Our medicalized approach to pain may be putting us in harms way. However, there are safe, natural approaches that can ease painful conditions.
How Coxibs Killed Tens of Thousands
Non-steroidal anti-inflammatory drugs (NSAIDs), which include over-the-counter pharmaceuticals such as ibuprofen, naproxen, and aspirin, rank among the most widely used pharmaceuticals worldwide. Their chief mechanism of action is inhibition of two forms of cyclo-oxygenase (COX), namely COX-1 and COX-2 (1). Also known as prostaglandin-endoperoxide synthase (PTGS), COX is responsible for the production of downstream mediators of pain and inflammation, such as thromboxane and prostaglandins. Due to their suppression of prostaglandins, which exert protective roles in the gastrointestinal tract, one of the most frequent adverse effects of NSAIDs is irritation of the gastric mucosa.
Thus, newer generation selective COX-2 drugs, known as the coxibs, were introduced in the 1990s to mitigate the risk of peptic ulceration that results from COX-1 suppression. By 2004, coxibs had dominated the prescription drug market for NSAIDs, with worldwide sales of approximately $10 billion (2). Their development was based on the premise that COX-1 was the source of the cytoprotective prostaglandins in the gastric epithelium, whereas COX-2 was the source of the inflammatory mediators, prostaglandins E2 and I2 (2). However, as early as 1999, scientists had reported that coxibs inhibit generation of prostaglandin I2, the primary product of COX in the endothelium, responsible for reducing platelet aggregation and proliferation of vascular smooth muscle cells and for inducing vascular vasodilation (2).