2246.pdf

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Scientific Opinion Part I on the substantiation of health claims related to various food(s)/food constituent(s) not supported by pertinent human data (ID 411, 559, 1174, 1184, 1197, 1380, 1409, 1656, 1667, 1670, 1763, 1767, 1806, 1884, 1908, 1997, 2141, 2159, 2243, 2244, 2325, 2331, 2333, 2336, 2652, 2717, 2727, 2752, 2788, 2861, 2870, 2885, 2894, 3077, 3101, 3516, 3595, 3726, 4252, 4288, 4290, 4406, 4509, 4709) pursuant to Article 13(1) of Regulation (EC) No 1924/2006[sup]1[/sup] EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA)2, 3 European Food Safety Authority (EFSA), Parma, Italy
Słowa kluczowe: Appetite   LDL cholesterol   UV-induced photo-oxidative damage   blood pressure   body weight   bowel function   cardiac function   health claims   oxidative damage   post-prandial glycaemic responses   satiety   venous walls  
ID:    1670      2717      1884      2885      4509      1667      2652      4709      1197      2894      4290      4252      1380      1806      3595      2159      3726      3516      1997      411      4406      1908      2788      3101      2752      2141      559      2861      1409      4288      1656      2325      2870      1174      1767      2331      2244      1763      2333      2243      1184      2336      3077      2727  
Produkty: Rzodkiew zwyczajna   Hesperydyna   Sok z winogron   Likopen, proantocyjanidyny, witamina C, witamina E, selen, beta-karoten (Seresis Pharmaton)   Winorośl właściwa   Trokserutyna   Marchew   Fruktoza, L-Karnityna   Alginian sodu, hydroksykwas cytrynowy, piperyna   Mangostan właściwy   Ocet jabłkowy (proszek)   Wycig z ananasa (standaryzowany na 2% bromelainę)   Jabłka   Aronia czarnoowocowa   Woda mineralna, chlorek sodu   Lakownica lśniąca   Diosmina   Kukurydza zwyczajna   Naturalna woda mineralna (z siarczanem magnezu i cynku)   Wyciąg z aronii czarnoowocowej   Białka ziemniaczane   Glikomakropeptydy   Flawonoidy z zielonej herbaty, jabłek, cebuli   Kiełki (mieszanka) SproutGarden®   Róg jeleni   Ryż siewny indyjski (też otręby ryżowe)   Porzeczka czarna   Jagodowe (borówka brusznica, borówka amerykańska, porzeczki, maliny, truskawki)   Arbuz zwyczajny   Wyciąg z borówki brusznicy   Ocet ryżowy   Witamina E, selen   Gorczyca biała   Śmietana w proszku o zmniejszonej zawartości tłuszczu (bogate źródło sfingomieliny)   Sok z kiszonej kapusty   Standaryzowany wyciąg z ziemniaków   Beta-karoten, Witamina C, witamina E, selen   Wyciąg ze śliwy japońskiej   Glukoza, fruktoza  

2. Znaczenie oświadczenia dla zdrowia człowieka


1.1. Wzrost apetytu po niezamierzonej utracie masy ciała prowadzący do zwiększenia ilości przyjmowanej energii (ID 411, 2141)

The claimed effects are “appetite (stimulation)” and “appetite/digestion”. The Panel assumes that the target population is underweight individuals who wish to increase their energy intake.
In the context of the proposed wordings, the Panel assumes that the claimed effects refer to the increase in appetite after unintentional weight loss.
The Panel considers that an increase in appetite after unintentional weight loss leading to an increase in energy intake, if sustained, might be a beneficial physiological effect.

1.2. Zwiększenie sytości prowadzące do redukcji przyjmowanej energii (ID 1656, 1884, 2870, 2894, 4252)

The claimed effects are “satiety/weight management/promotion of CCK release and soy foods”, “alginate forms a gel in the stomach and promotes an immediate feeling of satiety. It may also trap a portion of HCA. Piperine increases the bioavailability of the un-trapped HCA and enhances satiety”, “satiety”, and “weight management/satiety”. The Panel assumes that the target population is the general population.
In the context of the proposed wordings, the Panel assumes that the claimed effects refer to an increase in satiety. Satiety is the decrease in the motivation to eat after consumption of food. The effect may persist up to several hours, may reduce energy intake either at the next meal or across the day and, if sustained, may lead to a reduction in body weight.
The Panel considers that an increase in satiety leading to a reduction in energy intake, if sustained, might be a beneficial physiological effect.

1.3. Udział w utrzymaniu lub osiągnięciu prawidłowej masy ciała (ID 559, 1380, 1656, 1806, 2243, 2325, 2331, 2333, 2336, 2717, 2727, 2788, 2870, 3726, 4252, 4709)

The claimed effects are “weight control; carbohydrate metabolism and insulin sensitivity”, “weight management”, “satiety/weight management/promotion of CCK release and soy foods”, “weight control”, “weight loss management, carbohydrate & lipid metabolism improvement”, “weight loss management, acid base balancer”, “weight management, thermogenesis”, “amincissement”, “slimming (cellulitis draining)”, and “weight management/satiety”. The Panel assumes that the target population is the general population.
In the context of the proposed wordings, the Panel assumes that the claimed effects refer to the maintenance or achievement of a normal body weight.
Weight management and weight control can be interpreted as contribution to the maintenance of a normal body weight. In this context, weight loss in overweight individuals without achieving a normal body weight is considered to be a beneficial physiological effect.
The Panel considers that contribution to the maintenance or achievement of a normal body weight is a beneficial physiological effect.

1.4. Utrzymanie prawidłowego stężenia cholesterolu LDL we krwi (ID 1763, 2861, 3101, 4406)

The claimed effects are “cardiovascular health”, “control of blood lipids”, and “blood cholesterol”. 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 maintenance of normal blood LDL-cholesterol concentrations.
The Panel considers that maintenance of normal blood LDL-cholesterol concentrations is a beneficial physiological effect.

1.5. Utrzymanie prawidłowego ciśnienia krwi (ID 2159)

The claimed effect is “heart health”. The Panel assumes that the target population is the general population.
In the context of the proposed wordings, the Panel assumes that the claimed effect refers to the maintenance of normal blood pressure.
Blood pressure is the pressure (force per unit area) exerted by circulating blood on the walls of blood vessels. Elevated blood pressure, by convention above 140 mmHg (systolic) and/or 90 mmHg (diastolic), may compromise the normal arterial and cardiac function.
The Panel considers that maintenance of normal blood pressure is a beneficial physiological effect.

1.6. Utrzymanie prawidłowego funkcjonowania serca (ID 1767, 3595, 4509)

The claimed effects are “cardiovascular health”, “excellent source of sulforaphane known to help in the management of heart health”, and “help restoration of myocardial tissue”. 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 relate to the maintenance of normal cardiac function.
The Panel considers that maintenance of normal cardiac function is a beneficial physiological effect.

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.

1.8. Zmiany w funkcjonowaniu jelit (skrócenie czasu pasażu jelitowego, zwiększenie częstości ruchów jelit, zwiększenie objętości stolca) (ID 1409, 2141, 2752, 2885, 3516)

The claimed effects are “D/L-lactic acid - L(+)lactic acid activate the gut motility”, “appetite/digestion”, “improve digestion/transit”, “digestion/intestinal tract”, and “digestion". 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 changes in bowel function.
The Panel considers that changes in bowel function such as reduced transit time, more frequent bowel movements, increased faecal bulk, or softer stools may be a beneficial physiological effect, provided that these changes do not result in diarrhoea.

1.9. Ochrona skóry przed uszkodzeniem promieniami ultrafioletowymi (UV) (ID 4288, 4290)

The claimed effect is “antioxidant action”. The Panel assumes that the target population is the general population.
In the context of the proposed wordings, the Panel assumes that the claimed effect refers to the protection of lipids in the skin from UV-induced photo-oxidative damage.
The Panel considers that the protection of lipids in the skin from UV-induced photo-oxidative damage is a beneficial physiological effect.

1.10. Ograniczenie wzrostu stężenia glukozy (glikemii) po posiłku (ID 559)

The claimed effect is “weight control; carbohydrate metabolism and insulin sensitivity”. The Panel assumes that the target population is individuals who wish to reduce their post-prandial glycaemic responses.
In the context of the proposed wordings, the Panel assumes that the claimed effect refers to the reduction of post-prandial glycaemic responses.
Postprandial glycaemia is interpreted as the elevation of blood glucose concentrations after consumption of a food and/or meal. This function is a normal physiological response which varies in magnitude and duration and which may be influenced by the chemical and physical nature of the food or meal consumed, as well as by individual factors (Venn and Green, 2007). Reducing post-prandial glycaemic responses may be beneficial to subjects with, for example, impaired glucose tolerance as long as post-prandial insulinaemic responses are not disproportionally increased. Impaired glucose tolerance is common in the general population of adults.
The Panel considers that reduction of post-prandial glycaemic responses (as long as post-prandial insulinaemic responses are not disproportionally increased) may be a beneficial physiological effect.

1.11. Utrzymanie elastyczności i wytrzymałości ścian żylnych (ID 1670, 1908)

The claimed effect is “vascular health”. 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 effect refers to the maintenance of elasticity and strength of the venous walls.
The Panel considers that maintenance of elasticity and strength of the venous walls is a beneficial physiological effect.

3. Naukowe uzasadnienia wpływu na zdrowie człowieka - 


2.1. Wzrost apetytu po niezamierzonej utracie masy ciała prowadzący do zwiększenia ilości przyjmowanej energii (ID 411, 2141)

The references provided in relation to these claims included textbooks which did not provide any original data for the scientific substantiation of the claims. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claims.
No human studies which investigated the effect of the food(s)/food constituent(s) on appetite ratings, energy intake or body weight were provided in relation to any of the claims evaluated in this section.
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 a sustained increase in appetite after unintentional weight loss leading to an increase in energy intake.

2.2. Zwiększenie sytości prowadzące do redukcji przyjmowanej energii (ID 1656, 1884, 2870, 2894, 4252)

The references provided in relation to these claims included narrative reviews on the regulation of appetite, energy intake and body weight which did not provide any original data for the scientific substantiation of the claims, addressed the effects of food(s)/food constituent(s) other than those which are the subject of the claims, and/or investigated health outcomes (e.g. post-prandial blood glucose and insulin responses, body composition) unrelated to the claimed effect. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claims.
Some human intervention studies, which investigated the effect of the food(s)/food constituent(s) on appetite ratings and/or subsequent food intake and/or secretion of hormones with a putative role on the regulation of food intake (e.g. glucagon-like peptide-1, cholecystokinin, ghrelin) following a single meal or over 24 hours, were provided. The Panel notes that none of these studies tested the sustainability of an effect of the food(s)/food constituent(s) on appetite ratings and subsequent energy intake (i.e. effects were tested on a single occasion and no information was provided on the repeated consumption of the food(s)/food constituent(s)). The Panel considers that no conclusions can be drawn from these studies for the scientific substantiation of a claim on a sustained increase in satiety leading to a reduction in energy intake.
No human studies which investigated the effects of the food(s)/food constituent(s) on a sustained increase in satiety leading to a reduction in energy intake were provided in relation to any of the claims evaluated in this section.
A number of animal studies which addressed the effects of the food(s)/food constituent(s) on food intake, body weight, and/or secretion of hormones with a putative role on the regulation of food intake, and a number of animal and in vitro studies which addressed the mechanisms by which the food(s)/constituent(s) could exert the claimed effect were also provided. The Panel considers that, in the absence of human studies from which conclusions could be drawn for the scientific substantiation of the claim, the evidence provided in animal and in vitro studies is not sufficient to predict the occurrence of an effect of the consumption of the food(s)/food constituent(s) on an increase in satiety leading to a reduction in energy intake 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 a sustained increase in satiety leading to a reduction in energy intake.

2.3. Udział w utrzymaniu lub osiągnięciu prawidłowej masy ciała (ID 559, 1380, 1656, 1806, 2243, 2325, 2331, 2333, 2336, 2717, 2727, 2788, 2870, 3726, 4252, 4709)

Most of the references provided in relation to these claims were narrative reviews on the potential health effects of different food(s)/food constituent(s) which did not provide any original data for the scientific substantiation of the claims, addressed the effects of food(s)/food constituent(s) other than those which are the subject of the claims, and/or investigated health outcomes (e.g. delayed gastric emptying, appetite ratings and/or subsequent food intake following a single meal or over 24 hours, energy expenditure, post-prandial blood glucose responses, insulin sensitivity and/or long-term blood glucose control, treatment of chronic venous insufficiency, bioavailability of different food constituents, on plasma concentrations of carotenoids, blood lipids and/or lipid metabolism, antioxidant properties and/or oxidative stress) other than body weight. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claims.
For ID 2243 and 2325, summaries of two human intervention studies on the effects of the food constituents on body weight were provided. However, the limited methodological data available in the summaries did not allow a complete scientific evaluation. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claims.
For ID 1656 and 2870, some internal reports identified as proprietary by the company reported on human intervention studies on the effects of the food constituents on body weight. The Panel notes that Regulation (EC) No 1924/2006 does not foresee the protection of proprietary data for health claims under Article 13.1 of the Regulation and therefore considers that these data cannot be used for the scientific substantiation of the claims.
No relevant human studies which investigated the effects of the food(s)/food constituent(s) on changes in body weight were provided in relation to any of the claims evaluated in this section.
A number of animal studies which addressed the effects of some of the food(s)/constituent(s) on body weight, and a number of animal and in vitro studies which addressed the mechanisms by which the food(s)/constituent(s) could exert the claimed effect were also provided. The Panel considers that evidence provided in animal and in vitro studies is not sufficient to predict the occurrence of an effect of the consumption of the food(s)/food constituent(s) on body weight 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 contribution to the maintenance or achievement of a normal body weight.

2.4. Utrzymanie prawidłowego stężenia cholesterolu LDL we krwi (ID 1763, 2861, 3101, 4406)

The references provided in relation to these claims were book chapters and narrative reviews on the potential health effects of different food(s)/food constituent(s) which did not provide any original data for the scientific substantiation of the claims, addressed the effects of food(s)/food constituent(s) other than those which are the subject of the claims, and/or investigated health outcomes (e.g. resistance of LDL particles to peroxidation, liver steatosis, platelet aggregation, incidence of chronic diseases such as ischaemic heart disease, cancer, or asthma) other than blood cholesterol concentrations. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claims.
No human studies which investigated the effects of the food(s)/food constituent(s) on blood LDL-cholesterol concentrations were provided in relation to any of the claims evaluated in this section.
A number of animal studies which addressed the effects of some of the food(s)/food constituent(s) on the blood lipid profile, and a number of animal and in vitro studies which addressed the mechanisms by which the food(s)/food constituent(s) could exert the claimed effect were provided (e.g. activity of 3-hydroxy-3-methyl-glutaryl-CoA reductase, acyl CoA:cholesterol tranferases and/or microsomal triglyceride transfer protein in the liver). The Panel considers that evidence provided in animal and in vitro studies is not sufficient to predict the occurrence of an effect of the consumption of the food(s)/food constituent(s) on blood LDL-cholesterol concentrations 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 maintenance of normal blood LDL-cholesterol concentrations.

2.5. Utrzymanie prawidłowego ciśnienia krwi (ID 2159)

One reference on the antioxidant properties of different plant extracts and two reviews which did not address the effects of the food, which is the subject of the claim, on blood pressure were cited in relation to this claim. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claim.
No human studies, which investigated the effects of the food on blood pressure were provided in relation to the claim evaluated in this section.
The Panel concludes that a cause and effect relationship has not been established between the consumption of the food which is the subject of the claim evaluated in this section and maintenance of normal blood pressure.

2.6. Utrzymanie prawidłowego funkcjonowania serca (ID 1767, 3595, 4509)

The references provided in relation to these claims were book chapters and narrative reviews on the potential health effects of different food(s)/food constituent(s) which did not provide any original data for the scientific substantiation of the claims, addressed the effects of food(s)/food constituent(s) other than those which are the subject of the claims, and/or investigated health outcomes (e.g. treatment of infections, resistance of LDL particles to peroxidation, liver steatosis, platelet aggregation, incidence of chronic diseases such as ischaemic heart disease, cancer, asthma) unrelated to the claimed effect. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claims.
No human studies which investigated the effects of the food(s)/food constituent(s) on heart function were provided in relation to any of the claims evaluated in this section.
One animal study on a mice model of atherosclerosis was provided. The Panel considers that evidence provided in animal studies is not sufficient to predict the occurrence of an effect of the consumption of the food(s)/food constituent(s) on maintenance of normal cardiac function 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 maintenance of normal cardiac function.

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.

2.8. Zmiany w funkcjonowaniu jelit (skrócenie czasu pasażu jelitowego, zwiększenie częstości ruchów jelit, zwiększenie objętości stolca) (ID 1409, 2141, 2752, 2885, 3516)

The references provided in relation to these claims were textbooks, narrative reviews or monographs which did not provide any original data for the scientific substantiation of the claims, studies which addressed the effects of food(s)/food constituent(s) other than those which are the subject of the claims, and/or investigated health outcomes (e.g. glucose tolerance and lipid metabolism, hydrogen and methane production in the gastro-intestinal tract) unrelated to the claimed effect. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claim.
No human studies which investigated the effects of the food(s)/food constituent(s) on measures of bowel function were provided in relation to any of the claims evaluated in this section.
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 changes in bowel function.

2.9. Ochrona skóry przed uszkodzeniem promieniami ultrafioletowymi (UV) (ID 4288, 4290)

The references provided in relation to these claims were monographs which addressed food(s)/food constituent(s) other than those which are the subject of the claims. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claims.
No human studies which investigated the effects of the food(s)/food constituent(s) on protection of lipids in the skin from UV-induced photo-oxidative damage were provided in relation to any of the claims evaluated in this section.
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 lipids in the skin from UV-induced photo-oxidative damage.

2.10. Ograniczenie wzrostu stężenia glukozy (glikemii) po posiłku (ID 559)

The references provided in relation to this claim included narrative reviews which did not provide any original data for the scientific substantiation of the claims and studies which assessed the effects of food(s)/food constituent(s) other than the food which is the subject of the claim. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claim.
No human studies which investigated the effects of the food on reduction of post-prandial glycaemic responses were provided in relation to the claim evaluated in this section.
The Panel concludes that a cause and effect relationship has not been established between the consumption of the food which is the subject of the claim evaluated in this section and reduction of post-prandial glycaemic responses.

2.11. Utrzymanie elastyczności i wytrzymałości ścian żylnych (ID 1670, 1908)

The references provided in relation to these claims included human intervention and animal studies on the effects of the food constituent(s), either alone or in combination with other substances, on health outcomes (e.g. pharmacokinetics, treatment of chronic venous insufficiency, treatment of retinal venous occlusion, red blood cell aggregability, lipid peroxidation, profibrinolytic activity) unrelated
to the claimed effect. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claim.
No human studies which investigated the effects of the food constituent(s) on maintenance of the elasticity and strength of the venous walls were provided in relation to any of the claims evaluated in this section.
The Panel concludes that a cause and effect relationship has not been established between the consumption of the food constituent(s) which are the subject of the claims evaluated in this section and maintenance of the elasticity and strength of the venous walls.

Wnioski

On the basis of the data presented, the Panel concludes that:
A cause and effect relationship has not been established between the consumption of the food(s)/food constituent(s) and the claimed effects evaluated in this opinion.