2.1. Utrzymanie prawidłowego stanu stawów, ścięgien i tkanki łącznej (ID 1918, 1978, 3142)

The claimed effects are “joint health” and “beneficial for connective tissue and joints”. 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 maintenance of normal joints, tendons, and connective tissue.
The Panel considers that maintenance of normal joints, tendons, and connective tissue is beneficial to human health.

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.

2.3. Utrzymanie prawidłowej ostrości wzroku (ID 1448)

The claimed effect is “beneficial for eye health”. The Panel assumes that the target population is the general population.
In the context of the proposed wording, the Panel notes that the claimed effect relates to the maintenance of visual acuity.
The Panel considers that maintenance of normal visual acuity is beneficial to human health.

2.4. Utrzymanie prawidłowego stężenia cholesterolu we krwi i niskiego stężenia białka C-reaktywnego (CRP) (ID 1450)

The claimed effect is “supports a healthy cardiovascular system”. The Panel assumes that the target population is the general population.
In the context of the proposed wordings, the Panel assumes that the claimed effect relates to the maintenance of normal blood cholesterol concentration and to the maintenance of low plasma concentrations of C-reactive protein (CRP).
Low-density lipoproteins (LDL) carry cholesterol from the liver to peripheral tissues, including the arteries. Elevated LDL-cholesterol, by convention >160mg/dL, may compromise the normal function of the arteries.
CRP is an acute-phase protein whose plasma concentrations increase in response to inflammation.
The Panel considers that the maintenance of normal blood cholesterol concentrations is beneficial to human health and that the maintenance of low plasma concentrations of C-reactive protein (CRP) might be beneficial to human health.

3.1. Utrzymanie prawidłowego stanu stawów, ścięgien i tkanki łącznej (ID 1918, 1978, 3142)

Among the publications submitted to support these claims, one notification of placing on the market novel foods or novel food ingredients pursuant to Article 5 of Regulation (EC) No 258/97, one US patent describing the use of astaxanthin in the treatment of muscle diseases and disorders, one US patent describing a method for the prevention and treatment of the carpal tunnel syndrome, the pre- market notification form FDA on astaxanthin, a series of general reviews on the chemical properties and potential health effects of astaxanthin, one animal study and two human studies on the effects of astaxanthin on muscle damage/muscle endurance as a result of intense physical exercise are not considered directly pertinent for the substantiation of the claimed effect.
In addition, two unpublished reports on the effects of astaxanthin in the relief of pain and the improvement of performance in patients with carpal tunnel syndrome (Nir and Spiller, 2002a) and with tennis elbow (Spiller et al., 2006), and one intervention in patients with rheumatoid arthritis were presented to support the claimed effect (Nir and Spiller, 2002b). The Panel notes that the three studies
above are pilot single-centre, double-blind placebo-controlled parallel studies conducted with a product containing high oleic safflower oil, Haematococcus extract, lutein, vitamin A, vitamin E, gelatine and rosemary oil in addition to astaxanthin, and therefore no conclusions can be drawn from these studies on the food that is the subject of the health claim, astaxanthin, in relation to the claimed effect.
The Panel concludes that a cause and effect relationship has not been established between the consumption of astaxanthin and the maintenance of normal joints, tendons or connective tissue.

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.

3.3. Utrzymanie prawidłowej ostrości wzroku (ID 1448)

One notification of placing on the market novel foods or novel food ingredients pursuant to Article 5 of Regulation (EC) No 258/97 and four scientific references were provided to substantiate the claimed effect. Three were human intervention studies with astaxanthin and one was a mechanistic study indicating that carotenoids including astaxanthin were singlet oxygen quenchers in marine organisms (Shimidzu et al., 1996).
In a one-arm study (Takahashi and Kajita, 2005), nine volunteers consumed 6 mg/d of astaxanthin (from Astarioil, a product derived from Haematococcus) for 14 days and were evaluated by ophthalmological examination before and after the intervention. The examination was based on the Objective Diopter Value reading, the Accommodative Reaction Volume and the average value of the High-Frequency Component (HFC) in accommodative micro-fluctuation as well as on subjective measures using questionnaires to evaluate fatigue before and after operating electronic devices. Only the HFC value changed significantly with astaxanthin supplementation; the HCF after operation of the electronic devices decreased at the end of the intervention. The Panel notes the small number of subjects, the uncontrolled nature of the study design, and the limited relevance to the claimed effect of the endpoints measured; all of which limit the conclusions that can be drawn on the role of astaxanthin in supporting visual acuity.
Two small Japanese intervention studies with astaxanthin in humans could be accessed in abstract form only. One was a randomised placebo-controlled intervention study evaluating the effects of astaxanthin on accommodation, critical flicker fusion and pattern visual evoked potential in visual display terminal workers (Nagaki et al., 2002). The other study evaluated the effects of astaxanthin supplementation on visual acuity tests (Sawaki et al., 2002). The Panel notes that for both studies insufficient information was provided in the abstract (full papers in Japanese) for a complete evaluation in relation to the claimed effect.
In weighing the evidence, the Panel took into account the small number of subjects studied, the uncontrolled nature of the study design, and the limited relevance to the claimed effect of the endpoints measured in the only intervention study for which the full text was available.
The Panel concludes that a cause and effect relationship has not been established between the consumption of astaxanthin and the maintenance of visual acuity.

3.4. Utrzymanie prawidłowego stężenia cholesterolu we krwi i niskiego stężenia białka C-reaktywnego (CRP) (ID 1450)

One notification of placing on the market novel foods or novel food ingredients pursuant to Article 5 of Regulation (EC) No 258/97 and two references reporting the results from two human intervention studies were provided to substantiate the claimed effect.
One study investigated the effects of astaxanthin supplementation on lipid peroxidation (not on blood cholesterol concentrations) and is therefore not considered pertinent to substantiate the claimed effect (Karppi et al., 2007). The second reference is only available in summary form and reports data from a study were 15 healthy postmenopausal women were divided into three groups to consume supplements containing different doses of astaxanthin for 8 weeks (Kim and Chyun, 2004). It is unclear from the abstract the dose of astaxanthin consumed by each group daily (the Panel assumed those to be 0.2mg/d, 2mg/d, and 8mg/d, respectively), the number of subjects assigned to each intervention group, and how the assignment was carried out. Serum concentrations of total cholesterol, low density lipoprotein (LDL)-cholesterol, high density lipoprotein (HDL)-cholesterol,
and triglycerides were assessed at 4 and 8 weeks of the intervention. HDL-cholesterol concentrations in the 2 mg/d and 8 mg/d groups increased significantly and triglycerides decreased significantly in the 2 mg group after 8 weeks of intervention. Whether these changes were significant as compared to the control group (assumed to be the 0.2mg/d group), or whether any changes in either total or LDL- cholesterol were observed in the intervention groups are compared to controls is not reported.
From the information available, the Panel notes that none of these studies have assessed the effects of astaxanthin intake on plasma concentrations of CRP.
The Panel concludes that a cause and effect relationship has not been established between the consumption of astaxanthin and the maintenance of normal blood cholesterol concentrations or the maintenance of low plasma concentrations of C reactive protein.