Abstract
arch, I n early April 2013, Koeth et al 1 published in Nature Medicine an original article providing evidence that ingested L-carnitine can encourage the growth of intestinal microbiota capable of converting carnitine to trimethylamine; the latter compound, on absorption, can be oxidized in the liver to trimethylamine-N-oxide (TMAO), which the authors suggested was likely to be a key mediator of the adverse impact of red meaterich diets on human vascular health. This report immediately gained attention in the nation’s media. For example, Koeth et al’s research was a highlighted story on the CBS Evening News With Scott Pelley on the evening of Friday, April 5, 2013, and by Sunday, April 7, Gina Kolata of the New York Times had cited this research in an article questioning the safety of carnitine. Within days of this report,Mayo Clinic Proceedings electronically published ahead of print a meta-analysis by DiNicolantonio et al of 13 placebo-controlled clinical trials enrolling 3629 patients that had evaluated the clinical impact of L-carnitine administration (as a supplement, not in red meat) in patients who had previously experienced amyocardial infarction. This meta-analysis concluded that carnitine administration was associated with clinical benefit: decreased mortality and reduced onset of cardiac arrhythmias and angina. The journal also issued a press release noting the findings of DiNicolantonio et al and their relevance to the report by Koeth et al. Other media sources seized on the seeming inconsistency of these reports, with websites such as Forbes.com, hearthealth.com, and junkscience.com offering commentary. This second wave of media reports was followed shortly thereafter by many hundreds of media stories on one or both of the L-carnitine studies. In publications focusing on choline, which, similar to carnitine, can be converted to trimethylamine by intestinal microbiota, Koeth and his colleagues have made a case that TMAO may be a mediating risk factor for atherosclerosis.
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