ID 4680 - Arginina

PL: Arginina
EN: Arginin
Pdf: L-arginine

Oświadczenie (2)

1. Charakterystyka żywności / składnika

The food constituent that is the subject of the health claims is L-arginine.
Arginine is an alpha-amino acid present in foods from animal and vegetable origin. The L-form is the most commonly found form in nature and in food supplements. L-arginine is also known as (S)-2- amino-5-guanidinopentanoic acid and (S)-2-amino-5-[(aminoiminomethyl)amino] pentanoic acid. The terms L-arginine and arginine are frequently used interchangeably. The content of L-arginine in foods can be measured by established methods.
Arginine is a conditionally indispensable amino acid provided by mixed dietary protein intakes from different sources. Arginine can also be consumed in the form of food supplements as L-arginine.
The Panel considers that the food constituent, L-arginine, which is the subject of the health claims, is sufficiently characterised.

2.5. Poprawa rozszerzenia naczyń krwionośnych zależnego od śródbłonka (ID 664, 1443, 4680)

The claimed effects are “vascular system (blood pressure, circulation, vessels)”, “vascular health; blood circulation”, and “normal blood circulation as a nitric oxide precursor”. The Panel assumes that the target population is the general population.
In the context of the proposed wordings and the clarifications provided by Member States, the Panel assumes that the claimed effects refer to the improvement of endothelium-dependent vasodilation.
The Panel considers that an improvement of endothelium-dependent vasodilation may be a beneficial physiological effect.

3.4. Poprawa rozszerzenia naczyń krwionośnych zależnego od śródbłonka (ID 664, 1443, 4680)

The references provided for the scientific substantiation of the claim included narrative reviews and opinion papers with no original data on the effects of arginine intake on vasodilation, references on food constituents other than arginine, intervention studies using intravenous arginine administration, which is not relevant to human nutrition, and studies on the effects of arginine administration on health outcomes other than endothelium-dependent vasodilation (e.g. blood pressure, clinical course of myocardial infarction, insulin sensitivity, wound healing, immune parameters and erectile function). The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claim.
In one study in hypertensive patients, only the acute effect of arginine intake on endothelium-dependent vasodilation was assessed, and no information on sustained effects was provided (Lekakis et al., 2002). The Panel considers that no conclusions can be drawn from this study for the scientific substantiation of the claimed effect.
Miller (2006) investigated the effects of L-arginine (1,050 mg, as sustained-release preparation) twice daily (total 2.1 g daily) for one week on endothelial function in 29 healthy subjects in an open-label, single-arm intervention. The Panel considers that no conclusions can be drawn from this uncontrolled study for the scientific substantiation of the claim.
Lerman et al. (1998) performed a six-month randomised, double-blind, placebo-controlled parallel intervention to assess the effect of 3 g/day of L-arginine on coronary blood flow and epicardial coronary artery diameter in response to selective infusion of acetylcholine in 26 patients (age ≈49 years) with non-obstructive coronary artery disease. Patients were on cardiovascular treatment during the study, but all medication (except for study treatment) was discontinued at least 72 hours prior to the measurements. None of the subjects received cholesterol-lowering medications. All the patients were referred for the evaluation of stable exertional chest pain suspected to be of cardiac origin. Before the coronary angiogram, 10 patients (77 %) from each group underwent a non-invasive functional test, which was positive and consistent with myocardial ischemia in six patients from group 1 and five patients from group 2. Measures of peripheral endothelial function, for example flow-mediated dilation of the brachial artery, were not obtained in this study. The Panel considers that the evidence provided does not establish that patients with non-obstructive coronary artery disease including myocardial ischemia are representative of the general population with respect to the endothelial function of the coronary arteries. The Panel considers that no conclusions can be drawn from this study for the scientific substantiation of the claimed effect.
Blum et al. (2000) provided 9 g/day of L-arginine or placebo to ten healthy post-menopausal women (aged 55±5 years) in a randomised cross-over study. Intervention periods lasted one month and were separated by a one-month wash-out period. The study was powered to detect a difference of 1.7 % in flow-mediated (endothelium-dependent) dilation after hyperaemia between the study periods. Plasma L-arginine concentrations significantly increased during the intervention, whereas no significant changes were observed in serum nitric oxide or soluble cell adhesion molecules (E-selectin, ICAM-1
and VCAM-1). No significant differences between treatment periods were observed on endothelium-dependent vasodilation. The Panel notes that this study does not show an effect of L-arginine consumption on the improvement of endothelium-dependent vasodilation.
Clarkson et al. (1996) performed a randomised, double-blind, cross-over study in 27 hypercholesterolaemic subjects aged 19-40 years. Those taking HMG CoA reductase inhibitors in a stable dose for >6 months who met the entry criteria for blood cholesterol concentrations (>162 mg/dL) were recruited. Subjects on vasoactive medication were excluded. Subjects received 3x7 g L-arginine daily or placebo during four-week periods, separated by a four-week wash-out period. The non-invasive assessment of endothelium-dependent dilation was performed before and at the end of each treatment period. Post-treatment studies were performed between 1 and 2 h after the last dose of L-arginine or placebo. Plasma arginine concentrations rose from 115 to 231 μmol/L during L-arginine intake. There was a significant improvement in flow-mediated dilation in subjects while taking L-arginine (1.7±1.3 % to 5.6±3.0 %) compared with placebo (2.3±1.9 % to 2.3±2.4 %). The change with L-arginine was 3.9±3.0 % vs. 0.1±2.2 % with placebo (p<0.001). No significant differences were observed in endothelium-independent vasodilation (i.e. in response to nitroglycerine). Flow-mediated dilation improved, by more than 2 %, in 67 % of the subjects who consumed L-arginine. The Panel notes that the observed changes in endothelium-dependent vasodilation could have been due to an acute effect of arginine occurring 1-2 hours after intake in the second flow-mediated dilation test. The Panel also notes that the evidence provided does not establish that acute changes in endothelium-dependent vasodilation constitute a beneficial physiological effect per se.
In weighing the evidence, the Panel took into account that one study did not show an effect of L-arginine consumption on endothelium-dependent vasodilation, and that in a second study the observed changes in endothelium-dependent vasodilation could have been due to an acute effect of arginine rather than to a sustained effect.
The Panel concludes that a cause and effect relationship has not been established between the consumption of L-arginine and improvement of endothelium-dependent vasodilation.

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