A new study purports to demonstrate that the reason consumption of red meat seems to increase the risk of heart disease is not due to the presence of saturated fat and cholesterol.

One is tempted to say, “Duh!”

However, the “answer” creates more confusion than clarity, as the culprit is carnitine, a biological compound synthesized from the amino acids found in meat. Carnitine is essential to the transport of fatty acids inside cells, where they are metabolized for energy production.

Cleveland Clinic researchers identified a bacteria in the intestinal tract that interact with carnitine and turns it trimethylamine-N-oxide (TMAO), a metabolic waste product linked to the promotion of atherosclerosis, a disease where plaque builds up in arteries, compromising the circulation of oxygenated blood to the heart and other internal organs. Atherosclerosis is considered a serious risk factor for heart attacks and strokes.

“Carnitine metabolism suggests a new way to help explain why a diet rich in red meat promotes atherosclerosis,” Dr. Stanley Hazen stated in a Cleveland Clinic news release. Hazen is section head of preventive cardiology and rehabilitation in the Miller Family Heart and Vascular Institute at the Cleveland Clinic and the lead author of the study, which was published in the April 7 issue of Nature Medicine online.

According to the news release, Hazen and his team determined that not only do intestinal bacteria turn carnitine into TMAO, but a diet high in carnitine promotes the growth of those carnitine metabolizing bacteria, creating a vicious cycle.

The study was based on evaluations of 2,595 patients undergoing heart exams, and the data showed that increased carnitine levels raised the risks for cardiac events in subjects with high levels of TMAO.

What’s even worse, however (if you only read the clinic’s news release), the researchers found that the baseline TMAO levels were significantly lower among vegans and vegetarians, as opposed to omnivores. Even after consuming a large amount of carnitine, vegans and vegetarians did not produce significant levels of TMAO, whereas omnivores consuming the same amount of carnitine did.

“A diet high in carnitine actually shifts our gut microbe composition to those that like carnitine,” Hazen said, “making meat eaters even more susceptible to forming TMAO and its artery-clogging effects.”

A multi-faceted Rx

Okay, so it’s obvious, right? Less meat means less carnitine, which means less obnoxious gut bacteria producing waste products that turn your arteries into clogged sludge.

Well, not exactly.

First of all, carnitine is an essential metabolite, produced by the body to fulfill essential biological functions. Since we know that human physiology evolved over many millennia on a diet rich in meat, it doesn’t make sense that carnitine, synthesized from the amino acids in meat, could suddenly be the cause of our modern scourge of cardiovascular disease.

In fact, a whole raft of human genetic disorders affecting the internal production of carnitine are known to exist, and they produce all manner of problems with fatty acid metabolism and thus cellular energy production.

Second, as people—especially women—get older, cellular concentrations of carnitine diminish, adversely affecting bone structure. The administration of L-carnitine has been shown to increase serum concentrations of osteocalcin (a protein essential for bone-building) in animals and in fact has been patented as a treatment for osteoproposis in post-menopausal women. A few years ago, the National Institutes of Health even held a two-day symposium to determine research priorities for carnitine as a drug treatment, one of which was “for prevention of osteoporosis in older women who depend on thyroid-stimulating hormone.”

Other studies show that carnitine is far from merely a heart disease villain, as media reports portrayed it:

  • Regular supplements of L-carnitine contribute to energy metabolism and improved neurotransmitter function in the brains of elderly patients (American Journal of Clinical Nutrition December 2007).
  • Asthmatic children who received L-carnitine supplementation for six months showed statistically significant improvement in their “asthma control testing” and in their pulmonary function tests (Journal of Allergy 2012).
  • The use of carnitine showed promise in a controlled trial in selected cases of male infertility (Fertility and Sterility 2003).
  • A daily dosage of 2 to 4 grams of oral L-carnitine seemed to reverse hyperthyroid symptoms, even in the most serious form of hyperthyroidism (Annals of the New York Academy of Science, 2006).
  • Studies showed that while questionable as a weight loss aid, oral carnitine supplementation reduced fat mass, increased muscle mass and reduced fatigue (report from the University of Maryland Medical Center) and that L-carnitine and L-tartrate supplementation for six months improved muscle metabolism and performance (Journal of Physiology 2001).

One expert, Dr. Harlan Krumholtz, a professor of medicine and epidemiology and public health at Yale University School of Medicine, wrote in Forbes that while Hazen’s study may be potentially groundbreaking, the findings need to be repeated before doctors start measuring people’s intestinal bacteria to determine their disease risk from eating meat.

Not to mention that some prominent dieticians are sounding a note of caution.

“There’s no need to change our dietary recommendations from this [study],” Catherine Collins, a dietitian at the UK’s Science Media Centre, told Britain’s Business Insider. “A Mediterranean-style diet with modest meat, fish, dairy and alcohol intake, coupled with more beans, vegetables, fruits and whole grains remains the nutritional blueprint for a healthy and healthful life.”

You go, girl.

The opinions expressed in this commentary are solely those of Dan Murphy, a veteran food-industry journalist and commentator.