This mixmaster meta-analysis is junk science because…
… heart disease and death are complex, multifactorial health outcomes that are not easily studied through statistical studies, even clinical trials. For example, it would be no surprise to find that people taking high and regular doses of NSAIDS are less healthy and less physically active to start with — and so could be expected to have higher rates of heart disease and death. Researchers cannot wave statistical wands over data to correct for this. In the end, these statistically borderline results aren’t very impressive.
The media release is below.
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Meta-analysis confirms common painkillers increase risk of heart problems and death but suggests size of these risks can be predicted
NSAIDs have been the cornerstone in managing pain in people with inflammatory disorders like rheumatoid arthritis, and are some of the most commonly used drugs worldwide. Earlier research has linked their use with an increased risk of serious gastrointestinal complications, while a new generation of NSAIDs (coxibs) developed to reduce these gastrointestinal side effects have come under scrutiny for increasing the risk of heart attacks and death.
This new study now shows that higher dose regimens of older NSAIDs, such as diclofenac 150mg and ibuprofen 2400mg daily, are associated with similar risks of heart disease.
As such, for every 1000 individuals with a moderate risk of heart disease allocated to 1 year of treatment with high-dose diclofenac or ibuprofen, about three would experience an avoidable heart attack, of which one would be fatal.
In addition, all NSAIDs double the risk of heart failure and produce a 2? times increased risk of serious upper gastrointestinal complications such as bleeding ulcers.
The Coxib and traditional NSAID Trialists’ (CNT) Collaboration combined data on outcomes of over 353 000 patients comparing one NSAID with another NSAID or placebo.
The meta-analysis of patient data from 639 randomised trials shows that the size of these risks can be predicted, which may help physicians decide which types of patient are best suited to which NSAID regimen.
Importantly, the increased risk of heart attacks from individual NSAIDs seemed to be proportional to a patient’s underlying risk of such heart attacks, so that the risk is highest in those with a previous history of heart disease or those with cardiac risk factors such as raised blood pressure or cholesterol.
According to lead author Professor Colin Baigent from the Clinical Trial Service Unit and Epidemiological Studies Unit, University of Oxford, UK, “Whilst NSAIDs increase vascular and gastrointestinal risks to a varying extent, our analyses indicate that the effects of different regimens in particular patients can be predicted, which may help physicians choosing between alternative NSAID regimens to weigh up which type of NSAID is safest in different patients.”**
Writing in a linked Comment, Marie Griffin from Vanderbilt University Medical Center in the USA says, “The meta-analysis offers considerable certainty about relative and absolute major vascular risks of high doses of the most commonly prescribed NSAIDs, but leaves large gaps about risks associated with lower NSAID doses, longer durations of use, and residual effects after stopping treatment.”
She adds, “Identification of safe and effective strategies for chronic pain is sorely needed. In the meantime, long-term use of high dose NSAIDs should be reserved for those who receive considerable symptomatic benefit from the treatment and understand the risks.”
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Having read the notable Harvard study on negative aspects of using opiate use, I had a doctor give me a standard injection of a popular NSAID to reduce inflammation in my back.
Within two hours following the NSAID injection, I began feeling a malaise and uncomfortable sensations in both kidneys. Within four hours, the malaise increased, and kidneys began aching. The following day kidney pain was significant followed by nausea and vomiting. By evening of the second day, the nausea and vomiting was acute, and pain in both kidneys was excruciating. I went to an emergency room and was admitted. I was administered high levels of opioids for treatment of the associated pain, and placed on IVs. Much to my own surprise, I was informed by hospital staff that NSAID toxicity and associated loss in kidney and other organ function was not uncommon. I read annual mortality statistics associated with acetaminophen, NSAIDs, and opioid use. To my surprise, NSAID toxicity and related organ failures topped the list in global mortality values. Rereading the Harvard study, I began to realize narrowness of the published 2013 study, and identified some bias in their statistical findings, based on data selection criteria.
While I still prescribe NSAIDs to my own patients, I am often doing so at OTC levels, and am continuing to prescribe alternative pain treatments for acute and chronic patients. While the 2013 Harvard study indicates the origin for most pains are located in the head, I have incorporated alternative notable studies and practices of merit for treatment of acute and chronic pain. NSAIDs have a use, but are not a paneca for pain sufferers.
Howdy dr22
I’ve never heard ibuprofen recommended for heart maintenance, I was just guesstimating an equivalent dosage. Ibuprofen is usually thought of as a stronger pain reliever than aspirin.
Aspirin and acetaminophen are dosed at about the same levels — 650 to 1000mg per does — but acetaminophen has a narrower toxic range. Crowding up on aspirin may upset your stomach, make your ears ring and lead to gastric bleeding. Crowding up on acetaminophen may leave you in line for a liver transplant — happened to a member of our church.
The Marie Griffen comment seems to leave the door open to doubts about low doses and the type of NSAID, of which asprin (acetylsalicylic acid) is one, that can lead to heart problems. Potential problems with high doses of others, such as ibuprofen, have been known or mentioned for quite a while (high blood pressure, liver, etc.), so I’m not sure there is much new in this meta analysis.
Just to be clear, the standard “heart protection” dose recommended for aspirin is an 81 mg (baby aspirin) dose. A standard aspirin is 325 mg (about 4x the baby dose). So for say a headache 2 aspirin would be your standard dose, which sounds right on.
Your point about Ibuprofen indicates it’s ‘more powerful.’ I intuit your 50mg Ibuprofen dose is to equate to the 81 mg aspirin heart dose?
So then the 2400 mg / day of Ibuprofen tested (indicated) in this study is 48X the recommended heart does — even worse!!!!
Ibuprofen and acetasalycilic acid are quite different, although they are related. Both reduce pain, inflammation and fever but do not lower normal body temperature.
A typical pain-related dose of ASA or aspirin is 650mg to 1000mg, a typical pain-related dose of ibuprofen is 400mg to 600mg. Somebody with chronic pain might well take 2400-3000mg of aspirin daily but that wouldn’t be a heart-maintenance regimen.
According to their warnings, both have some “blood-thinning” effect, that is, they reduce clotting tendency. But I’ve never heard a recommendation for 50mg of ibuprofen as a heart-attack measure or as a daily regimen.
“Aspirin” was a trademark of Bayer, at the time a German corporation. The US government “seized” the trademark during WWI and that made the term a generic instead of a brand name like “Advil”.
It seems mute on that subject. Indeed, assuming aspirin and Ibuprofin are the same, it seems they’re talking about taking 30X the dose (2400 mg) of aspirin than a low dose regimen (81 mg). 30X the normal dose of anything sounds dangerous to me.
So, this analysis says that the low dose aspirin is not a heart attack preventative?