ID 1099 - Kofeina

PL: Kofeina
EN: Caffeine
Pdf: caffeine

Oświadczenie (2)

1. Charakterystyka żywności / składnika

The foods/food constituents that are the subjects of the health claims are coffee, Coffea Arabica L., chlorogenic acids from coffee, and antioxidants in coffee.
Coffee contains a wide range of “bioactive” compounds including caffeine and other purine derivatives, polyphenolic compounds such as chlorogenic acid derivatives and its degradation product caffeic acid, and specific diterpenes such as kahweol and cafestol. No information is provided on the concentration of such compounds in coffee, but this will likely depend on the coffee variety, on the roasting of the beans and on the brewing process, such as the use of coffee filters. Also, no specifications were provided on the compounds or molecules generically referred to as “antioxidants in coffee”.
The Panel notes that chlorogenic acid from coffee has been specified as the “active” food constituent responsible for the claimed effects considered in this opinion. Chlorogenic acids from coffee are well defined compounds which can be measured in foods by established methods.
The Panel considers that whereas the food/food constituents, coffee and antioxidants in coffee, are not sufficiently characterised in relation to the claimed effects evaluated in this opinion, the food constituent, chlorogenic acids from coffee, is sufficiently characterised.

2.1. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1099, 3152, 4301)

The claimed effects are “protection of body tissues, lipids, cells and DNA from oxidative damage”, “oxidative stress reduction” and “coffee naturally contains antioxidants that may support the body's natural cell defences”. 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 and pollutants). These reactive intermediates damage molecules such as DNA, proteins
and lipids if they are not intercepted by the antioxidant network which includes radical scavengers like antioxidant nutrients.
The Panel considers that protection of DNA, proteins and lipids from oxidative damage may be a beneficial physiological effect.

3.1. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1099, 3152, 4301)

Some of the references provided in the consolidated list reported on the association between coffee drinking and disease risk (e.g. hepatocellular carcinoma, liver cirrhosis, breast cancer, colon cancer, and inflammatory and cardiovascular disease) in observational (cohort) studies. Other references were general reviews on claim substantiation, on biomarkers for chronic disease risk, on the chemistry and absorption of chlorogenic acids and other polyphenols from coffee, and on the effects of coffee drinking on liver enzyme activity (a marker of liver damage), and on endothelial and vascular function. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claimed effect.
Some experimental, and generally small-scale, human intervention studies on the effects of coffee consumption, or of individual compounds present in coffee, on markers of antioxidant status (e.g. antioxidant activity/capacity/potential of plasma (Natella et al., 2002)), on the induction of antioxidant enzymes such as super-oxide dismutase (SOD) or glutathione S-transferases (GSTA and
GSTP) and/or on plasma concentrations of glutathione (GSH) (Bichler et al., 2007; Esposito et al., 2003; Grubben et al., 2000; Mursu et al., 2005; Steinkellner et al., 2005), on the formation of malondialdehyde (MDA), on thiobarbituric acid reactive substances (TBARS), and/or on LDL oxidation lag time (Mursu et al., 2005; Yukawa et al., 2004) were provided. The Panel notes that measurements of the total antioxidant activity/potential of plasma are not considered as markers of oxidative damage, and that the formation of TBARS or of MDA assessed by colorimetric assays, as well as the resistance of LDL to oxidation, are not suitable markers to assess lipid peroxidation (Dalle-Donne et al., 2006; Dragsted, 2008; Griffiths et al., 2002; Knasmuller et al., 2008; Mayne, 2003). Also two small intervention studies on the effects of coffee consumption on DNA damage measured ex vivo in lymphocytes using single cell gel electrophoresis (Comet assay) after incubation with restriction enzymes and treatment with H2O2 or a heterocyclic compound (Bichler et al., 2007), and on benzo[a]pyrene diolepoxide (BPDE) induced DNA-migration using the Comet assay (Steinkellner et al., 2005), were presented. The Panel notes that these measurements do not provide information about oxidative damage to DNA in vivo (Dusinska and Collins, 2008). The Panel also notes that coffee has not been sufficiently characterised in these studies in relation to the claimed effect, and that its content of chlorogenic acids has not been reported. The Panel considers that no conclusions can be drawn from these studies for the scientific substantiation of the claimed effect.
In a multiple-dose supplementation trial, 43 healthy non-smoking men consumed daily either no coffee, 3 cups (450 mL) or 6 cups (900 mL) of filtered coffee (7–8 g of grounds per 150 mL cup) for three weeks. In vivo LDL oxidation using conjugated dienes, plasma hydroxy fatty acids, activity of antioxidant enzymes, and plasma F2-isoprostanes were assessed (Mursu et al., 2005). The Panel notes that coffee has not been sufficiently characterised in this study in relation to the claimed effect, and that its content of chlorogenic acids has not been reported. The Panel considers that no conclusions can be drawn from this study for the scientific substantiation of the claimed effect.
Data from in vitro studies on the effect of caffeic acid on LDL resistance to oxidation (lag time), and on glutathione (GSH) depletion (Nardini et al., 1995; 1997; Richelle et al., 2001), and studies on the chemopreventive effects of chlorogenic acids in human cancer cell lines, on transcription factors and biomarkers of cell proliferation (Bandyopadhyay et al., 2004; Feng et al., 2005), and on the effects of kahweol and cafestol on induced DNA damage in cultured NIH3T3 cells (Lee and Jeong, 2007), were submitted. The Panel considers that evidence provided in in vitro studies is not sufficient to predict the occurrence of an effect of coffee on protection of DNA, lipids or proteins from oxidative damage in vivo in humans.
The Panel concludes that a cause and effect relationship has not been established between the consumption of chlorogenic acids from coffee and protection of DNA, lipids or proteins from oxidative damage.

Warunki i możliwe ograniczenia stosowania oświadczenia

1 or 2 cups per day