Nature medicineApr 9, 2013

Gut bacteria breaking down L-carnitine from red meat may promote artery hardening

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Mar 28, 2026

Abstract

Omnivorous human subjects produced more trimethylamine-N-oxide (TMAO) than vegans or vegetarians after ingesting L-carnitine.

Intestinal microbiota metabolizes dietary L-carnitine, found in red meat, to produce TMAO, which is linked to atherosclerosis.
Specific bacterial taxa in human feces are associated with both plasma TMAO levels and dietary status.
In a large cohort of 2,595 cardiac evaluation subjects, plasma L-carnitine levels predicted increased cardiovascular disease risk, but only with high TMAO levels.
Chronic L-carnitine supplementation in mice significantly altered gut bacteria, increased TMA and TMAO production, and enhanced atherosclerosis.
Dietary supplementation with TMAO or L-carnitine or choline reduced reverse cholesterol transport in mice with intact intestinal microbiota.

Simplified

Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO). We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice. Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism. The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status. Plasma L-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels. Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed. In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport. Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk.

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Gut bacteria breaking down L-carnitine from red meat may promote artery hardening

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