L-Carnitine Improves Oxidative Stress in Coronary Artery Disease Patients

Written by Angeline A. De Leon, Staff Writer. L-carnitine supplementation significantly reduced plasma malondialdehyde and significantly increased catalase, superoxide dismutase, and glutathione peroxidase in participating subjects with coronary artery disease.

Coronary artery disease (CAD), involving the narrowing or blockage of the coronary arteries due to the buildup of cholesterol plaque, is the most common type of heart disease and the leading cause of death worldwide (1). Decades of research provide evidence for a distinct association between oxidative stress and atherosclerotic plaque formation (2), leading to the development of antioxidant therapy as a strategy to improve clinical outcomes in patients with CAD and other types of cardiovascular diseases (3). A number of in vitro studies suggest that L-carnitine (LC), a derivative of amino acids lysine and methionine involved in energy metabolism and mitochondrial protection (4), may function as a potent free radical scavenger which protects antioxidant enzymes from oxidative damage (5). In healthy human subjects, supplementation with LC at 2000 mg/d has been found to significantly boost activity levels of antioxidant enzymes (6). At higher doses, LC also demonstrates a protective effect on cardiac metabolism in patients with ischemic heart disease (7) and has been linked to lower rates of CAD-related death (8). Researchers at the Chung Shan Medical University in Taiwan (2014) conducted the first clinical study to examine the effects of LC supplementation on markers of oxidative stress and antioxidant enzyme activities in patients with CAD.

A total of 39 patients with CAD (identified by cardiac catherization as having at least 50% narrowing of one major coronary artery) were enrolled in a single-blind, randomized, placebo-controlled trial. At baseline and at 12-week follow-up, fasting venous blood samples were obtained to measure serum LC, plasma malondialdehyde (MDA, biomarker for oxidative stress) and antioxidant enzyme activities [catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx)]. Participants were randomized to ingest 1000 mg of LC or matching placebo (starch capsule) daily for 12 weeks.

After 12 weeks of LC supplementation, researchers observed a significant reduction in MDA levels (from 2.0 +/- 0.3 to 1.8 +/- 0.3 µmol/L, p = 0.02), along with a significant increase in LC (from 33.6 +/- 13.6 to 40.0 +/- 12.0 µmol/L, p = 0.04), CAT (from 12.7 +/- 5.5 to 13.1 +/- 5.8 U/mg of protein, p = 0.02), SOD (from 14.8 +/- 2.9 to 20.7 +/- 5.8 U/mg, p < 0.01), and GPx (from 20.3 +/- 3.4 to 23.0 +/- 3.1, U/mg of protein, p = 0.01). A significant positive correlation was also reported between LC level and antioxidant enzyme activity (CAT: β = 0.87, p = 0.02; SOD: β = 0.72, p < 0.01).

Based on findings, LC supplementation at a dose of 1000 mg/d proved capable of significantly reducing oxidative stress while also increasing antioxidant capacity, based on antioxidant enzyme activity levels in CAD patients. LC appears to be an effective antioxidant agent in models of cardiovascular disease and should be considered as part of an integrative approach to reducing CAD. However, current findings require replication in a larger sample of participants and further studies are needed to confirm if cardioprotective benefits vary as a function of LC dosage. 

Source: Lee B, Lin J, Lin Y, et al. Effects of L-carnitine supplementation on oxidative stress and antioxidant enzymes activites in patients with coronary artery disease: a randomized, placebo-controlled trial. Nutrition Journal. 2014; 13: 79. DOI: 10.1186/1475-2891-13-79.

© 2014 Lee et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the CreativeCommons Attribution License (http://creativecommons.org/licenses/by/4.0) ,which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Posted May 1, 2018.

Angeline A. De Leon, MA, graduated from the University of Illinois at Urbana-Champaign in 2010, completing a bachelor’s degree in psychology, with a concentration in neuroscience. She received her master’s degree from The Ohio State University in 2013, where she studied clinical neuroscience within an integrative health program. Her specialized area of research involves the complementary use of neuroimaging and neuropsychology-based methodologies to examine how lifestyle factors, such as physical activity and meditation, can influence brain plasticity and enhance overall connectivity.

References:

1. Braunwald E. Shattuck lecture-cardiovascular medicine at the turn of the millennium: triumphs, concerns, and opportunities. N Engl J Med. 1997; 337: 1360–1369.
2. Harrison D, Griendling KG, Landmesser U, et al. Role of oxidative stress in atherosclerosis. Am J Cardio. 2003; 91: 7–11.
3. Gaby AR. Nutritional treatments for acute myocardial infarction. Altern Med Rev. 2010; 15: 113–123.
4. Kendler BS. Carnitine: an overview of its role in preventive medicine. Prev Med. 1986; 15: 373–390.
5. Bremer J. Carnitine metabolism and function. Physiol Rev. 1983; 63: 1420–1479.
6. Cao Y, Qu HJ, Li P, et al. Single dose administration of L-carnitine improve antioxidant activities in human subjects. Tohoku J Exp Med. 2011; 224: 209–213.
7. Singh RB, Niaz MA, Agarwal P, et al. A randomised, double-blind, placebo-controlled trial of L-carnitine in suspected acute myocardial infarction. Postgrad Med J. 1996; 72: 45–50.
8. Guby AR. Nutrition treatments for acute myocardial infarction. Altern Med Rev. 2010; 15: 113–123.