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Meat, Carnitine and Heart Disease


7208-eat1A study released in April 2013 implicated beef as a primary cause of cardiovascular disease.1 What was surprising about the study, which was published in the journal Nature Medicine, was that the alleged reason for this risk factor wasn’t the fat or cholesterol content of the meat but rather its carnitine content.

Carnitine is an amino acid product familiar to most bodybuilders for its use in supplements, where it’s often touted as a fat burner. That’s based on the primary function of carnitine, which is to shuttle fatty acids into the mitochondrial portion of cells, where the fat is oxidized. Carnitine is essential for this process and is made in the liver and kidneys from the amino acids lysine and methionine, with the assistance of vitamins C, B6 and niacin and the mineral iron. How can an essential nutrient such as carnitine cause cardiovascular disease?

In fact, it isn’t carnitine itself that is the alleged culprit but a breakdown product of carnitine called trimethylamine-oxide. TMAO is produced from trimethylamine, which is degraded into TMAO through the actions of specific intestinal bacteria. According to the new study, that increase in TMAO leads to increased cholesterol being deposited in arterial linings, which can lead to cardiovascular disease, including heart attacks and strokes.

The biochemical basis of those findings regarding TMAO conversion was that it occurred in lab mice and did accelerate the progression of cardiovascular disease in the animals. The problem, however, is that the type of bacteria that converted TMA into TMAO in the mice doesn’t exist in humans. The authors conjecture that eating beef habitually does boost the intestinal content of this type of bacteria, but they offer only indirect proof. The bacteria doesn’t exist in vegetarians, so they directed one vegetarian to eat a 12-ounce serving of beef and also take a carnitine supplement. Even so, the vegetarian showed no increased production of TMAO, and that was the primary basis of their assertion that beef causes changes in intestinal bacteria that favor the buildup of the type of bacteria that readily converts TMA into TMAO. Even in the mice that did have the dangerous bacteria, the production of TMAO from carnitine was completely suppressed when the rodents were given an antibiotic before eating beef.

Initially, this study appears alarming for those who eat beef—until you consider a few other facts. For one thing, numerous studies have shown that carnitine exerts a beneficial effect on cardiovascular disease, which isn’t hard to understand when you consider that the heart’s preferred fuel is fat, not sugar, and carnitine allows the heart to use fat more effectively. For that reason, carnitine is suggested as an effective treatment for various heart ailments, including congestive heart failure, characterized by a failing heart muscle unable to produce sufficient adenosine triphosphate, or ATP, the body’s primary elemental energy source.

Indeed, less than two weeks after the Nature Medicine study was released, another study appeared in the Mayo Clinic Proceedings which found that carnitine significantly improves patient outcomes following a heart attack.2 The review looked at 13 controlled studies involving 3,629 patients who took L-carnitine and found the following:

1) A 27 percent reduction in all-cause mortality

2) A 65 percent reduction in heart rhythm disturbances, a common cause of heart attacks

3) A 40 percent reduction in the development of angina, or “heart pain.”

4) A significant reduction in the size of infarcted tissue in the heart, meaning heart tissue that has been destroyed during heart attacks. Carnitine helps the heart because it not only aides the use of fat more efficiently but also boosts mitochondrial function, which boosts the output of ATP, and that protects heart cells from dying.

From a bodybuilding standpoint, carnitine provides many benefits. Although its fat oxidation effect is questionable (because supplemental carnitine tends to increase carnitine mainly in the blood rather than in muscle, where fat is oxidized), with some studies showing definite effects and other none, other benefits are more apparent. That includes an upgrade in cell androgen receptors, which boosts testosterone availability to cells.

A recent study showed that carnitine (although in massive amounts) also blunts catabolic effects in muscle through blocking catabolic pathways and increasing the anabolic hormone IGF-13.

Other studies show that carnitine increases work efficiency by an average of 11 percent, accomplishing that through lowered glycogen use and decreased lactate production in muscle during exercise. Carnitine also boosts nitric oxide by an average of 18 percent, far more than any “NO-boosting” supplement on the market. That, however, involves a specific form of carnitine, propionyl-L-carnitine, which has been used in Europe for years as a heart medication.

Thus, the theory that carnitine—and by extension, red meat—are dangerous seems to be based on flimsy evidence, and the evidence to the contrary is quite robust. So eat your meat, put on muscle, and relax! —Jerry Brainum

 

Editor’s note: Have you been ripped off by supplement makers whose products don’t work as advertised? Want to know the truth about them? Check out Natural Anabolics, available at JerryBrainum.com.

1 Koeth, R.A., et al. (2013). Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis. Nature Medicine. 19(5):576-85.

2 Dinicolantonio, J.J., et al. (2013). L-carnitine in the prevention of cardiovascular disease: Systemic review and metanalysis. Mayo Clinic Proceedings. 88.

3 Keller, J., et al. (2013). Supplementation of carnitine leads to an activation of the IGF-1/P13K/Akt signalling pathway and downregulates the E3 MuRF1 in skeletal muscle of rats. Nut Metabol. 10:28.

 

Commentary by Dr. Steven Zeisel

Dr. Hazen and colleagues have published a series of three papers suggesting that choline and carnitine are precursors of trimethylamine oxide formation. In a special mouse model, where the animals have been genetically modified to have very high cholesterol and develop atherosclerosis, Hazen finds that administration of TMAO is sufficient to increase heart disease in the mice. That’s the most interesting piece of data and indicates that additional research should be conducted on TMAO.

The other data presented in the three papers is more problematic. All of the human population data presented by Hazen shows that people with heart disease have a slightly higher blood concentrations of TMAO than people who don’t have heart disease. That’s an association and is not evidence of causality. If you examine the data carefully, you can see that people with heart disease have bad kidney function. Atherosclerosis is also damaging to the kidneys, which excrete TMAO. Thus, TMAO could be higher just because kidney function is lower. That would make it a marker of kidney function and not the cause of heart disease.

In the mouse studies giving the animals choline, in the presence of gut microbes, forms TMA, which in the liver is converted to TMAO. That has been known for decades. The bacteria colonize all the way up to the stomach in the mice, but in humans there are very few bacteria above the large intestine. Choline is absorbed in the small intestine—so in humans only large doses actually reach the bacteria in the small intestine. We knew that because patients treated with very large doses of choline smell fishy, which is the odor of TMA. In the mice bacteria easily get to choline; in humans choline should be absorbed before bacteria can get to it.

Regarding carnitine, the Hazen paper researchers had to give a large amount of meat to humans to see TMAO formed. Likely that amount was large enough that the meat was not fully digested before reaching the bacteria in the large intestine. Note that carnitine treatment generated much less TMAO. In the study where eggs were administered, there was no statistically significant bump in TMAO after two eggs. When labelled phosphatidylcholine was administered, there was an increase in labeled TMAO at six hours after the meal. That is likely the small portion of label that got to the large intestine, and the amount of TMAO formed was tiny.

So, while it is an intriguing theory, the supporting data are very preliminary and confounded. People should not overdose on choline or carnitine, but they should realize that these are needed nutrients, and that deficiency in them has serious consequences. Eat a diet of normal foods, and don’t worry.

 

Steven Zeisel M.D., Ph.D.
Professor of Nutrition
Nutrition Research Institute
University of North Carolina at Chapel Hill

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