In those who have suffered heart attacks …

Carnitine Significantly Reduces
All-Cause Mortality

Along with highly significant reductions in ventricular arrhythmias
and significant reductions in angina

By Will Block

A recent meta-analysis review, subsuming 13 controlled trials with a total of 3629 participants and published in the journal Mayo Clinic Proceedings, indicates that L-carnitine (hereafter carnitine) is helpful for heart disease.1 This type of review, identifying the common patterns of multiple studies, specifically tested carnitine on hard outcomes in humans who had already experienced a heart attack. The study found that carnitine was associated with significant reduction in death from all causes and a highly significant reduction in ventricular arrhythmias and anginal attacks (chest pain due to ischemia of the heart muscle) following a heart attack, compared with placebo or control. In other words, carnitine is extremely helpful to the heart, so much so that it actually heals it!

Carnitine Can Keep You Alive After a Heart Attack

The Mayo Clinic study provides strong evidence for carnitine’s benefits in heart health and represents the largest, most powerful scientific review of carnitine’s cardiovascular benefits to date. Its authors found that carnitine supplementation was associated with a 27% reduction in all-cause mortality, a 65% reduction in ventricular arrhythmias, and a 40% reduction in angina symptoms in patients who had experienced a heart attack. These effects were thought to occur through multiple mechanisms, including improved energy metabolism in the mitochondria, decreased ischemia, and enhanced left ventricle function.

Carnitine Provides Fuel for Mitochondria Thereby Producing Energy

Carnitine is manufactured by the human body and also occurs in various animal foods, particularly red meat. Chief among its functions in the body is the facilitation of the transport of fatty acids into mitochondria, where they are metabolized to produce energy. According to a recent review, “L-carnitine is intrinsically involved in mitochondrial metabolism and function as it plays a key role in fatty acid oxidation and energy metabolism. In addition to the transportation of free fatty acids across the inner mitochondrial membrane, L-carnitine modulates their oxidation rate and is involved in the regulation of vital cellular functions such as apoptosis.”2 The carnitines (including acetyl L-carnitine and propionyl L-carnitine) exert a substantial antioxidant action, thus providing a protective effect against lipid peroxidation of phospholipid membranes and against oxidative stress induced at the myocardial and endothelial cell level.

Carnitine Decreases Post-Heart Attack Mortality by 90%

Double-blind clinical trials have shown that carnitine supplements can increase exercise capacity in people with heart disease-related chest pain (angina),3 and indeed this was found in the meta-analysis. Furthermore, people with intermittent claudication (a condition caused by atherosclerosis of the lower extremities) were able to walk farther without pain after they were treated with carnitine for six months.4 Moreover, in those with congestive heart failure, carnitine increased exercise capacity, improved heart function, and increased survival times.5 Finally, in a randomized controlled trial, those who took carnitine shortly after suffering a heart attack had a 90 percent decrease in mortality over the next 12 months, compared with people who did not receive carnitine.6

Carnitine supplementation
was associated with a 27% reduction
in all-cause mortality,
a 65% reduction in ventricular
arrhythmias, and a 40% reduction in
angina symptoms in patients who had
experienced a heart attack.

In addition to all this, the carnitines have been found to be helpful with kidney disease (which depletes carnitine), male infertility, muscle metabolism and performance, energy metabolism and improved neurotransmitter function in the brain, the control of asthma, for the treatment of hypothyroidism, and more.

If Carnitine Is Actually Good for Us, What about Meat?

While the health benefits or liabilities of meat are controversial, an extremely large meta-analysis published by ­Circulation (over 1.2 million participants) found that fresh and unprocessed red meat consumption was not associated with increased heart disease risk, stroke, or diabetes.7 It is important to note that the meat used in this review was not industrialized factory farm meat, which is very different from organic, local, grass-fed meat in its nutrient composition. Factory meat contains twenty times the amount of omega-6 fatty acids (which is associated with inflammation, arthritis, and cancer) than healthier omega-3 fatty acids, have much more fat marbling, and may be full of antibiotics. Grass-fed beef has nearly seven times more omega-3s than omega-6s, so when eaten in moderation offers healthier levels of essential fats. As well, grass-fed beef is lower in total fat, and higher in vitamin E complex, beta-carotene, thiamin, riboflavin, calcium, magnesium, potassium, and conjugated linoleic acid. Thus these differences may have a tremendous impact on the types of bacteria in the gut along with the amount of inflammation produced (see sidebar, “Red Meat and Egg Studies Flawed”).

New studies imply that we should move toward veganism …
Red Meat and Egg Studies Flawed
A herd of trigger-happy press-release journalists cash in on the latest confusion

Dr. Stanley Hazan, M.D., PhD., section head of Preventive Cardiology and Rehabilitation at the Cleveland Clinic in Ohio does not like dietary supplements, and thinks that we should move toward veganism with reduced meat, egg, and fish consumption, but without dietary supplementation. Two new papers, for which Dr. Hazen is the senior editor, conclude that the consumption of meat, eggs, and fish may cause an increase in atherosclerosis and cardiovascular risk.8,9

Dr. Hazen is particularly concerned about the potential effect of meat and carnitine supplements. He told the Cleveland Plain Dealer10 that, ”the amount of carnitine in many energy drinks is equivalent to a porterhouse steak, or more. Especially if you’re talking about kids who are being targeted with all this advertising, drinking these drinks is like eating steaks every day and they’re getting it in a can and don’t even realize it.”

“Another remarkable finding is that choline—a natural semi-essential vitamin—when taken in excess, promote[s] atherosclerotic heart disease. Over the past few years we have seen a huge increase in the addition of choline into multi-vitamins—even in those marketed to our children—yet it is this same substance that our study shows the gut flora can convert into something that has a direct, negative impact on heart disease risk by forming an atherosclerosis-causing by-product,” averred Dr. Hazen in 2011.11 He also warned, “Choline is an essential nutrient, but “We have no idea how much is too much … Our data would suggest that’s a bad thing,” he says. “It suggests that’s like eating a tub of cholesterol.”12

And in 2013, according to The New York Times, “Dr. Hazen said it also may be wise to avoid supplements or vitamins with added choline.”

No, meat, eggs, and fish are not unsafe—nor is ­carnitine; nor is choline. Strangely, by the standards of Dr. Hazen and colleagues, fish produce gigantic amounts of the substance that is the principle subject of the Dr. Hazen papers, trimethylamine-N-oxide (TMAO) (see below and sidebar, “A Red Halibut?”), dwarfing the amounts found in meat or eggs.

Indictment of Supplements

The first paper of Dr. Hazen,9 published in the journal Nature Medicine, associates the nutrient carnitine, found in red meat, supplements, and sports supplements, with the risk of heart disease. Here are some examples of what the media said about it “Red meat nutrient used in weight-loss and muscle-building supplements could cause heart disease”! “Put down that steak! (and energy drinks, too); the carnitine in these foods may increase risk of cardiovascular disease”!

Here is a summary of the study:

  • A diet high in carnitine promotes the growth of certain bacteria that metabolize the nutrient

  • During that metabolization, an organic compound called TMAO is produced in the blood

  • This compound increases risk of heart disease

The study further states that vegetarians and vegans have different gut bacteria, which do not produce a burst of TMAO after consuming carnitine. This study has many faults. First, there’s the question of the study participants. Most of the study was done on mice, though there was a human component—a tiny sample of only six people, five meat-eaters and one vegan. Amazingly, their conclusion that vegetarians and vegans have different gut bacteria that don’t produce an abundance of TMAO after consuming carnitine was based on just one individual.

Furthermore, how healthy were the five meat-eaters in this study? That is not revealed. Also, the study found that the red meat eaters did not produce TMAO after a course of antibiotics. Could it be that these subjects’ immune systems were already sub-par, not impugning that all meat eaters’ are? At the same time, the study does not clarify whether TMAO production is caused by eating red meat (this was just an assumption), or whether raised TMAO levels actually cause heart disease. That was an association, not a causal connection.

Carnitine Does Not Increase TMAO in Healthy Subjects

A study published in 2006, examined the pharmacokinetics of carnitine and its metabolites in 7 healthy subjects following the oral administration of 0, 0.5, 1, and 2 g taken 3 times a day for 7 days (a total of 0, 1.5, 3, and 6 g/day).13 Mean plasma concentrations of carnitine across an 8-hour dose interval increased significantly following the 0.5-g dose (3 times/day), but there was no further increase at higher doses. A significant increase in the plasma concentrations of TMAO from baseline was evident only for the 6-g dose of carnitine per day (that’s more than 33 half-pound sirloin steaks/day or 16.5 pounds of steak per day), and its renal clearance decreased with increasing dose.

Media Blank Out: No Mention of Carnitine’s Benefits

When the media reports came out, nary a one bothered to mention any of the positive effects of carnitine—even those mentioned in the study itself. Carnitine also helps with kidney disease and male infertility, reduces fat mass, increases muscle mass, and reduces fatigue. And in the elderly, it also helps energy metabolism and improves neurotransmitter function in the brain.

What none of these overhyped media reports—not to mention the study itself—take into account bioindividuality. No one diet, and no one selection of supplements, should be advocated for everyone. Only a balanced diet tailored to each individual body’s personal needs will ensure one’s health in the long run.

Once again, although the study found an association between higher levels of TMAO in the blood and increased risk of cardiovascular problems, it did not prove a cause-and-effect relationship.

Association Between Carnitine and Heart Disease Statistically Insignificant

In an analysis published in the Huffington Post (of all places), Alan Gaby, M.D. (an associate of Jonathan Wright, M.D.) developed two significant arguments.14 “With regard to the observational study of 2,595 subjects that linked higher blood carnitine levels to heart disease, the researchers were able to demonstrate such an association only after manipulating the data.” Dr. Gaby went on to say that, “Normally, statisticians are supposed to adjust their numbers to account for ‘multiple comparisons.’ For example, five heads in a row when flipping a coin five times would be considered a statistically significant event. In contrast, it would be easy to find five heads in a row when searching through 100 consecutive coin flips, and that finding would not be considered statistically significant. The researchers acknowledged that their supposed carnitine-heart-disease link was not statistically significant, according to commonly accepted criteria. It only became significant when they used ‘less stringent’ (i.e., mathematically inappropriate) criteria.”

Furthermore, “Even if a true association did exist between blood levels of carnitine and heart disease, there would be no reason to assume that such an association indicates cause-and-effect. Cardiovascular disease is often associated with impaired kidney function, and weak kidneys have a reduced capacity to excrete carnitine. Thus, higher carnitine levels might be a consequence, rather than a cause, of heart disease. It is noteworthy that the observed association between heart disease and carnitine levels disappeared completely when the researchers corrected for differences in kidney function. That key point was not mentioned in the media reports, and the researchers themselves were apparently unaware of its importance.” [Emphasis added.]

Moreover, according to Stephen L. DeFelice, M.D., Founder and Chairman of FIM, The Foundation for Innovation in Medicine, who brought carnitine into the United States, “In a series of clinical studies conducted in patients with congestive heart failure, cardiomyopathy and coronary artery disease they discovered that, in these conditions of cardiac stress, cardiac muscle levels of L-carnitine are very low while blood levels are significantly higher than normal. [] This indicates that the high blood levels are due to leakage from the myocardium or heart muscle. Elevated L-carnitine blood levels, therefore, is a highly promising biomarker for serious cardiac distress and is due to and not a cause of atherosclerosis as misinterpreted in the Cleveland clinical study.”

The Mice were Fed the Equivalent of 80 Half-Pound Steaks Per Day

Out of curiosity, why did the Koeth et al researchers choose to use a linear dose conversion when adjusting for body weight between mice and humans when trying to determine the human equivalent dose of carnitine used in this study? Shouldn’t a scaling conversion be used that takes into consideration body surface area ratios between species? So the mouse dose would be 3,250 mg/kg carnitine (assuming 20 g mice and 65 mg carnitine dose), which would only be 263.5mg/kg in humans (human equivalent dose = 3,250 mg/kg x 3 (mouse Km) / 37 (human Km)).* For a 70 kg adult human that would be 18,446 mg of carnitine per day or 80 half-pound steaks per day (at 454 mg carnitine per pound of steak) instead of a “thousand steaks per day.”

Still, the carnitine dose is ridiculously high and no human can come remotely close to consuming anywhere near this much, but the distinction/correction is still important (80 vs. 1000 is a pretty big difference).

Missing Findings

The major precursors of TMAO are choline and betaine, not carnitine. Lecithin, betaine, and carnitine have been supplemented for decades without any reports of excess heart disease. According to Koeth et al, “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.”

Yet, the researchers ignored that it has been known for about a decade that choline and betaine blood levels are caused by heart disease, not contributory to it. They can, in fact, be used as acute markers in troponin negative patients (meaning that a heart attack has not occurred) to predict the presence of heart damage. These would, of course, have been the sources for the TMAO, a consequence rather than a cause. This could be the reason Koeth and Hazen decided to study a cohort of patients presenting with suspected heart disease, and misrepresented the causal pathway.

Also, in the rodent portion of the paper they used an inappropriate mouse model, (an APOE null cross that develops atherosclerosis at 20 weeks) and still reported no atherosclerosis in coronary arteries, only the aorta. Apparently this model does not develop atherosclerosis in coronary arteries.

Furthermore, any rodent study dependent on large bowel bacteria can be assumed inappropriate for humans due to longer transit time, unless adjusted for large bowel levels, which was not reported.

A Red Halibut?
The halibut fish contains 107 times the amount of
TMAO than an equal amount of beef

As you can gather from reading the encompassing article, TMAO is thought to be the culprit in atherosclerosis. However, the following table indicates that TMAO is not exclusive to meat or eggs. In fact, it is much higher in fish (and highest in halibut) and there are even some vegetables that have higher amounts than meat.

Even if physiological levels of TMAO contribute to heart disease in humans and even if red meat were to raise TMAO substantially more than most other foods (which is false; see table), it doesn’t follow that eating red meat causes heart disease.

The effects of a food on biology cannot be reduced to one of the biological effects of one of the food’s components. A particular component has other relevant biological effects, and there are multiple relevant biological effects of the other tens of thousands of components of that food. Nonetheless, when the researchers (Koeth et al)8 compared the risk of cardiovascular events to the levels of carnitine and TMAO, they found that the risk was higher in those with higher TMAO levels, independent of the carnitine levels.

If the carnitine in red meat were promoting atherosclerosis through its conversion to TMAO, however, then red meat should be no more dangerous than potatoes and carrots and the real killer should be seafood. How likely is this to be true? Who would believe that regular consumers of halibut have rampant cardiovascular disease.

Urinary trimethylamine production from foods (227 g) following human ingestion

Foodstuff TMA & TMAO
(mmol/8 hr)*
Foodstuff TMA & TMAO
(mmol/8 hr)*
Fruit & Vegetables
Apple 38.7 ± 30.8
Banana 22.1 ± 9.5
Carrots 128.8 ± 104.0
Cauliflower 173.1 ± 108.4
Orange 27.5 ± 13.7
Peanut 113.1 ± 28.2
Pear 32.0 ± 6.5
Peas 191.5 ± 148.1
Pineapple 53.1 ± 42.1
Potato 139.8 ± 58.3
Soya bean 87.9 ± 46.5
Tomato 85.7 ± 79.5
Beef 76.5 ± 48.5
Chicken 71.6 ± 24.7
Duck 29.1 ± 34.5
Lamb 62.9 ± 60.5
Lamb's Liver 203.1 ± 64.9
Pork 94.3 ± 22.9
Cereal Products & Miscellaneous
Biscuit 31.4 ± 13.1
Bread 132.7 ± 52.8
Mushroom 172.5 ± 75.2
Rice 48.1 ± 32.3
Dairy Product
Cheese 117.4 ± 42.5
Egg 139.5 ± 77.2
Milk 70.6 ± 46.4
Fish & Seafoods
Clam 377.1 ± 12.8†
Cockles 167.5 ± 10.0
Cod 5135.3 ± 1983.7†
Cod roe 691.9 ± 107.9†
Coley 3436.4 ± 446.5†
Crab 1562.0 ± 250.0†
Haddock 4001.0 ± 392.3†
Halibut 8230.2 ± 564.8†
Herring 4345.0 ± 490.3†
Lumpfish roe 286.0 ± 33.3†
Mackerel 2614.3 ± 700.4†
Octopus 1786.9 ± 313.3†
Plaice 805.4 ± 335.2†
Prawn 3647.9 ± 254.2†
Sardine 1424.1 ± 318.1†
Squid 5648.1 ± 1426.7†
Skate 5454.4 ± 622.7†
Swordfish 2769.4 ± 568.7†
Trout (rainbow) 495.2 ± 280.7
Tuna 301.8 ± 19.9†
Whiting 1667.5 ± 312.7†
Control Background
150.7 ± 64.4

* It is assumed that about 50% trimethylamine N-oxide undergoes reduction to trimethylamine in the gut and then reoxidaton to the N-oxide in the liver before reaching the urine. The remaining 50% passes through the body unchanged and is therefore not available to provide trimethylamine.

† Signicantly greater than control values (Student’s t-test, P <0.01)


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