Commonly known as “hardening of the arteries,” atherosclerosis is a major public health threat as it is the underlying cause of a broad spectrum of diseases associated with a western diet and lifestyle. Atherosclerosis refers to the process of narrowing, hardening, and ultimately the blockage of arterial blood vessels. These blood vessels, of course, are responsible for supplying the body’s organs with oxygen, energy, and nutrients.
In light of the important function of these blood vessels, the consequences of poor circulation and limited vascular function are serious and manifold.
Risk Factors for Atherosclerosis
- Age: the likelihood of developing atherosclerosis increases with age
- Gender: Men evidence atherosclerosis more often than women
- Elevated homocysteine levels (particularly homocysteinemia)
- Excess weight/obesity
- Elevated blood pressure.
With the exceptions of age and gender, all risk factors can be influenced and managed. A healthy diet, sufficient exercise, and avoidance of nicotine play an important role in reducing the risk of developing atherosclerosis.
L-arginine is the raw material necessary to influence vascular toning. The molecule NO (nitric oxide), which plays a vital role in signaling dilation in the interior wall of blood vessels (endothelium), can only be produced from L-arginine in the body. If the endothelium is damaged, increased amounts of nitric oxide, and subsequently L-arginine, are required. Low blood levels of L-arginine are often recorded in individuals with poor arterial function.
Many studies have shown that patients with risk factors such as high blood pressure, diabetes mellitus, lipid (fat) metabolism disorders, obesity, lack of exercise, smoking, atherosclerosis, etc., all evidence disease-related deficiencies in L-arginine, and consequently NO.
The correlation between arginine and vascular health has been researched extensively and can be deemed as valid. A meta-analysis by Bai et al. in 2009 confirmed that regular intake of L-arginine over a period of several months can significantly improve vascular health.
The positive effects of L-arginine on vascular function can be explained by two mechanisms: (1) the body is able to produce enough nitric oxide, the molecule that signals vascular relaxation, only if sufficient amounts of L-arginine are available; and (2) L-arginine reduces the catabolism of vascular damaging ADMA (asymmetric dimethylarginine, a byproduct of protein metabolism that interferes with the production of NO, nitric oxide).2
L-arginine and Folic Acid, B6 and B12
Homocysteine is a product of normal metabolic processes, but it is harmful to vascular and nerve tissues. While it is found naturally in the blood, its concentration should be kept as low as possible. The body requires the vitamin B trio: folic acid (B9), vitamin B6, and vitamin B12 to break down homocysteine.
In a larger German study, the effects of long-term supplementation with 2,400 mg of L-arginine in combination with folic acid, vitamin B6, and vitamin B12 were observed on 477 participants.3 At the end of the study period, more than 85% of users described the combination therapy as good or very good. The combination of arginine with the vitamin B trio slowed the development of plaque deposits in arterial walls, and also helped in lowering blood pressure to normal levels. Participants reported an approximately 50% improvement in various symptoms such as circulatory disorders, limited physical capacity, as well as difficulty concentrating.4
In the course of the study, homocysteine levels were reduced by 28%. Supplementation also had a positive effect on cholesterol levels.
The combination of L-arginine with the vitamin B trio produces optimal results: on one hand, harmful homocysteine is broken down; on the other, the interior walls of blood vessels (endothelia) have greater availability of NO (nitric oxide). This supports vascular flexibility and blood flow.
In addition to the vitamin B trio, betaine may also be beneficial in breaking down homocysteine and help improve effects on vascular health.
Betaine and Choline
Betaine is a plant substance derived from beets that, in addition to the vitamin B trio, is also responsible for the break down of homocysteine in the body. The European Food Safety Authority (EFSA) has also confirmed that betaine can contribute to the reduction of homocysteine levels.5
The same applies to choline, since choline is converted to betaine in the body. The effects of choline on homocysteine levels have also been confirmed by the EFSA.
L-carnitine transports fatty acids into the cell interior. There, the power plants of cells, the mitochondria, convert them to energy. One study found that bad LDL cholesterol levels can be reduced though L-carnitine in diabetics.6
Plant materials, particularly seed and bark extract, contain OPC (oligomeric proanthocyanidines) and polyphenols that serve in their protection. These extracts, specifically Grape Seed Extract and Pine Bark Extract, have been extensively studied in terms of their effects on the interior walls of blood cells (endothelia). Improved vascular function 7 and a normalization of blood pressure were often observed. 8
These OPC-containing extracts from pine bark or grape seeds were found to promote metabolic processes in vascular tissue, especially when paired with L-arginine. Results of several studies show improved circulation, lower blood pressure, and increased sexual potency in men.
Pine Bark Extract
The extract from the French maritime pine (pinus pinaster) contains proanthocyanidins. According to a study conducted in 2007, these antioxidative plant substances appear to improve the function of the endothelium (interior wall of blood vessels).9
Additionally, studies have shown that the daily intake of approximately 100 mg to 150 mg of Pine Bark Extract can reduce the danger of platelet aggregation (thrombosis/blood clot).10
Pine Bark Extract is therefore a good addition to a regimen of L-arginine (for improved NO production) and the vitamin B trio B6, B12, and B9 – folic acid (for the reduction of harmful homocysteine) to support vascular health.
- Bai Y., Sun L., Yang T., Sun K., Chen J., Hui R. (2009); “Increase in fasting vascular endothelial function after short-term oral L-arginine is effective when baseline flow-mediated dilation is low: a meta-analysis of randomised controlled trials.”; Am. J. Clin. Nutr. 89, 77-84. ↩
- Boger RH, Ron ES. “L-Arginine improves vascular function by overcoming deleterious effects of ADMA, a novel cardiovascular risk factor.”; Altern Med Rev. 2005 Mar;10(1):14-23. ↩
- Jung K., Petrowicz O. (2008); “L-Arginin und Folsäure bei Arteriosklerose. Ergebnisse einer prospektiven, multizentrischen Verzehrsstudie.” (L-arginine and folic acid in incidences of atherosclerosis. Results of a prospective, multi-center consumption study) Perfusion 21, 148-156. ↩
- Robenek, H.; “Arteriosklerose, Herzinfarkt, Schlaganfall. Therapeutisches Potential von L-Arginin” (Atherosclerosis, heart attack, stroke. The therapeutic potential of L-arginine); 7. Aufl. (Edition) 2013; S. 7 ↩
- http://www.efsa.europa.eu/en/efsajournal/doc/2052.pdf ↩
- Deprosa, G., et al.; “The effect of L-Carnitine on plasma lipoprotein (a) levels in hypercholesterolemic patients with type 2 diabetes mellitus”; Clin Ther 2003; 25(5): S.1429-1439 ↩
- Edirisinghe, I., Randolph, J., et al, “Effect of grape seed extract on postprandial oxidative status and metabolic responses in men and women with the metabolic syndrome – randomized, cross-over, placebo-controlled study”; Functional Foods in Health and Disease, 2013, Vol 2, Issue 12 ↩
- Roninson, M., et al.; “Effect of Grape Seed Extract on Blood Pressure in Subjects with Pre-Hypertension”; Journal of Pharmacy and Nutrition Sciences, Vol. 2, pp 155-159, 2013 ↩
- Nishioka K, Hidaka T, Nakamura S, et al. Pycnogenol, French maritime pine bark extract, augments endothelium-dependent vasodilation in humans. Hypertens Res. 2007;30(9):775-780 ↩
- Araghi-Niknam M, Hosseini S, Larson DF, Rodhewald P, Watson RR.; “Pine bark extract reduces platelet aggregation.”; Int Med. 1999;2(2):73-77; and also in: Putter M, Grotemeyer KH, Wurthwein G, et al.; “Inhibition of smoking induced platelet aggregation by aspirin and pycnogenol.”; Thromb Res. 1999;95(4):155-161 ↩