ID 3141 -
Astaksantyna
PL: Astaksantyna
EN: Astaxanthin
Pdf: astaxanthin
Oświadczenie (2)
- wysokiej silnym przeciwutleniaczem
- wspiera zdrowe oksydacyjnym równowagi
1. Charakterystyka żywności / składnika
The food constituent that is the subject of the health claim is astaxanthin, which is a red (non- provitamin A) oxygenated carotenoid found in phytoplankton and is responsible for the colour of certain fish (e.g. salmon) and shellfish (e.g. crab).
Astaxanthin is measurable in foods by established methods. Astaxanthin occurs naturally in foods and also in synthetic forms as free form or as esters. Astaxanthin is absorbed into the bloodstream as the free form and bioavailability can be enhanced in lipid matrices. This evaluation applies to astaxanthin naturally present in foods and to those forms authorised for addition to foods.
The Panel considers that the food constituent, astaxanthin, which is the subject of the health claim is sufficiently characterised.
2.2. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1449, 3141)
The claimed effects are “high potent antioxidant” and “supports a healthy oxidative balance”. The Panel assumes that the target population is the general population.
In the context of the proposed wordings, the Panel assumes that the claimed effects relate to the protection of DNA, proteins and lipids from oxidative damage caused by free radicals.
Reactive oxygen species (ROS) including several kinds of radicals are generated in biochemical processes (e.g. respiratory chain) and as a consequence of exposure to exogenous factors (e.g. radiation, pollutants). These reactive intermediates damage biologically relevant molecules such as
DNA, proteins and lipids if they are not intercepted by the antioxidant network which includes free radical scavengers like antioxidant nutrients.
The Panel considers that protection of DNA, proteins and lipids from oxidative damage is beneficial to human health.
3.2. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1449, 3141)
Among the publications provided to substantiate these claims, some are general reviews on the potential health effects of astaxanthin and other carotenoids and were not considered directly pertinent to the claim.
Studies in cell cultures and algae model systems show that astaxanthin is an efficient antioxidant in vitro (Palozza and Krinsky, 1992; Terao, 1989; O'Connor and O'Brien, 1998; Kobayashi and Okada, 2004).
In humans, the effects of astaxanthin on lipid peroxidation were investigated in a small placebo controlled study conducted in 15 postmenopausal women (YooKyung and JongHee, 2004). Subjects were randomly assigned to consume either 0 (control), 2 or 8 mg/d astaxanthin for 8 weeks (five subjects per group). Blood and urine samples were collected at weeks 0, 4 and 8 of the study and the following parameters were determined as biomarkers of lipid peroxidation: thiobarbituric acid reactive substances (TBARS) in plasma, total antioxidant status (TAS) of plasma, and urinary 8- isoprostanes. TBARS significantly decreased in both of the supplemented groups, whereas they slightly increased in the control group. The effect seen in the astaxanthin groups was not dose dependent (changes observed were similar in the 2 and 8 mg/d groups). TBARS alone are not generally accepted as a valid biomarker of lipid peroxidation and should only be interpreted in context with other markers. No changes in urinary 8-isoprostanes, a validated marker of total lipid peroxidation, were observed in any astaxanthin group during the study. Total antioxidant status of plasma was measured by the ABTS method. This parameter was significantly different from baseline only at 8 weeks and only in the high dose astaxanthin group. The Panel notes that antioxidant status of plasma is not a validated marker of oxidative damage. The Panel also notes the limited number of subjects included in the study and that no comparisons between changes in the outcome variables between intervention and control groups were reported.
Another publication (Karppi et al., 2007) reported a double blind randomized controlled intervention in 39 healthy, non-smoker Finnish men (19-33 years). Subjects were randomised to consume either 8mg/d astaxanthin (n=20) or placebo (n=19) for 12 weeks. Plasma concentrations of astaxanthin significantly increased (0 to 0.032 µmol/L) during the study in the astaxanthin group as compared to placebo. Values in this concentration range are consistent with available literature (Rüfer et al., 2008). Eight different hydroxy fatty acid derivatives and F2-isoprostane concentrations in plasma were assessed as markers of lipid peroxidation. There was a significant decrease in 12-hydroxy fatty acids and 15-hydroxy fatty acids within the astaxanthin group as compared to baseline, but these changes were not statistically significant as compared to placebo. In addition, the Panel notes that the biological validity of 12-hydroxy fatty acids and 15-hydroxy fatty acids as markers of oxidative damage has not been established by the evidence provided.
In weighing the evidence, the Panel took into account that, although astaxanthin has antioxidant properties in vitro, the human studies presented do not provide any evidence in support of an in vivo antioxidant effect in terms of lipid peroxidation following the consumption of astaxanthin. No studies have been presented using markers of DNA or protein oxidative damage as outcomes.
The Panel concludes that a cause and effect relationship has not been established between the consumption of astaxanthin and the protection of DNA, proteins or lipids from oxidative damage.
Warunki i możliwe ograniczenia stosowania oświadczenia
3.85 mg astaxanthin (low dose) -19.25 mg astaxanthin (high dose) for 8 weeks - No negative effects on health have been described for 8 weeks