket'' tests like CT scans that deliver a lot of radiation to the chest and abdomen—places where cancer is likely to develop. "You shouldn't get too excited about feet and knee X-rays,'' he adds
Quote:
Before Your Scan ...
Consider asking these questions, says Fred Mettler, a radiation-safety expert and radiology chief at the New Mexico Veterans Administration health-care system.
Is it truly needed? How will it change my care?
Have you or another doctor done this test on me before?
Are there alternatives, such as ultrasound or MRI?
How many scans will be done? Could one or two be enough?
Will the dose be adjusted for my gender, age and size?
Will lead shields be used to keep radiation away from places it can do harm?
Do you have a financial stake in the machines that will be used?
How much radiation will I get from the scan?
Can I have a digital copy of my scan? (Bring a blank CD or thumb drive with you.)
Source: Associated Press
Reanalysis of a landmark cholesterol-lowering trial of people typically considered at low risk for heart attacks indicated that the results are flawed -- and do not support the primary-prevention benefits that made headlines, authors of the review asserted.
The reanalysis of the massive JUPITER trial involving almost 18,000 people with low or normal cholesterol but elevated levels of the inflammatory biomarker C-reactive protein (CRP) -- turned up no evidence of the "striking decrease in coronary heart disease complications" reported by the trial investigators. Instead, the reanalysis has called into question the involvement of drug companies in such clinical trials, according to an article in the June 28 issue of the Archives of Internal Medicine.
Moreover, Michel de Lorgeril, MD, of Joseph Fourier University and the National Center of Scientific Research in Grenoble, France, and co-authors argue that a major discrepancy exists between the JUPITER trial's report of significant reductions in nonfatal stroke and myocardial infarction (MI) but a lack of effects on fatal stroke or MI. Moreover, cardiovascular mortality and the case-fatality rate for MI fell far below predicted rates.
"The JUPITER data set appears biased," de Lorgeril and co-authors concluded.
Paul Ridker, MD, of Harvard Medical School and Brigham and Women's Hospital in Boston, a major proponent of high-sensitivity CRP (hsCRP) as a marker of coronary risk, dismissed de Lorgeril's criticisms. Ridker initially reported the JUPITER results at the American Heart Association meeting in 2008.
In an e-mail to MedPage Today, Ridker said that JUPITER data "overwhelmingly stand for themselves. Among a group of individuals with low levels of cholesterol, we clearly demonstrate that those with elevated levels of hsCRP are in fact a high risk population, and that using statin therapy in this group cuts event rates for myocardial infarction and stroke in half."
And Ridker pointed out that the "FDA has extensively reviewed these data, found the trial to be well conducted, and recently provided a new indication for the use of statins in primary prevention on the basis of the JUPITER data."
AstraZeneca, the maker of rosuvastatin (Crestor), also defended the JUPITER results and the way in which the study was conducted.
Donna Huang, an AstraZeneca spokesperson, told MedPage Today in an e-mail that the study "was undertaken with a fully independent steering committee, data and safety monitoring board, and academic study statistician."
And, she pointed out that Ridker and his co-investigators controlled all the data. "AstraZeneca played no role in conducting data analyses and had no access to unblinded trial data," she wrote.
But the authors of reanalysis say that the links between study sponsor and study investigators are too strong to ignore.
"Three other trials involving rosuvastatin (Crestor) therapy in high-risk patients did not show any protection. The authors of the JUPITER study fail to comment on these negative trials but go on to report secondary endpoint and subgroup analyses that appear to support the efficacy and safety of rosuvastatin therapy," de Lorgeril and colleagues wrote.
Moreover, de Lorgeril and co-authors point out that nine of 14 authors of the JUPITER article have financial relationships with AstraZeneca, which sponsored the trial. First author Ridker has a patent interest in the assay for CRP, an inflammation biomarker evaluated in all JUPITER trial participants.
"The sponsor's pervasive role is clearly described in the second paragraph of the 'Methods' section of the report: 'the sponsor collected the trial data and monitored the study sites,'" the authors wrote.
De Lorgeril and co-authors concluded that "the results of the JUPITER trial are clinically inconsistent and therefore should not change medical practice or clinical guidelines. The results of the JUPITER trial support concerns that commercially sponsored clinical trials are at risk of poor quality and bias."
Adding to the controversy, authors of another article in the same issue of Archives reported that a meta-analysis of 11 large primary-prevention trials showed no effect of statin therapy on all-cause mortality in high-risk patients.
The JUPITER trial (Justification for the Use of Statins in Primary Prevention) has stood alone in its finding of a significant benefit in patients with no evidence of CHD (N Engl J Med 2008; 170: 1032-36). The trial examined the effect of rosuvastatin in patients with normal or low cholesterol levels but elevated levels of CRP.
Investigators randomized 17,802 apparently healthy men and women to rosuvastatin or placebo. The primary endpoint was the composite of MI, stroke, arterial revascularization, hospitalization for unstable angina, and cardiovascular mortality. The trial ended prematurely after a median follow-up of 1.9 years, when an interim analysis showed a 44% reduction in the composite endpoint in the rosuvastatin group.
De Lorgeril and co-authors cited the early termination as one of several methodologic problems with JUPITER. Although prespecified early stopping points are a well-accepted feature of clinical trials, the rules for stopping should be clearly described. That was not the case in the published description of the JUPITER protocol.
"Indeed, we still do not know which endpoint was used to define [the rules for stopping], or which level of benefits -- unexpected on the basis of the a priori calculated hypothesis -- was required to justify early termination," de Lorgeril and co-authors wrote.
The authors also expressed concern that the trial ended early despite the fact that the data were not consistent with a large difference between rosuvastatin and placebo. Considering only "hard endpoints," such as fatal and nonfatal MI and stroke, the trial ended after 240 events, a small number given the size of the trial.
"Moreover, a close examination of the all-cause mortality curves shows that the curves were actually converging when the trial ended, suggesting that the borderline significant difference between groups may have disappeared in the case of a slightly longer follow-up," the authors wrote.
De Lorgeril and co-authors also could not resolve what they considered implausible differences in hard endpoints. Performing their own calculations based on data reported in the JUPITER published article, the authors concluded that total cardiovascular mortality was identical in the rosuvastatin and placebo groups. Despite the JUPITER investigators' statement of an "unequivocal reduction in cardiovascular mortality" as the justification for stopping the trial, the published article included no cardiovascular mortality data.
Another inconsistency related to the mix of fatal and nonfatal cardiovascular endpoints.
"The ratio of fatal myocardial infarction (nine for rosuvastatin and six for placebo) to nonfatal myocardial infarction (22 and 62) is incredibly low, especially in the placebo group," de Lorgeril and co-authors wrote. "Mortality from acute myocardial infarction is a very important issue in cardiology. The data would suggest that the hearts of the JUPITER patients were unexpectedly -- and inexplicably -- highly resistant to acute ischemic and infarction."
De Lorgeril and co-authors also take JUPITER investigators to task for failure to describe the criteria used to define cardiovascular death and for omission of any discussion of sudden cardiac death (SCD).
"It is therefore very surprising that no SCD is reported in the JUPITER trial because SCD usually represents about 65% to 70% of total cardiac mortality," the authors of the reanalysis observed.
On the basis of their review, de Lorgeril and co-authors concluded that "the time has come for a critical reappraisal of cholesterol-lowering and statin treatments for the prevention of CHD complications. The emphasis on pharmaceuticals for the prevention of CHD diverts individual and public health attention away from the proven efficacy of adopting a healthy lifestyle, including regular physical activity, not smoking, and a Mediterranean-style diet."
The meta-analysis reported in the same issue of the journal encompassed 11 randomized clinical trials involving 65,229 patients and 244,000 person-years of follow-up. The primary objective was to determine whether statin therapy reduces all-cause mortality among intermediate and high-risk people with no history of cardiovascular disease, wrote Kausik K. Ray, MD, of the University of Cambridge in England, and co-authors.
Collectively, the trials documented a total of 2,793 cardiovascular deaths. Analysis of all-cause mortality showed a nonsignificant 9% reduction in relative risk in patients treated with statins (95% CI 0.83 to 1.01). The analysis also showed no statistical heterogeneity among the studies.
The findings call into question current clinical guidelines regarding use of statins' cardiovascular prevention.
"Current prevention guidelines endorse statin therapy for subjects at high global risk of incident CVD as a means to reduce fatal and nonfatal events," Ray and co-authors wrote. "Due consideration is needed in applying statin therapy in lower-risk primary prevention populations."
In an editorial that accompanied the two articles, Lee A. Green, MD, of the University of Michigan in Ann Arbor, said the de Lorgeril and Kay studies add fuel to a high-stakes debate.
"Most patients who have major coronary events do not have previously known disease, so primary prevention could deliver large outcome benefits," wrote Green.
Extending the discussion of large risks and benefits, Green added that "three quarters of the patients who take statins are taking them for primary prevention, so enormous expenditures (from payors' perspectives) or revenues (from industry's perspective) are at stake."
The uncertainty surrounding the outcomes of such clinical trials also is high, Green continued. Given the short-term nature of clinical trials versus the need for long-term treatment in clinical practice, "no data settle the increasing-returns versus the diminishing-returns extrapolations."
"Ray and colleagues' meta-analysis makes it clear that in the short term, for true primary prevention, the benefit, if any, is very small," Green wrote. "In the long term, although sincere advocates on both sides will try to convince us otherwise, we really must admit that we do not know. We need good research to find out, and, as de Lorgeril and colleagues point out, that search must be free of incentives to find any particular desired answer."
Ray and a co-author have received honoraria for lectures and advisory boards from the majority of companies that market lipid-lowering agents, inclusive of statins and nonstatins.
One of de Lorgeril's co-authors has served as an expert for plaintiffs' attorneys in litigation involving the pharmaceutical industry (not involving rosuvastatin), as an unpaid consultant to the Federal Bureau of Investigation and the Department of Justice in investigations involving the pharmaceutical industry, and as a consultant to Wells Fargo Insurance Services.
Green declared no financial conflicts.
Ridker is the co-inventor of the high-sensitivity CRP test and, along with Brigham and Women's Hospital. Ridker holds the patent on the test. Ridker also reported financial support from AstraZeneca, Novartis, Merck, Abbott, Roche, sanofi-aventis, Merck-Schering-Plough, Isis, Dade Behring, and Vascular Biogenics.
To heartwire, Seshasai commented: "We didn't find a significant reduction in death despite having such a huge sample size. This is the totality of evidence in primary prevention. So if we can't show a significant reduction with this data, it is unlikely to be there. We are not saying don't use statins in this population, as they do have benefits on other outcomes, such as MI. But we are saying that we should be cautious in prescribing these agents for a mortality reduction. That is, don't expect wonders to happen. If it is for a reduction of all-cause death that you are prescribing a statin, you probably need to reconsider. And our population was primary prevention at high risk of heart disease, so if we extend it to those at lower risk the benefits will be even more modest."
In an accompanying editorial, Dr Lee Green (University of Michigan Medical School, Ann Arbor) says: "Ray and colleagues present what is to date the cleanest and most complete meta-analysis of pharmacological lipid lowering for primary prevention. Limiting the analysis to patients without existing coronary disease is critical because studies that include both groups of patients may appear to show benefit for all patients, when all the benefit accrues to those with existing disease."
He adds that this analysis "makes it clear that in the short term, for true primary prevention, the benefit, if any, is very small. In the long term, although sincere advocates on both sides will try to convince us otherwise, we really must admit that we do not know."
Nissen: "Not surprising"
Commenting on the meta-analysis for heartwire, Dr Steve Nissen (Cleveland Clinic, OH) said he did not find the results surprising. "Because mortality is low in primary-prevention patients, it is difficult to show a mortality benefit. This has been established previously. The primary benefit in this setting is reduction in nonfatal MI, which remains a worthwhile goal of therapy," he added.
Many patients with diabetes may not benefit from aggressive management of cardiovascular risk factors and some may even be harmed, according to a statistical model based on a government health survey.
Intensive, stepped-care management of dyslipidemia and hypertension led to gains of 1 to 1.5 quality-adjusted-life-years (QALY) in people who had a life expectancy of 10 to 11 years. But adjustment for potential harms of treatment reduced the benefits.
Only the patients at highest risk benefited from intensification beyond the first step of management protocols, suggesting that current clinical guidelines often recommend inherently flawed strategies, authors of the study reported in the June 28 issue of Archives of Internal Medicine.
"Below average to average-risk patients seem to receive virtually no net benefit from titrating beyond standard dose of a statin and two to three blood pressure medications, even if commonly recommended LDL-C and blood pressure goals have not been met," Justin W. Timbie, PhD, of the RAND Corp. in Arlington, Va., and co-authors wrote.
"Given the large set of factors that moderate the benefit of treatment intensification ... the diminishing effects of combination therapy, and increasing polypharmacy and adverse effects, we recommend a strategy of tailoring treatments to individual patients on the basis of their expected benefit of intensifying treatment. Current treatment approaches that encourage uniformly lowering risk factors to common target levels can be both inefficient and cause unnecessary harm."
Almost all clinical guidelines for diabetes recommend aggressive treatment of LDL cholesterol and blood pressure. However, the recommendations are based on averaging of benefits from clinical trials, the authors wrote.
Tailoring treatment to individual patient risk has received little or no attention in diabetes risk management, apparently because of "an implicit assumption that all patients with diabetes are at equally high risk, requiring all patients to be treated aggressively."
In fact, the benefit of intensified stepped-care therapy or treating to targets could vary substantially across the diabetic population, depending on the distribution of cardiovascular disease risk in the population, the authors continued.
Recent substudies of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial showed no survival advantage and suggested possible harm associated with a blanket approach to aggressive treatment of dyslipidemia and high blood pressure (N Engl J Med 2010; 362: 1563-74, N Engl J Med 2010; 362: 1575-85). Nonetheless, some high-risk patients might still benefit from an aggressive strategy.
In an effort to clarify the role of aggressive risk-factor management in diabetic patients, Timbie and co-authors designed a study to assess the variability in benefit and harm associated with treating to target. They identified adult diabetic participants in the third National Health and Nutrition Examination Survey (NHANES III) and developed models to simulate treat-to-target strategies for LDL and blood pressure.
The LDL target was 100 mg/dL and the blood pressure target was 130/80 mm Hg. Patients could progress through five titrations of statin therapy for LDL and eight titrations of antihypertensive therapy. The models incorporated adverse effects of treatment and the risks and burdens of polypharmacy.
Treating to the specified target for LDL resulted in a gain of 1.50 QALY and 1.35 QALY for treatment to the blood pressure target. After accounting for treatment-related harms, the QALY gain declined to 1.42 for LDL and 1.16 for blood pressure.
"Most of the total benefit was limited to the first few steps of medication intensification or to tight control for a limited group of very high-risk patients," the authors wrote.
"Intensifying beyond the first step for LDL or third step for blood pressure resulted in either limited benefit or net harm for patients with below-average risk," they added.
Statistical modeling has inherent limitations in its ability to simulate reality. Even so, "the lessons to be gleaned from this simulation are profound," Andrew L. Avins, MD, of Kaiser Permanente Northern California in Oakland, wrote in an editorial.
"Most important, the results starkly challenge some fundamental assertions regarding the appropriate treatment of patients with diabetes mellitus. Over the years, practice guidelines have advocated increasingly tighter control of blood glucose and cardiovascular risk factors, often relying on logical inference to extend thresholds beyond the available empirical evidence."
"The more and more tightly risk factors are controlled, the less benefit there will be in treating each additional risk factor," Avins continued. "The failure to account for this effect results in substantial overtreatment. Despite the fact that this phenomenon has been known for many years, it is generally ignored, to the detriment of our patients and our limited healthcare resources."
The principles reflected in the model by Timbie and colleagues apply to virtually all preventive interventions.
"One wonders why such examinations are not generally incorporated into the guideline development process rather than, as in this case, conducted in response to it," Avins concluded.
I don't know what is so hard to grasp about the idea that aggressively adding one medication on top of another as a way of managing cardio risk factors is counterproductive. What is needed is a re examination of the causes of diabetes.
How about recognising the role of carbohydrates in a condition like diabetes which clearly is a failure in the response to carbohydrate consumption.
As diabetes is in effect an inability to safely consume refined carbohydrates why not reduce the carbohydrate burden?
Instead of adding one medication after another why not consider the role of inflammation in diabetes and ensure the natural anti inflammatory status of all diabetics is optimized. It's pretty easy, cheap, simple to check vitamin D status and ensure all diabetics have a reserve store of D3 on board and a circulating plasma level around 60ng/ml the natural level of vitamin D homoeostasis.
Now we understand better the anti inflammatory role of omega 3 and the potential of omega 6 to be pro inflammatory is it really too difficult to recommend an effective omega 3 intake alongside the elimination of industrial seed oils such as corn, soybean, safflower, sunflower and cottonseed oil omega 6 rich sources.
As we know that only 10% of US adults achieve the RDA intake for magnesium isn't it about time all diabetics were reminded to take a form of magnesium the body actually is able to absorb. Now we know diabetes worsens magnesium status in diabetics surely it's a simple and straightforward matter to ensure ALL DIABETICS TAKE MAGNESIUM SUPPLEMENTS.
Instead of aggressively piling one medication on top of the last so Treating diabetes becomes unaffordable we need to think smarter and instead of using expensive medications to treat symptoms we need to use cheap natural OTC supplements with a proven track record to curb inflammation at source and dietary lifestyle changes (low carb + exercise) to prevent symptoms in the first place. Humans evolved for hundreds of thousands of years before the invention of farming, it's only in the last 60yrs we've seen the escalation in diabetes incidence.
We can turn the clock back.
We can tax sodas and stop cheap booze deals.
We could easily tax HFCS and sugars.
We can reduce the use of omega 6 oils.
What we can't do is afford the cost of an exponential increase in the cost of diabetes medications treatments and related complications.
Des Spence, general practitioner, Glasgow
Interesting to see some UK doctors with similar thoughts. This time it's about Chronic Kidney Disease.
the article is in the BMJ and ends with the line
Quote:
Chronic kidney disease is a failed experiment, a mockery of evidence based medicine, and just more bad modern medicine.
It's quite interesting also to read the replies to see the response he got.
I like this one
Quote:
If the road to hell is paved with QoF intentions, CKD was the last paving stone before the entrance. We are now poisoning half the population over 65 with mass medication. We know the cost and workload is astronomical - leaving aside side-effects and iatrogenic deaths. Where are the outcome data?
Silence.
from Dr Malcolm Kendrick. (who wrote the Cholesterol Con)
and this from the original author of the article
Quote:
the unregulated widespread use of medications in the USA is a testimony to the dangers of profit before care.
ScienceDaily (Aug. 17, 2010) � The pharmaceutical industry is a "market for lemons," a market in which the seller knows much more than the buyer about the product and can profit from selling products less effective and less safe than consumers are led to believe, according to an analysis that will be presented at the 105th Annual Meeting of the American Sociological Association.
"Sometimes drug companies hide or downplay information about serious side effects of new drugs and overstate the drugs' benefits," said Donald Light, the sociologist who authored the study and who is a professor of comparative health policy at the University of Medicine and Dentistry of New Jersey. "Then, they spend two to three times more on marketing than on research to persuade doctors to prescribe these new drugs. Doctors may get misleading information and then misinform patients about the risks of a new drug. It's really a two-tier market for lemons."
Three reasons why the pharmaceutical market produces "lemons" are: Having companies in charge of testing new drugs, providing firewalls of legal protection behind which information about harms or effectiveness can be hidden, and the relatively low bar set for drug efficacy in order for a new drug to be approved, Light said.
According to his study, independent reviewers found that about 85 percent of new drugs offer few if any new benefits. Yet, toxic side effects or misuse of prescription drugs now make prescription drugs a significant cause of death in the United States.
Light's paper, "Pharmaceuticals: A Two-Tier Market for Producing 'Lemons' and Serious Harm," is an institutional analysis of the pharmaceutical industry and how it works based on a range of independent sources and studies, including the Canadian Patented Medicine Prices Review Board, the Food and Drug Administration, and Prescrire International.
The foundation for the paper is the work Light did for a forthcoming book he edited, titled 'The Risk of Prescription Drugs," which is scheduled for publication this fall by Columbia University Press.
In both his paper and his book, Light describes the "Risk Proliferation Syndrome" that is maximizing the number of patients exposed to new drugs that have relatively low efficacy and effectiveness but have greater risk of adverse side effects. Building on clinical trials designed to minimize evidence of harm and published literature that emphasizes a drug's advantages, companies launch massive campaigns to sell it, when a controlled, limited launch would allow evidence to be gathered about the drug's effects. Companies recruit leading clinicians to try using the drug for conditions other than those for which it is approved and to promote such off-label or unapproved uses. Physicians inadvertently become "double agents" -- promoters of the new drug, yet trusted stewards of patients' well-being, said Light. When patients complain of adverse reactions, studies show their doctors are likely to discount or dismiss them, according to Light.
Despite the extensive requirements for testing the efficacy and safety of each new drug, companies "swamp the regulator" with large numbers of incomplete, partial, substandard clinical trials, Light said. For example, in one study of 111 final applications for approval, 42% lacked adequately randomized trials, 40% had flawed testing of dosages, 39% lacked evidence of clinical efficacy, and 49% raised concerns about serious adverse side effects, said Light.
"Just recently, major reports have come out about biased, poor trials for Avandia and Avastin," Light said, who noted that orphan drugs are tested even less well.
"The result is that drugs get approved without anyone being able to know how effective they really are or how much serious harm they will cause," Light said. The companies control the making of scientific knowledge and then control which findings will go to the FDA or be published.
"A few basic changes could improve the quality of trials and evidence about the real risks and benefits of new drugs," Light said. "We could also increase the percentage of new drugs that are really better for patients."
The paper, "Pharmaceuticals: A Two-Tier Market for Producing 'Lemons' and Serious Harm," was presented on Aug. 17 in Atlanta at the American Sociological Association's 105th Annual Meeting.
When I was little, my mom took me to the doctor every time I got even the sniffles! I always ended up with an antibiotic... I'm not sure if it was the doctor or if my mom was pushing the doctor to prescribe one. I would get sick at least once every 2 months, sometimes more. I had terrible asthma which would get worse each time I had an infection. My immune system was never able to fight them on it's own...I mean, I can't count the times I remember taking the liquid antibiotics because I was too small to swallow pills! I knew the names of all of them and I knew exactly how each one was taken and how it tasted. It was THAT often!
When I got to be about 14, I realized that cold medicine and antibiotics weren't doing me any good. So I would refuse to go to the doctor for minor things. I even stopped taking my inhaler! I said I was going to train my body to not react to exercise and allergens with asthma. It worked! I only had to do that for a few months and my attacks decreased in frequency...significantly!
I finally don't get sick every month and I haven't had an asthma attack in about 5 years. I don't believe I have asthma anymore. I can be engaged in heavy exercise for hours and I don't feel a thing. I also think that singing helped strenghthen my lungs. Now my respiration rate is always on the low end.
Statistics show that whenever there was a strike by doctors, the death rate in the affected population fell dramatically. In 1976, the death rate fell by 35%in Bogota, Colombia. In Los Angeles County, CA, it fell by 18% during a strike in the same year. While in Israel it fell by 50% during a strike in 1973. Only once before was there a similar drop in the death rate in Israel and that was during another doctor's strike 20 years earlier. After each strike the death rate jumped again to its normal level - Walter Last
Statistics show that whenever there was a strike by doctors, the death rate in the affected population fell dramatically. In 1976, the death rate fell by 35%in Bogota, Colombia. In Los Angeles County, CA, it fell by 18% during a strike in the same year. While in Israel it fell by 50% during a strike in 1973. Only once before was there a similar drop in the death rate in Israel and that was during another doctor's strike 20 years earlier. After each strike the death rate jumped again to its normal level - Walter Last
Bear in mind knightofalbion, the quy who is put that quote here, has suggested in another thread, you take the advice of health professionals when it comes to taking an effective amount of vitamin D, even though in practice the amount they suggest always, inevitably, leaves everyone vitamin D insufficient.
Statistics show that whenever there was a strike by doctors, the death rate in the affected population fell dramatically. In 1976, the death rate fell by 35%in Bogota, Colombia. In Los Angeles County, CA, it fell by 18% during a strike in the same year. While in Israel it fell by 50% during a strike in 1973. Only once before was there a similar drop in the death rate in Israel and that was during another doctor's strike 20 years earlier. After each strike the death rate jumped again to its normal level - Walter Last
I dont hold any brief for big pharma but I always wince a bit whenever I hear this quotation, which seems to turn up quite a lot on alt med forums.
The assumption appears to be that patients in hospitals will receive fewer drugs and therefore have less chance of damaging side effects or being victims of wrong prescribing of drugs.
Whenever doctors go on strike in a hospital its never a mass walkout of all staff. Normally A&E and existing inpatients are treated as normally and patients will still get the same amount of drugs. Doctors are well aware of possible class action malpractice if a patient is denied their drugs in a strike situation.(Even if we believe these drugs are killing them quicker.)
Where the workload is usually drastically cut is in 'elective surgery', that is they dont do any of those operations that are not classed as urgent. These are mainly in the elderly,such things as hip joints, coronary bypasses and back surgery etc.
Normally, these type of operations have a 5% or thereabouts chance of mortality especially in the elderly, so in a lengthy strike you are going to get a fair reduction in the number of deaths from not doing this type of surgery.
The only study I know that has looked into the statistics of these strikes appears to agree with this.
I think there is quite enough evidence against the normal medical paradigm without constantly bringing up the question of Doctors Strikes which to me doesnt quite hold water.
Avonex (was $10,000/year): Minimum price = $23,736; Maximum price = $30,660
Betaseron (was $10,000/year): Minimum price = $22,272; Maximum price = $32,616
Copaxone (was $10,000/year): Minimum price = $23,208; Maximum price = $33,804
Rebif was (was $15,600/year): Minimum price = $25,068; Maximum price = $30,756
Tysabri (was $28,400/year): Now costs 31,332 for the drug itself, with additional charges for the infusion facility or clinic fees.
Read the full articles:
You can see why the drugs industry is pressing for more drugs to be used and trying to suppress the use of effective supplements.
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Men with low prostate-specific antigen (PSA) values may face more risks than benefits from aggressive approaches to prostate cancer screening and evaluation -- along with potential overtreatment -- data from a large cohort study suggest.
The retrospective study of more than 85,000 men (ages 55 to 74) found that those with low serum PSA levels were likely to undergo aggressive evaluation (such as biopsies) and treatment -- with little or no decrease in mortality -- according to Pim J. van Leeuwen, MD, of Erasmus University Medical Center in Rotterdam, Netherlands, and colleagues.
Using a PSA cutoff of less than 2 ng/mL, every life saved would require investigation and workup of almost 25,000 men and treatment of more than 700, van Leuwen and co-authors wrote in an article published online in the journal Cancer
In contrast, a PSA value of 10 to 19.9 ng/mL was associated with a number needed to investigate (NNI) of 133 and a number needed to treat (NNT) of 60, they found.
"For men with a low serum PSA level, the benefits of aggressive investigation and treatment may be limited because they are associated with a large increase in cumulative incidence and potential overtreatment," van Leeuwen and co-authors concluded.
Prostate cancer incidence and mortality increased with baseline PSA values among men who were aggressively screened and followed or who had routine clinical follow-up, the researchers noted.
Patients who were followed aggressively had a prostate cancer incidence that was almost three times higher than that of the clinical group, but prostate cancer mortality was less than 1% in both groups, they added.
"In the absence of standardized early detection programs, PSA level can be used for a risk assessment that balances the harms and benefits of early detection in men aged 55 to 74 years," van Leeuwen's team wrote. "Current analyses suggest that the significant reduction in disease-specific mortality with screening and early detection may be limited to men with baseline elevated PSA levels."
Prostate cancer screening remains controversial and the subject of continual investigation aimed at identifying optimal screening strategies.
Recently, a large European study showed a 20% reduction in prostate cancer mortality relative to a control group. However, the reduction in mortality came at a cost of a substantial increase in cumulative excess incidence, associated with a number needed to screen of 1,410 and NNT of 48 (N Engl J Med 2009; 360: 1320-1328).
Moreover, an even larger North American study published simultaneously with the European study showed no effect of PSA screening on prostate cancer mortality (N Engl J Med 2009; 360: 1310-1319).
In a study aimed at continuing the evaluation of the benefits and harms of prostate cancer screening, van Leeuwen and co-authors analyzed data on two large cohorts: 43,987 men randomized to the intervention arm in a study of prostate cancer screening and 42,503 men in an unrelated clinical population that served as a control group.
The men in the intervention group had serial PSA screening and PSA-triggered investigation, including biopsy. In the control group men had a baseline PSA test and then were followed clinically in accordance with local standards.
The ages of men in both groups were 55 to 74, and all had baseline serum PSA values less than 20 ng/mL and no history of prostate cancer. Median follow-up was eight to nine years and ended Dec. 31, 2006.
Men in the control group were older (median age 65 versus 61, P<0.001), had a higher median baseline PSA value (1.60 versus 1.18 ng/mL, P<0.001), and a significantly lower proportion of patients with PSA values of 0 to 1.99 ng/mL (60.1% versus 72.8%, P<0.001).
The intervention group had a prostate cancer incidence of 9.9% compared with 3.6% in the control group (P<0.001). In the control group, men who had prostate cancer diagnoses were significantly older (71 versus 66, P<0.001), and their median time to diagnosis was significantly longer (5.3 versus 4.1 years, P<0.001).
The significant excess in incidence rates mainly resulted from repeated systematic screening using a lateralized sextant biopsy technique, the researchers wrote.
At the end of follow-up, overall mortality was 25.5% in the control group and 14.5% in the intervention group. However, prostate cancer-related mortality did not differ significantly between the control (0.6%) and intervention (0.2%) groups.
The main limitation of the study was the absence of randomization, resulting in different patient characteristics at study entry. "Statistical adjustment was needed for the difference in age and serum PSA level at study entry. Furthermore, the large difference in all-cause mortality might have biased the outcomes," van Leeuwen and co-authors wrote. Another limitation that could have led to bias was the different PSA assays used, they added.
This study is controversially proposing that small increases in PSA levels indicate that the body is trying to defend itself against tumour angiogenesis (increased tumour blood supply)thereby slowing cancer growth,and by attempting to lower PSA this would be counterproductive. This makes the case that sometimes its better not to attempt over medication or testing procedures. This does not apply to people with rapidly rising PSA levels which signals that the cancer is out of control.
Antiangiogenic Activity of Prostate-Specific Antigen
Anne H. Fortier, Barbara J. Nelson, Davida K. Grella, John W. Holaday
Affiliation of authors: EntreMed, Inc., Rockville, MD.
BACKGROUND:
Measurement of serum levels of prostate-specific antigen (PSA) is widely used as a screening tool for prostate cancer. However, PSA is not prostate specific, having been detected in breast, lung, and uterine cancers. In one study, patients whose breast tumors had higher levels of PSA had a better prognosis than patients whose tumors had lower PSA levels. To test the hypothesis that PSA may have antiangiogenic properties, we evaluated the effects of PSA on endothelial cell proliferation, migration, and invasion, which are key steps in angiogenesis, the process by which tumors develop a blood supply.
METHODS: To assess the antiproliferative effects of PSA, we treated bovine endothelial cells and human endothelial cell lines (HUVEC and HMVEC-d) with purified human PSA (0.1-10 �M) and then stimulated them with 10 ng/mL fibroblast growth factor-2 (FGF-2). Effects on FGF-2- or vascular endothelial growth factor (VEGF)-stimulated endothelial cell migration, invasion, and tube formation were measured by use of one cell line only (HUVEC). PSA was administered to mice at 9 �M for 11 consecutive days after intravenous inoculation of B16BL6 melanoma cells to assess its ability to inhibit the formation of lung colonies (i.e., metastatic tumors).
RESULTS:
PSA inhibited endothelial cell proliferation, migration, and invasion at IC50 (i.e., the concentration at which inhibition was 50%) values ranging from 0.3-5 �M. In addition, PSA inhibited endothelial cell responses to both angiogenic stimulators tested, FGF-2 and VEGF. In a mouse model of metastatic disease, daily PSA treatment resulted in a 40% reduction in the mean number of lung tumor nodules compared with phosphate-buffered saline treatment (two-sided P = .003).
CONCLUSION:
To our knowledge, this is the first report that PSA may function in tumors as an endogenous antiangiogenic protein. This function may explain, in part, the naturally slow progression of prostate cancer. Our findings call into question various strategies to inhibit the expression of PSA in the treatment of prostate cancer.
"From inability to let well alone; from to much zeal for the new and contempt for what is old; from putting knowledge before wisdom,science before art, and cleverness before common sense; from treating patients as cases and making the cure of the disease more grievous than the endurance of the same, good Lord deliver us."
Sir Robert Hutchinson, President of The Royal College of Physicians (1871-1960)
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