A review in the British Medical Journal found that anti-inflammatory drugs cause heart disease. The use of selective cyclooxygenase-2 inhibitors (a type of anti-inflammatory) is associated with a 1.4-fold increase in the risk of heart attack, stroke, or death from vascular disease compared with placebo. Further, large doses of diclofenac and ibuprofen are also associated with an increased risk. In a meta-analysis of 138 randomised trials and almost 150 000 participants, Kearney et. al. (1) found that the hazard was not confined to long term use only.

Cyclooxygenase-2 (COX 2) inhibitors were regarded as a preferable alternative to conventional non-steroidal anti-inflammatories (NSAIDS) for some conditions, particularly arthritis. The inhibition of cyclooxygenase-2 has been more directly implicated in ameliorating inflammation, whereas the inhibition of cyclooxygenase-1 (older NSAIDS like diclofenac and ibuprofen inhibit COX 1 along with COX 2) has been related to adverse effects in the gastrointestinal tract (indigestion, abdominal pain, gastric or duodenal perforation or bleeding). Therefore, it was hoped that coxibs would be better tolerated than nonselective NSAIDs but equally effective.

The suspicion that COX 2 inhibitors could cause heart problems was raised by a 2001 review in the New England Journal of Medicine (2).

We must gather additional information on the pharmacology of the coxibs. Given the cardiovascular findings in the VIGOR (Vioxx Gastrointestinal Outcomes Research) trial and the association of both rofecoxib and celecoxib with small, but potentially clinically relevant, changes in blood pressure, elucidation of the cardiovascular and renal effects of these drugs and their interactions with potential adjuvant therapies, such as low-dose aspirin, is imperative.

A risk analysis was therefore required as to which was worse in individuals who could not tolerate conventional NSAIDs: increased risk of heart disease vs. pain from arthritis.

Add this average increased global risk of adverse myocardial and vascular events for people taking NSAIDS to the already elevated risk of individuals with blood group A, AB and non-secretors or Lewis negative, and you may feel your heart miss a beat.

The choice between different anti-inflammatory regimens requires assessment of the individual expected absolute attributable risks of cardiovascular and serious gastrointestinal events.

This sounds like wise advice from the BMJ, but how much can orthodox medicine judge "individual expected absolute attributable risks" without knowing the individual patient in depth?

In naturopathic medicine simply blocking the pain and saying a person is cured is like opening the windows to let the smoke out while the fire rages below. There are numerous anti-inflammatory herbs and natural medicines (ignored in mainstream studies) with far fewer side effects than pharmaceuticals, but a naturopathic physician will also address the cause of the problem in the individual.

Kidney disease is a side effect of high-dose analgesic paracetamol (acetaminophen), but remains widely available. Rofecoxib (a COX 2 inhibitor) was withdrawn from the market on September 30th 2004 because of concerns over myocardial infarction. Let's hope the other pharmaceutical NSAIDs follow soon, people will have to look into dietary and lifestyle changes to prevent inflammation, and natural medicines will get the attention they deserve.

Follow up:

References:

1. Kearney PM, Baigent C, Godwin J, et. al.

Do selective cyclo-oxygenase-2 inhibitors and traditional non-steroidal anti-inflammatory drugs increase the risk of atherothrombosis? Meta-analysis of randomised trials.

BMJ. 2006 Jun 3;332(7553):1302-8.

PMID: 16740558

2. FitzGerald GA, Patrono C.

The coxibs, selective inhibitors of cyclooxygenase-2.

N Engl J Med. 2001 Aug 9;345(6):433-42.

PMID 11496855