Sensational news headlines hyping results from a recent Nature Medicine study may have your clients convinced that L-carnitine, a popular supplement and nutrient in red meat, causes heart disease. A closer look at the study suggests that a byproduct of L-carnitine metabolism promotes atherosclerosis in mice, but what about men? Human studies show carnitine’s heart-healthy benefits. With these conflicting reports, it’s no wonder consumers and health professionals alike are confused about L-carnitine’s role in maintaining health and well-being.
L-carnitine is a conditionally essential micronutrient synthesized in the liver and kidneys from lysine and methionine. Synthesized L-carnitine is delivered to skeletal and cardiac muscle, where its main job is to shuttle long-chain fatty acids into the mitochondria for beta-oxidation and energy prodcution.
L-carnitine is abundant in animal products and nearly negligible in plant sources. While as much as 54-87% of food-derived L-carnitine is bioavailable and well-absorbed in the body, oral supplements of L-carnitine have low bioavailability with only14-18% absorbed (Rebouche 2004).
L-carnitine levels are tightly controlled through a combination of synthesis, diet and kidney reabsorption (Reuter & Evans 2012). Vegans synthesize and reabsorb more L-carnitine than omnivores (Rebouche & Chenard 1991). The intestines can absorb up to about about 2,000 milligrams (Reuter & Evans 2012) of L-carnitine. Microbes in the intestines degrade excessive, unabsorbed L-carnitine into gamma-butyrobetaine, which is eliminated in the feces; and trimethylamine-N-oxide (TMAO), which is excreted by the kidneys (Rebouche & Chenard 1991).
Koeth et al. found that elevated TMAO accelerates atherosclerosis in mice. In humans, omnivores produced more TMAO than vegans in response to ingestion of 250 mg of a heavy isotope labeled L-carnitine supplement and 180 mg of L-carnitine from steak. In the observational portion of the study, higher blood carnitine was linked to greater cardiac event risk. The authors concluded that the association was due to TMAO rather than carnitine.
Within days of the Koeth et al. study, a Mayo Clinic systematic review of 13 controlled trials involving 3,629 people found that L-carnitine reduces abnormal heart rhythms and angina in patients experiencing heart attacks (DiNicolantonio 2013). Compared with control or placebo, L-carnitine was linked to a 27% reduction in all-cause mortality, a 65% reduction in ventricular arrhythmias and a 40% reduction in angina in patients experiencing an acute myocardial infarction (MI). However, there was no link between L-carnitine and a reduced risk of heart failure and MIs.
Should consumers shun or run to carnitine? Dietary and supplemental sources of L-carnitine have a long history of safety and health benefits (Higdon & Drake 2012; Reuter & Evans 2012). The Koeth et al. study sheds light on a potential mechanism for the development of heart disease, but is not conclusive and should not discourage use of L-carnitine. Health professionals should critically evaluate the available literature while noting the absorptive differences between food-derived and supplemental forms of L-carnitine, the limitations of the Koeth et al. study, and the large body of evidence that supports carnitine’s role as a vital micronutrient.
Photography By: RJ Dollen