Written by Greg Arnold, DC, CSCS. 2 grams of Acetyl-L-Carnitine for 6 months demonstrated a 6.2 % decrease in systolic blood pressure.  

Cardiovascular diseases, including heart disease and stroke, which are the first and third leading causes of death for both men and women in the United States, account for 1 in 3 of all U.S. deaths. Heart disease and stroke are expected to cost our healthcare system $473 billion in 2009. If all major types of cardiovascular disease were eliminated, U.S. life expectancy would increase by nearly 7 years (1).

Now recent research (2) suggests Acetyl-L-Carnitine may benefit blood pressure and blood sugar health in those at risk for cardiovascular disease. In the study, 32 patients between the ages of 34 and 54 and without diabetes were given 1,000 milligrams of Acetyl-L-Carnitine twice daily for 6 months. The patients were divided into two groups: those at risk for cardiovascular disease because of a glucose disposal rate less than or equal to 7.9 milligrams per kilogram of bodyweight (16 patients) and those with a glucose disposal rate greater than 7.9 mg/kg/bw (16 patients). Glucose disposal rate is a measure of how fast glucose is taken up by muscles once it has entered the bloodstream (3).

Before the study began, those in the lower glucose disposal rate group (less than or equal to 7.9 mg/kg/bw) had 10% higher systolic blood pressure (144 vs. 130.8 mmHg) compared to those in the higher glucose disposal rate group (greater than 7.9 mg/kg/bw) (p = 0.0072) while the difference in diastolic blood pressure was not statistically significant (p = 0.1255).

By the end of the study, those in the lower glucose disposal rate group saw 3 significant improvements from Acetyl-L-Carnitine supplementation:

  • Glucose Disposal Rate increased by 37.4% (4.89 to 6.72 mg/kg/bw, p < 0.05)
  • Oral Glucose Tolerance Test improved by 13.3% (17,690 to 15,339 milligrams x minute/deciliter, p < 0.005)
  • Systolic Blood Pressure decreased by 6.2% (144 to 135.1 mmHg, p < 0.05)

For those in the higher glucose disposal group, they saw a 5.4% decrease in their systolic blood pressure (130.8 to 123.8 mmHg, p < 0.05) but no statistically significant changes in glucose disposal rate and oral glucose tolerance test.

When suggesting how Acetyl-L-Carnitine is able to elicit these healthful effects, the researchers pointed to studies showing Acetyl-L-Carnitine to positively affect enzymes that control blood sugar control (4, 5). As for the effects on blood pressure, the researchers noted a 27.6% increase in a protein called adiponectin (4.7 to 6.0 milliequivalents/Liter, p < 0.05) across all of the patients and this increased adiponectin may increase nitric oxide levels, thereby helping relax blood vessels and lower blood pressure (6 , 7, 8).

For the researchers, “Acetyl-L-carnitine safely ameliorated [systolic high blood pressure], insulin resistance, impaired glucose tolerance, and [low levels of adiponectin] in subjects at increased cardiovascular risk.”

Source: Ruggenenti, Piero, et al. “Ameliorating Hypertension and Insulin Resistance in Subjects at Increased Cardiovascular Risk.” Hypertension 54.3 (2009): 567-574.

© 2009 American Heart Association, Inc.

Posted January 20, 2014.

Greg Arnold is a Chiropractic Physician practicing in Hauppauge, NY. You can contact Dr. Arnold directly by emailing him at PitchingDoc@msn.com or visiting his web site at www.PitchingDoc.com

References:

  1. “Cardiovascular Disease at a Glace” posted on the CDC Website.
  2. Ruggenenti P. Ameliorating hypertension and insulin resistance in subjects at increased cardiovascular risk: effects of acetyl-L-carnitine therapy.  Hypertension. 2009 Sep;54(3):567-74. doi: 10.1161/HYPERTENSIONAHA.109.132522. Epub 2009 Jul 20.
  3. “Glucose Disposal Rate” posted on the National Diabetes Education Initiative website.
  4. Stephens FB, Constantin-Teodosiu D, Greenhaff PL. New insights concerning the role of carnitine in the regulation of fuel metabolism in skeletal muscle. J Physiol. 2007;581:431– 444.
  5. Foster DW. The role of the carnitine system in human metabolism. Ann N Y Acad Sci. 2004;1033:1–16.
  6. Cheng KK, Lam KS, Wang Y, Huang Y, Carling D, Wu D, Wong C, Xu A. Adiponectin-induced endothelial nitric oxide synthase activation and nitric oxide production are mediated by APPL1 in endothelial cells. Diabetes. 2007;56:1387–1394.
  7. Chen H, Montagnani M, Funahashi T, Shimomura I, Quon MJ. Adiponectin stimulates production of nitric oxide in vascular endothelial cells. J Biol Chem. 2003;278:45021– 45026.
  8. Zhu W, Cheng KK, Vanhoutte PM, Lam KS, Xu A. Vascular effects of adiponectin: molecular mechanisms and potential therapeutic intervention. Clin Sci (Lond). 2008;114:361–374.