You may have seen media reports about a scientific study suggesting that carnitine could be linked to heart disease. Carnitine – found naturally in red meat, poultry, and fish (and also available as a dietary supplement) – is an amino acid. Unlike most amino acids, carnitine is not used in the body to make proteins. Instead, carnitine is used to transport fat inside a cell to allow fat burning and energy metabolism.
The scientific study found that high plasma levels of carnitine in human subjects are associated with an increased risk of cardiovascular disease, including heart attacks and strokes. Furthermore, when they used a mouse model, increasing the level of carnitine they ate seemed to promote atherosclerosis, one of the underlying causes of cardiovascular disease.
The authors of the study found carnitine isn’t the bad guy here, at least not directly. Gut bacteria can convert carnitine into a substance called trimethylamine oxide (TMAO), which is absorbed into the body. The level of TMAO seems to be what is causing the increased risk for heart disease. In a related study, the same authors reported that lecithin and choline, two nutrients abundant in meat and egg yolk, also can give rise to TMAO in the body after conversion by intestinal bacteria.
Both studies were published in prestigious scientific journals, and the principal investigator and senior author, Dr. Stanley Hazen, is a highly respected, first-rate scientist.
Yet my reaction to the carnitine study is that it is intriguing and novel but far from definitive. To call carnitine a culprit in heart disease in humans, as the press labeled it, is premature. I still believe the main culprit in red meat for causing atherosclerosis and increasing cardiovascular risk is high levels of saturated fat, and not carnitine, lecithin, and choline.
I doubt the link between TMAO and atherosclerosis, because other studies have shown that TMAO is associated with a healthy diet. A British study published in 1999 found that the consumption of 8 oz. of marine fish, such as cod, haddock, halibut, or herring, elevated urinary levels of TMAO and its precursor, trimethylamine, on average about 35 times, whereas eating 8 oz. of beef, other meats, or dairy products such as cheese, eggs and milk had no effect on the background levels of these compounds! And we know that the consumption of fish is associated with a lower risk for heart disease.
A large body of work, accumulated over decades, indicates that one form of carnitine called acetyl-L-carnitine is safe to use at appropriate doses. Acetyl-L-carnitine has been given clinically at very high doses – as much as 8 grams per day – with no observed side effects. Furthermore, we know from studies in rodents that acetyl-L-carnitine improves mitochondrial function, lowers lipid levels (which would lower cardiovascular risk), and improves muscle and brain function.
Therefore, based on current evidence, carnitine appears to have significant health benefits, and the balance – or “benefit-to-risk ratio”– favors the use of carnitine supplements.
Personally, I will continue to take a daily supplement containing 1,000 mg of acetyl-L-carnitine. In addition, I exercise regularly, eat a heart-healthy diet, and avoid red meat.
As a resource of trusted nutrition information for the public, we at the Linus Pauling Institute continually reassess our recommendations, based on new scientific information. We will let you know if we find compelling evidence against carnitine supplementation.
In addition to our Research Newsletter and Micronutrient Information Center (MIC), we are enhancing our communication efforts, such as with this new blog, to help you make informed personal decisions towards achieving optimum health.
To your health!
Balz Frei, Ph.D.
Director and Endowed Chair, Linus Pauling Institute
Joan H. Facey Linus Pauling Institute Professor
Distinguished Professor of Biochemistry and Biophysics