Acetaminophen and NSAID Toxicity
Non-steroidal anti-inflammatory drugs (NSAIDs) are a diverse group of drugs with analgesic, anti-inflammatory, and antipyretic (fever-reducing) properties. NSAIDs are typically used to relieve mild to moderate pain related to a variety of conditions (Conaghan 2012; Goldman 2011; Mayo Clinic 2011).
Acetaminophen, also called paracetamol, is not an NSAID, but a distinct analgesic and fever reducing drug with a similarly broad usage (Amar 2007; Harvard Medical School 2006).
Acetaminophen overdose is the leading cause of acute liver failure in the developed world (Larson 2005; Craig 2010), accounting for more than 56,000 emergency room visits, 26,000 hospitalizations, and 450 deaths per year in the U.S. (Amar 2007). Acetaminophen can also contribute to kidney toxicity (Bessems 2001).
Although the “safe” dose of acetaminophen is up to 4 grams daily, chronic daily ingestion of this dose has been shown to cause elevations of liver enzymes, even in healthy people (Watkins 2006). Since alcohol, especially when consumed chronically, augments the toxic potential of acetaminophen, many people unknowingly put themselves at risk of significant liver damage by consuming acetaminophen and alcohol together (Sharma 2009; van Mil 2001).
Aspirin and NSAID usage has been associated with gastrointestinal toxicity including bleeding ulcer (Singh 1998; Vonkeman 2010). Certain NSAIDs (e.g., selective COX-2 inhibitors) have been linked to an increased risk of cardiovascular events, in particular heart attack. In addition, chronic use of some types of NSAIDs has been associated with kidney damage that may persist even after drug withdrawal in some cases (Trelle 2011; Back 2011; Moodley 2008; Ejaz 2004).
This protocol discusses the mechanisms of acetaminophen and NSAID function and toxicity, and outlines dietary and lifestyle approaches for minimizing their toxic potential.