ID 3077 -
Marchew
PL: Marchew
EN: Carrot
Pdf: various food(s)/food constituent(s) not supported by pertinent human data
1.7. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1174, 1184, 1197, 1667, 1997, 2244, 2652, 3077)
The claimed effects are “heart health vascular health”, “cardiovascular system”, “maintenance of cardiovascular system”, “for cardiovascular health”, “antioxidant properties/source of anthocyanins and polyphenols with antioxidant activity”, “antioxidant properties”, “antioxidant effects”, and “immune system, antioxidant properties”. 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 protection of cells and molecules 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 such as antioxidant nutrients.
The Panel considers that protection of DNA, proteins and lipids from oxidative damage may be a beneficial physiological effect.
2.7. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1174, 1184, 1197, 1667, 1997, 2244, 2652, 3077)
Most of the references provided in relation to these claims addressed potential health effects of dietary antioxidants in general, of food(s)/food constituent(s) other than those which are the subject of
the claims, and/or reported on claimed effects other than the protection of body cells and molecules from oxidative damage. The latter included references on the development or progression of acute or chronic diseases (e.g. immune dysfunction/susceptibility to infections, cardiovascular diseases, cancer, and degenerative diseases, among others) presumed to be associated with increased levels of oxidative stress and 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 claim.
Some intervention studies in humans which investigated the effects of the food(s)/food constituent(s) on the overall antioxidant capacity of plasma assessed by different methods have been provided. These methods included total reactive antioxidant potential (TRAP), trolox-equivalent antioxidant capacity (TEAC), ferric reducing ability of plasma (FRAP), oxygen radical absorbance capacity (ORAC), and dichlorofluorescein (DCF) fluorescence. The Panel considers that the evidence provided in these studies does not predict the occurrence of an effect of the food(s)/food constituent(s) on the protection of body cells and molecules from oxidative damage (Dalle-Donne et al., 2006; Griffiths et al., 2002; Knasmuller et al., 2008; Mayne, 2003).
A number of intervention studies assessed changes in antioxidant enzymes (e.g. superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), haemoxigenase) and compounds (e.g. glutathione (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 not specific (e.g. induction of antioxidant enzymes may also be achieved in response to the pro-oxidant effect of a dietary component) and does not reflect oxidative damage to cells or molecules (Niki, 2009).
Some intervention studies in humans which investigated the effects of the food(s)/ food constituent(s) on markers of lipid peroxidation have been provided. Such markers are thiobarbituric acid-reactive substances (TBARS), malondialdehyde (MDA) and/or oxidation lag time of LDL ex vivo and/or autoantibodies against oxidised LDL particles. The Panel considers that both TBARS and MDA, when used alone, are not reliable markers of lipid peroxidation (Griffiths et al., 2002; Knasmuller et al., 2008; Lykkesfeldt, 2007). The Panel also considers that no evidence has been provided to establish that the oxidation lag time of LDL particles ex vivo or that autoantibodies against oxidised LDL particles predict the resistance of LDL particles to peroxidation in vivo (Griffiths et al., 2002; Lapointe et al., 2006; Verhoye and Langlois, 2009).
No human studies which investigated the effects 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 were provided in relation to any of the claims evaluated in this section.
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 intake 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 evidence provided in animal and in vitro studies is not sufficient to predict the occurrence of an effect of the food(s)/food constituent(s) consumption on the protection of body cells and molecules from oxidative damage in vivo in humans.
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 the claims evaluated in this section and protection of DNA, proteins or lipids from oxidative damage.
Warunki i możliwe ograniczenia stosowania oświadczenia
At least 1 glass ( = 150 ml) lactic acid fermented carrot juice per day