2.1. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1647)

The claimed effect is “antioxidant properties”. The Panel assumes that the target population is the general population.
The Panel considers that claims made on the antioxidant capacity/content or properties of food/food constituents based on their capability to scavenge 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 exerts a beneficial physiological effect in humans as required by Regulation (EC) No 1924/2006.
The proposed wordings include “antioxidant containing foods support of healthy aging” and “antioxidants contribute to the total antioxidant capacity of the body and may help strengthen our body's defences”.
No definition has been provided of “healthy aging” in relation to the antioxidant properties of foods. The Panel considers that this claimed effect is general and non-specific, and does not refer to any specific health claim as required by Regulation (EC) No 1924/2006.
In the context of the references provided, the Panel assumes that the claimed effect refers to the protection of DNA, proteins and lipids from oxidative damage.
Reactive oxygen species (ROS), including several kinds of radicals, are generated in biochemical processes (e.g. the respiratory chain) and as a consequence of exposure to exogenous factors (e.g. radiation and 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 the protection of DNA, proteins and lipids from oxidative damage may be a beneficial physiological effect.

2.2. Układ sercowo-naczyniowy (ID 1844)

The claimed effect is “cardiovascular system”. The Panel assumes that the target population is the general population.
The claimed effect is not sufficiently defined and no further details were provided in the proposed wording. No clarifications have been provided by Member States.
The Panel considers that the claimed effect is general and non-specific, and does not refer to any specific health claim as required by Regulation (EC) No 1924/2006.

2.3. Stan psychiczny (ID 1845)

The claimed effect is “mental state and performance”. The Panel assumes that the target population is the general population.
The claimed effect is not sufficiently defined and no further details were provided in the proposed wording. No clarifications have been provided by Member States.
The Panel considers that the claimed effect is general and non-specific, and does not refer to any specific health claim as required by Regulation (EC) No 1924/2006.

2.4. Wątroba, nerki (ID 1846)

The claimed effect is “liver, kidneys”. The Panel assumes that the target population is the general population.
The claimed effect is not sufficiently defined and no further details were provided in the proposed wording. No clarifications have been provided by Member States.
The Panel considers that the claimed effect is general and non-specific, and does not refer to any specific health claim as required by Regulation (EC) No 1924/2006.

3.1. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1647)

Some references provided in the consolidated list were narrative reviews or textbooks that did not contain any original data which could be used to substantiate the claim. Several references referred to intake, bioavailability and plasma kinetics of quercetin and other polyphenols, or were related to
effects of quercetin (and polyphenol) on body functions unrelated to the claimed effect. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claimed effect.
One human intervention study compared the effects of a high flavonol (HF) diet to a low flavonol (LF) diet in 36 healthy human subjects using a randomised cross-over design (Beatty et al., 2000). Subjects consumed each diet for 14 days with a 14-day wash-out period in between. Subjects were asked to avoid foods containing flavonols, flavones and flavanols during the LF dietary treatment period and to consume one 150 g onion cake containing 89.7 mg of quercetin and one 300 mL cup of black tea containing 1.4 mg quercetin daily during the HF dietary treatment. Oxidative damage to DNA was measured in isolated DNA from leukocytes using Gas Chromatography-Mass Spectrometry (GC-MS) analysis of DNA bases. No significant differences between the HF and the LF treatment periods were observed with respect to changes in oxidative damage to DNA.
Chopra et al. (2000) investigated the effects of quercetin supplementation on ex vivo low density lipoproteins (LDL) resistance to (copper-initiated) oxidation (lag time) in healthy male subjects. The Panel notes that this method is not appropriate to assess oxidative damage of blood lipids and considers that no conclusions can be drawn from this study for the scientific substantiation of the claimed effect.
Among the references provided were also in vitro and ex vivo studies on the antioxidant capacity of quercetin or on effects of quercetin on markers of lipid peroxidation. The Panel considers that evidence provided in in vitro and ex vivo studies is not sufficient to predict the occurrence of an effect of quercetin consumption on protection of DNA, proteins and lipids from oxidative damage in humans.
In weighing the evidence, the Panel took into account that the only human intervention study provided which used a valid marker of oxidative damage to DNA did not show an effect of quercetin on the protection of DNA from oxidative damage.
The Panel concludes that a cause and effect relationship has not been established between the consumption of quercetin and protection of DNA, proteins or lipids from oxidative damage.