ID 2527 - Koper morski

PL: Koper morski
EN: Christe marine
Pdf: various food(s)/food constituent(s)

Oświadczenie (2)

1.1. Ochrona komórek przed przedwczesnym starzeniem (ID 1668, 1917, 2515, 2527, 2530, 2575, 2580, 2591, 2620, 3178, 3179, 3180, 3181, 4329, 4415)

The claimed effects are “antioxidant”, “anti-cancer”, “anti-ageing”, “healthy ageing”, “antioxidant mainly due to phenolic compounds as well as high amounts of carotenoids and vitamin C and E” and “skin anti-ageing agent”. The Panel assumes that the target population is the general population.
The proposed wordings and clarifications provided by Member States include “lowers the ageing process”, “fighting oxidation induced ageing”, “fights against cellular ageing”, and “protects the skin from the effects of premature ageing”.
The Panel considers that the claimed effect “anti-cancer” relates to the prevention of a disease and does not comply with the criteria laid down in Regulation (EC) No 1924/2006.
No definition has been provided of “premature (skin) ageing”, “healthy ageing”, “oxidation-induced ageing”, “ageing process” or “cellular ageing” in relation to the antioxidant properties of foods.
The Panel considers that the claimed effects are general and non-specific and do not refer to any specific health claim as required by Regulation (EC) No 1924/2006.

1.2. Aktywność antyoksydacyjna, zawartość antyoksydantów, właściwości antyoksydacyjne (ID 857, 1306, 2515, 2527, 2530, 2575, 2580, 2591, 2629, 2728, 4327, 4365, 4380, 4390, 4394, 4455, 4464, 4507, 4694, 4705)

The claimed effects are “antioxidant”, “andioxidative capacity”, “antioxidant properties”, “antioxidant activity”, “purifying/ detoxifying properties” and “antioxidant effect”. The Panel assumes that the target population is the general population.
In the context of the proposed wording, the Panel assumes that the claimed effect refers to the capacity of foods/food constituents to scavenge free radicals and/or to their reducing capacity.
The Panel considers that claims made on the antioxidant capacity/content or properties of foods/food constituents based on their capability of scavenging free radicals in vitro refer to a property of the food/food constituent measured in model systems, and that the information provided does not establish that this capability as such exerts a beneficial physiological effect in humans.
The Panel considers that no evidence has been provided to establish that having antioxidant activity/content and/or antioxidant properties is a beneficial physiological effect.
The Panel concludes that a cause and effect relationship has not been established between the consumption of the food(s)/food constituent(s) which are the subject of this opinion and a beneficial physiological effect related to antioxidant activity, antioxidant content or antioxidant properties.

1.3. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1196, 1211, 1216, 1306, 1312, 1440, 1441, 1666, 1668, 1692, 1900, 1914, 1948, 2023, 2158, 2517, 2522, 2527, 2575, 2591, 2620, 2637, 2639, 2663, 2860, 3079, 3276, 3564, 3818, 4324, 4329, 4351, 4397, 4416, 4424, 4507, 4527, 4528, 4542, 4611, 4629, 4659)

The claimed effects refer to the protection of body cells and molecules (such as DNA, proteins and lipids) from oxidative damage, including UV-induced oxidative damage. The Panel assumes that the target population is the general population.
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 can damage molecules such as DNA, proteins and lipids if they are not intercepted by the antioxidant network which includes free radical scavengers such as antioxidant nutrients.
The Panel considers that protection of DNA, proteins and lipids from oxidative damage may be a beneficial physiological effect.

2.1. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1196, 1211, 1216, 1306, 1312, 1440, 1441, 1666, 1668, 1692, 1900, 1914, 1948, 2023, 2158, 2517, 2522, 2527, 2575, 2591, 2620, 2637, 2639, 2663, 2860, 3079, 3276, 3564, 3818, 4324, 4329, 4351, 4397, 4416, 4424, 4507, 4527, 4528, 4542, 4611, 4629, 4659)

Most of the references provided addressed potential health effects of dietary antioxidants in general, or of foods/food constituents other than those for which the specific claims are proposed, and/or health outcomes other than the protection of body cells and molecules from oxidative damage. These health outcomes refer to the development or progression of acute or chronic diseases presumed to be associated with increased levels of oxidative stress (e.g. immune dysfunction/susceptibility to infections, cardiovascular diseases, cancer and degenerative diseases) where oxidative damage to cells or molecules has not been considered as an outcome. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claimed effect.
No human studies that investigated the effects of the consumption of the food(s)/food constituent(s) on reliable markers of oxidative damage to body cells or to molecules such as DNA, proteins and lipids have been provided in relation to any of the health claims evaluated in this opinion.
Some intervention studies in humans which investigated the effects of the consumption of the food(s)/food constituent(s) on the overall antioxidant capacity of plasma assessed by different methods have been provided. These methods include total reactive antioxidant potential (TRAP), trolox- equivalent antioxidant capacity (TEAC), ferric reducing ability of plasma (FRAP), oxygen radical absorbance capacity (ORAC) and ferrous oxidation-xylenol orange (FOX). The Panel considers that the evidence provided in these studies does not predict the occurrence of an effect of the consumption of the food(s)/food constituent(s) on the protection of body cells and molecules from oxidative damage (Griffiths et al., 2002; Mayne, 2003; Dalle-Donne, et al., 2006; Knasmuller et al., 2008). A number of intervention studies assessed changes in antioxidant enzymes (e.g. superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), haemeoxigenase) and compounds (e.g. glutathion (GSH)) belonging to the antioxidant network system, or on HDL-associated paraoxonases (e.g. PON-1). The Panel notes that induction of antioxidant enzymes and HDL-associated paraoxonases provides an indication of response to oxidative stress, but it is non specific and does not reflect oxidative damage to cells or molecules (e.g. induction of antioxidant enzymes may also be achieved in response to the pro-oxidant effect of a dietary component) (Niki, 2009).
Some intervention studies in humans that have investigated the effects of the consumption of specific food(s)/food constituent(s) for which the claims are made on markers of lipid peroxidation were provided (ID 1196, 2620, 2860, 4528). Such markers are thiobarbituric acid-reactive substances (TBARS), malondialdehyde (MDA), conjugated dienes and/or oxidation lag time of low-density lipoproteins (LDL) ex vivo. The Panel considers that MDA (when used alone), and TBARS and conjugated dienes (when used either alone or in combination) are not reliable markers of lipid peroxidation (Griffiths et al., 2002; Lykkesfeldt, 2007; Knasmuller et al., 2008). The Panel also considers that no evidence has been provided to establish that the oxidation lag time of LDL particles ex vivo predicts the resistance of LDL particles to oxidation in vivo (Griffiths et al., 2002; Lapointe et al., 2006; Verhoye and Langlois, 2009).
Thus, for claims supported by references to human studies on the overall antioxidant capacity of plasma only, or on MDA/TBARS/conjugated dienes and/or oxidation lag time of LDL particles ex vivo as the only markers of lipid peroxidation, either alone or in combination with animal and/or in vitro studies, the Panel considers that a cause and effect relationship has not been established between the consumption of the food(s)/food constituent(s) and the claimed effect.
A number of in vitro studies were provided which addressed the antioxidant properties of different food(s)/food constituent(s), either by testing their capacity to scavenge free radicals under controlled conditions or by testing their capacity to prevent or delay protein, lipid or DNA oxidation in different in vitro models. Also, studies were provided on the relationship between the consumption of the food(s)/food constituent(s) and the claimed effect by measuring markers of protein, lipid and/or DNA oxidation in animals, either in vivo or ex vivo. The Panel considers that the evidence provided in the animal and in vitro studies submitted is not sufficient to predict the occurrence of an effect of the consumption of the food(s)/food constituent(s) on the protection of body cells and molecules from oxidative damage in vivo in humans. The Panel considers that while effects shown in animal and in vitro studies may be used as supportive evidence, human studies are required for the substantiation of a claim. Thus, for claims supported by references to animal studies and/or in vitro studies only, the Panel considers that a cause and effect relationship has not been established between the consumption of the food(s)/food constituent(s) and the claimed effect.
The Panel concludes that a cause and effect relationship has not been established between the consumption of the food(s)/food constituent(s) which are the subject of this opinion and the protection of DNA, proteins and lipids from oxidative damage.

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