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Rebuttal to Attack Against Carnitine

August 2013

By By William Faloon, Steven V. Joyal, MD, Luke Huber, ND, MBA, Blake Gossard, and Richard A. Stein, MD, PHD

People with angina, an early sign of impaired blood flow (ischemia) to the heart muscle, benefited from carnitine supplements. A natural derivative of L-carnitine, propionyl-L-carnitine, at a dose of 500 mg 3 times daily , increased the average time patients could exercise without EKG signs of ischemia by an impressive 450%.10 That result indicated improved blood flow to heart muscle cells following ischemia, an effect amply demonstrated in animal studies.13,14

Carnitine also increases concentrations of nitric oxide, which helps endothelial cells relax and increase blood flow, an effect that can help lower blood pressure.15-17 Three weeks of supplementation with 2 grams of L-carnitine improved blood flow by 17% during the critical after-meal period in a group of people fed a high-fat meal; placebo patients had a 12% decrease in blood flow.18 And a daily 6-gram intravenous dose of propionyl-L-carnitine for one week improved walking distance in people with peripheral arterial disease by 28%.19

What You Need to Know
Media Deception of Carnitine’s Established Benefits

Media Deception of Carnitine’s Established Benefits

  • Carnitine is a fat-transporting compound that is absolutely essential for normal heart function.
  • L-carnitine supplementation also prevents the progression of heart muscle damage in people with congestive heart failure and improves exercise tolerance in people who develop chest pain (angina) with exertion.
  • Carnitine also has multiple favorable effects on blood sugar and insulin resistance, the hallmarks of type II diabetes.
  • Studies also indicate that some forms of carnitine are effective at relieving clinical symptoms of cardiovascular conditions such as peripheral arterial disease, angina, coronary artery disease, cardiomyopathy, intermittent claudication, ischemic heart disease, atherosclerosis, and congestive heart failure.
  • A recent investigational study examined levels of a compound called trimethylamine-N-oxide (TMAO) in relationship to microbial metabolism of carnitine in the gut.
  • The researchers cite very recent, limited research suggesting TMAO may be a risk factor for cardiovascular disease.
  • Despite an exceedingly small subject number, they then provocatively propose that carnitine consumption may increase cardiovascular risk in some individuals due to increasing TMAO levels following microbial metabolism of the compound.
  • What the media reports didn’t say was that these results are very preliminary, based on limited research (versus the extensive body of peer-reviewed research attesting to carnitine’s benefits), applicable only in red-meat consumption, and contradictory to the vast majority of research on carnitine.

Carnitine Fights Diabesity

Carnitine Fights Diabesity  

As obesity rates skyrocket, more and more Americans are developing type II diabetes as a result, producing a syndrome called “diabesity.”20,21

Since carnitine helps the mitochondria utilize energy, it plays a critical role in reducing the occurrence and impact of diabesity.22,23 Studies show that in addition to helping the mitochondria burn fat as energy, carnitine is also vital for removing waste products from mitochondria.23,24 This is important, because we now recognize that the buildup of mitochondrial waste products is one of the most important contributors to insulin resistance, which further promotes high blood sugar and obesity.25

Obesity and aging contribute to low carnitine levels, which compromises mitochondrial performance and increases insulin resistance, promoting further obesity and carnitine reduction. Restoring carnitine levels to their youthful values is an effective way to break this deadly cycle.23

Human volunteers who took L-carnitine 3 grams/day for 10 days had favorable changes in body composition.26 Supplemented patients used their fat for energy, burning it 22% faster than control patients, without any increase in muscle protein breakdown. Another study,using 2 grams/day for 6 months, demonstrated a loss of total fat mass of 4 pounds, with a gain in lean muscle mass of 8.4 pounds.27

Animal studies confirm and extend these findings, showing that propionyl-L-carnitine decreases body weight gain, food intake, and fat composition, while improving insulin resistance.22

Carnitine also has multiple favorable effects on blood sugar and insulin resistance, the hallmarks of type II diabetes.24 Animals fed a high fat diet develop the same symptoms and signs that humans do: obesity, insulin resistance, abnormal lipid profiles, and liver damage, which are known as metabolic syndrome. Just 4 weeks of treatment with L-carnitine reversed all of those abnormal parameters.20,28,29

Similar effects have been found in diabetic humans. Two grams of L-carnitine twice daily for 10 daysimproved insulin sensitivity and reduced insulin levels.30 L-carnitine supplementation of 2 grams/day caused a significant reduction in plasma free fatty acids, which contribute to insulin resistance.31 Three grams/day were shown to reduce simulated after-meal blood sugar spikes from 157 mg/dL to 132 mg/dL (oral glucose tolerance test).32 A significant number of studies document the deadly impact of elevated after-meal glucose levels.

Carnitine Protects Against Heart Disease

Carnitine Protects Against Heart Disease  

Research suggests that a specific form of carnitine, called propionyl-L-carnitine (PLC), plays an important role in protecting the function and health of endothelial cells.33-35 Studies also indicate that PLC may act as a nutritional corrective agent, relieving clinical symptoms of cardiovascular conditions such as peripheral arterial disease, angina, coronary artery disease, cardiomyopathy, intermittent claudication, ischemic heart disease, atherosclerosis, and congestive heart failure.36-42

PLC passes across the mitochondrial membrane to supply L-carnitine directly to the mitochondria, the energy-producing organelles of all cells.43 This is important because heart muscle cells and endothelial cells burn fatty acids rather than glucose for 60% of their energy. 44

Carnitine deficiency has been associated with congestive heart failure.45 PLC supplementation has been reported to increase exercise capacity, optimize energy production, and reduce ventricular size in patients with congestive heart failure.38

The myocardium, the muscular substance of the heart, comprises cells called cardiomyocytes. A study of cardiomyocytes found that PLC helped to correct an imbalance between the production and utilization of adenosine triphosphate (ATP), the energy currency used throughout the body. This suggests that PLC may improve cardiac performance by improving energy metabolism and optimizing ATP levels.46

An animal study suggests PLC may help to prevent or decrease the severity of atherosclerosis. In rabbits fed a high-cholesterol diet, which normally induces endothelial dysfunction and subsequent atherosclerosis, supplementation with PLC resulted in reduced plaque thickness, markedly lower triglyceride levels, and reduced proliferation of foam cells, thereby preventing the progression of atherosclerosis.41

PLC has been shown to have a protective role against vascular cell inflammation that other carnitines do not. When rodents were exposed to irritating chemicals, PLC protected their vascular cells from this source of damage, but L-carnitine and acetyl-L-carnitine did not, leading the study authors to support “a specific protective role of PLC in the vascular component of the inflammatory process.”34

PLC improves endothelial function by increasing nitric oxide production in animals with normal blood pressure and in animal models of hypertension. The increased nitric oxide production induced by PLC is related to its antioxidant properties; PLC reduces reactive oxygen species and increases nitric oxide production in the endothelium in the presence of superoxide dismutase (SOD) and catalase.47

Oxygen-deprived endothelial cells produce large amounts of free radicals. Laboratory findings suggest that PLC protects these cells during periods of oxygen deprivation. When blood flow is restored, PLC also allows the cells to regain their lost energy charge much faster.35

An animal study indicates that PLC prevents abnormal heart muscle function associated with diabetes. The researchers found that PLC significantly increased both fatty acid and glucose utilization while restoring cardiac muscle function. These findings suggest PLC prevents diminished cardiac function associated with diabetes, possibly by promoting a favorable shift in glucose and fatty acid metabolism.46