2.1. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 612, 1658, 1959)

The claimed effects are “antioxidant activity, detoxifying properties, and protection of body cells from oxidative damage”. The Panel assumes that the target population is the general population.
In the context of the proposed wordings, the Panel notes that the claimed effects relate to the protection of body cells and tissues from oxidative damage caused by free radicals.
Reactive oxygen species 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.

2.2. Metabolizm energetyczny (ID 614)

The claimed effect is “energy metabolism”. The Panel assumes that the target population is the general population.
In the context of the proposed wordings, the Panel notes that the claimed effect relates to the conversion of energy from foods into energy in the form of ATP which may be readily used by the body.
The Panel considers that normal energy-yielding metabolism is beneficial to human health.

2.3. Opóźnienie wystąpienia zmęczenia i poprawa wydolności fizycznej (ID 1660)

The claimed effect is “ergogenic role in sports and exercise”. The Panel assumes that the target population is sports men and women.
In the context of the proposed wordings, the Panel notes that the claimed effect relates to the delay of the onset of fatigue and to enhanced physical performance.
The Panel considers that delaying the onset of fatigue and enhancing physical performance might be beneficial for sports men and women.

3.1. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 612, 1658, 1959)

The references provided for the substantiation of the claimed effect include general reviews on the role of taurine in human nutrition, on the role of antioxidants in free-radical scavenging, on the role of oxidative stress in the development of chronic disease; studies on the role of taurine in the prevention/treatment of hypoxia and oxidative stress-induced tissue injury in animal models; and human intervention studies on taurine supplementation, both orally and intravenously, for the treatment of various disease conditions.
The Panel considers that no conclusions can be drawn from these references in relation to the claimed effect. The Panel also considers that the evidence provided in the animal studies does not predict an effect of taurine consumption on the protection of body tissues from oxidative damage in humans.
One human intervention study which investigated the effects of taurine supplementation on the prevention of exercise-induced oxidative damage was presented (Zhang et al., 2004). In an open label, single arm intervention, 11 young men (18-20 years of age) underwent an identical exhaustive test procedure using a bicycle ergometer before and after taurine supplementation (6 g/d for 7 days). Single cell gel assay was used to study DNA damage in white blood cells (WBC). Plasma lipid oxidation products were assessed using the plasma thiobaribituric acid reactive substance (TBARS) assay. Pre-supplementation of taurine, a significant negative correlation was found between plasma taurine concentrations before exercise and TBARS 6 hr after exercise. WBC showed a significant increase in DNA strand breakage 6 hr and 24 hr after exercise. Seven-day taurine supplementation reduced serum TBARS before exercise and resulted in a significantly reduced DNA migration 24 hr after exercise. The Panel notes that the small number of subjects studied, the lack of an appropriate control group, the high doses of taurine used in the study as compared to those proposed in the conditions of use, and the lack of appropriate methods to assess either lipid or DNA oxidative damage limit the conclusions that can be drawn from this study in relation to the claimed effect under the proposed conditions of use.
The Panel concludes that a cause and effect relationship has not been established between the consumption of taurine and the protection of DNA, proteins and lipids from oxidative damage.

3.2. Metabolizm energetyczny (ID 614)

One monograph was provided for the substantiation of the claimed effect (Jellin et al., 2000).
The role of taurine on carbohydrate metabolism is mentioned in some of the references provided to substantiate other claims on taurine (Huxtable, 1992; Birdsall, 1998; Bouckenooghe et al., 2006). Although a role for taurine on glucose absorption and metabolism has been suggested in animal and in vitro experimental studies via interactions with the insulin receptor, the clinical studies, which were performed in patients with type 1 diabetes mellitus, are too small and too short duration to draw any conclusions (Franconi et al., 2006). In addition, taurine supplementation has no effect on insulin secretion/action in non-diabetic overweight subjects (Bouckenooghe et al., 2006).
The Panel concludes that a cause and effect relationship has not been established between the consumption of taurine and normal energy-yielding metabolism.

3.3. Opóźnienie wystąpienia zmęczenia i poprawa wydolności fizycznej (ID 1660)

The ergogenic effect of taurine in sports and exercise is not mentioned in any of the reviews and textbooks provided for the substantiation of the claimed effect.
Out of the references provided, three human intervention studies (Yatabe et al., 2003; Baum and Weiss, 2001; Alford et al., 2001) and one animal study (Zhang et al., 2004) investigated the relationship between the consumption of taurine and the claimed effect.
In a crossover double blind intervention study (Baum and Weiss, 2001), 13 endurance trained athletes consumed 500 ml of a so-called “energy drink” containing 2 g taurine, 160 mg caffeine, 1.2 g glucuronolactone, 43 g saccharose, and 10.5 g glucose (and vitamins), 500 ml of a similar (control) drink without taurine and glucuronolactone, and 500 ml of a drink containing only saccharose and glucose (placebo) 40 minutes before a controlled intense exercise. Parameters of cardiac contractility were assessed by echocardiography before and after exercise. Some parameters of cardiac contractility (e.g., left ventricular end systolic diameter) improved after exercise following consumption of the “energy drink” compared to the control and placebo drinks. The Panel notes that no conclusions can be drawn from this study for the substantiation of the claim on taurine alone.
In the study by Alford et al. (2001), a total of 36 volunteers were included in three different small double-blind crossover studies comparing the effects of 250 ml of an energy drink containing 1 g taurine, 80 mg caffeine and 600 mg glucuronolactone to those of 250 ml of carbonated water (control) consumed before aerobic and anaerobic endurance testing. When compared to the control drink (carbonated water), the energy drink significantly improved aerobic endurance (maintaining 65– 75% max. heart rate) and anaerobic performance (maintaining max. speed) on cycle ergometers. The Panel notes that no conclusions can be drawn from this study for the substantiation of the claim on taurine alone.
The study by Zhang et al. (2004) was an open label, single arm intervention which investigated the effects of taurine supplementation (6 g/d for 7 days) on exercise performance in 11 young men (18-20 years of age). Subjects were asked to undergo an identical exhaustive test procedure using a bicycle ergometer before and after the taurine supplementation period. Workload, VO2 max, and exercise duration before fatigue significantly increased after taurine supplementation compared with baseline (pre-treatment). The Panel notes that the small number of subjects studied, the lack of an appropriate control group, and the high doses of taurine used in the study (6 g/d, 60 times higher than the 100mg/d dose proposed in the conditions of use) limit the conclusions that can be drawn from this study in relation to the claimed effect under the proposed conditions of use.
In a rat study (Yatabe et al., 2003), a modest but significant increase in time to exhaustion was observed with very high doses of taurine (0.5 g/kg) that are not relevant for human nutrition.
In weighing the evidence, the Panel took into account the small number of subjects studied, the lack of measurements related to physical performance in one of the studies, the difficulty in attributing any effects to the consumption of taurine alone in two of the studies, and the high doses of taurine used in one human intervention study and in the animal study, which limit the conclusions that can be drawn from these studies in relation to the consumption of taurine and the claimed effect under the proposed conditions of use.
The Panel concludes that a cause an effect relationship has not been established between the consumption of taurine and the delay in the onset of fatigue or the enhancement of physical performance.