2.2. Zwiększenie sytości prowadzące do redukcji przyjmowanej energii (ID 851, 852)

The claimed effect is “increases satiety, prolongs satiety”. The Panel assumes that the target population is the general population.
Satiety is the decrease in 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.

2.3. Ograniczenie wzrostu stężenia glukozy (glikemii) po posiłku (ID 821, 824)

The claimed effect is “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 that 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). Decreasing 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 adult population.
The Panel considers that the reduction of post-prandial glycaemic responses (as long as post-prandial insulinaemic responses are not disproportionally increased) may be a beneficial physiological effect.

2.4. Funkcje trawienne (ID 850)

The claimed effect is “beta-glucan improves digestive function”. The Panel assumes that the target population is the general population.
Improved digestion or absorption of nutrients might be considered as beneficial physiological effects in a situation where digestion or absorption is a limiting factor for the maintenance of adequate status of the nutrient. The Panel considers that “improving digestive function” without identification of the nutrients which are the target of the claim is not sufficiently defined.
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. Zwiększenie sytości prowadzące do redukcji przyjmowanej energii (ID 851, 852)#ID:34244

The two references provided for the scientific substantiation of the claim reported on human intervention studies which assessed the effects of oat or barley products on appetite ratings (including satiety) after eating the test food on a single occasion (Berti et al., 2005; Granfeldt et al., 1994). One of the studies also reported on the effects of barley and oat product consumption (on a single occasion) on subsequent energy intake (Berti et al., 2005). The Panel notes that none of these studies tested the sustainability of an effect of beta-glucans on appetite ratings and subsequent energy intake (i.e. effects were tested on a single occasion and no information has been provided on the repeated consumption of the food constituent). The Panel considers that no conclusions can be drawn from these studies for the scientific substantiation of the claim.
The Panel concludes that a cause and effect relationship has not been established between the consumption of beta-glucans from oats and barley and a sustained increase in satiety leading to a reduction in energy intake.

3.2. Ograniczenie wzrostu stężenia glukozy (glikemii) po posiłku (ID 821, 824)

The references provided for the scientific substantiation of the claim included publications on the health effects of dietary fibre in general, on the health effects of low glycaemic foods and/or diets, and on the effects of barley and/or oat products and/or beta-glucans on health outcomes unrelated to the claimed effect (e.g. blood lipids). The references also included human intervention studies which reported on measures of blood glucose in which the amount of beta-glucans consumed was not specified (Granfeldt et al., 1994; Liljeberg et al., 1992), or in which the study population was insulin-dependent or non-insulin dependent diabetic subjects on either insulin or oral hypoglycaemic medications (Braaten et al., 1994; Jenkins et al., 2002; Pick et al., 1996; Pick et al., 1998; Tappy et al., 1996). The evidence provided does not establish that results obtained in patient populations treated with anti-diabetic medications can be generalised to the target population with respect to post-prandial glycaemic responses. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claim.
Three human intervention studies investigated the effects of barley and/or oat beta-glucans on post- prandial glycaemic and insulinaemic responses in healthy subjects using a standardised meal protocol in which whole-meal bread products (from oats, barley, and rye) were compared to white wheat bread (Juntunen et al., 2002; Liljeberg et al., 1996; Östman et al., 2006). All of these studies had a randomised cross-over design with washout periods longer than three days, and sample sizes between 9 and 20 subjects (men and women). Two out of the three studies (Liljeberg et al., 1996; Östman et al., 2006) observed a statistically significant reduction in post-prandial glycaemic and insulinaemic responses following consumption of the test meals which included beta-glucan-containing products (from oats or barley), compared to the test meals not containing beta-glucans, at doses between 4.6-14 g beta-glucans per 30 g of available carbohydrates. The study by Juntunen et al. (2002) did not show a significant effect on post-prandial glycaemic responses of rye bread containing 5.4 g beta-glucans in 50 g of available carbohydrate compared to white wheat bread, whereas post-prandial insulinaemic responses were significantly reduced.
Two human intervention studies investigated the effects of incorporating oat (Holm et al., 1992) or barley (Yokoyama et al., 1997) beta-glucans into pasta products (control pasta made with plain durum wheat flour) in 10 and 5 healthy subjects, respectively. These studies had a randomised cross-over design with washout periods longer than three days. Consumption of pasta with 12 g of beta-glucans in a 100 g available carbohydrate portion (about 3.6 g/30 g available carbohydrates) resulted in significantly lower and delayed peak glucose responses, and in lower peak insulin responses
(Yokoyama et al., 1997), whereas enrichment with oat bran (28 %) giving 6 % beta-glucans in the final product only slightly decreased post-prandial insulinaemic responses, while post-prandial glycaemic responses were unchanged compared to the control pasta (Holm et al., 1992).
Another test meal study, which investigated the effects on post-prandial blood glucose and insulin responses of oat and barley beta-glucan products in healthy subjects, used a standardised protocol in which sucrose was used as a control (Behall et al., 2005). Ten overweight women (mean age 50.1±7.7 years; BMI 30.3±2.2 kg/m2) consumed glucose (1 g/kg body weight) and four test meals consisting of 0.33 g/kg body weight of carbohydrate from pudding (predominantly sucrose) plus 0.67 g/kg body weight of carbohydrates from oat flour, oatmeal, barley flour, or barley flakes to constitute a total of 1 g carbohydrates/kg body weight at breakfast after a 10 h fast. The content of beta-glucans in the test food grains was 4 and 15 g/100 g dry matter in the oat and barley test foods, respectively (about 1.8 and 6.5 g/30 g available carbohydrates, respectively). Blood samples were collected at fasting and every 30 min up to 180 min after the acute loads. Peak glucose and insulin concentrations after the barley test foods were significantly lower than those after the glucose or oat test foods. Post-prandial glucose responses (area under the curve) were significantly reduced after the consumption of oat and barley test foods when compared to sucrose. Post-prandial glucose responses after barley (flour and flakes) were significantly lower than the post-prandial glucose responses after oat (flour and oatmeal). Post-prandial insulinaemic responses were significantly reduced by barley test foods only (44-56 %, p<0.005). The content of beta-glucans in the barley test foods was almost four times higher than in the oat test foods, which could have explained the differential effects of the barley and oat test foods on post-prandial glucose and insulin responses.
The Panel notes that the studies above consistently show an effect of oat and barley beta-glucans in decreasing post-prandial glycaemic responses, without disproportionally increasing post-prandial insulinaemic responses, at doses of at least 4 g per 30 g of available carbohydrates.
The mechanism by which beta-glucans from oats or barley could exert the claimed effect is well established, and relates to the increased viscosity of the meal bolus when beta-glucans are added. When the meal bolus reaches the small intestine, a high viscosity delays the rate of absorption of nutrients, including glucose (Battilana et al., 2001; Wood et al., 2000; Wursch and Pi-Sunyer, 1997).
In weighing the evidence, the Panel took into account that intervention studies in healthy subjects consistently show an effect of oat and barley beta-glucans in decreasing post-prandial glycaemic responses, without disproportionally increasing post-prandial insulinaemic responses, at doses of about 4 g per 30 g of available carbohydrates in bread and pasta products when consumed alone or in the context of a meal, and that the mechanism by which beta-glucans could exert the claimed effect is well established.
The Panel concludes that a cause and effect relationship has been established between the consumption of beta-glucans from oats and barley and a reduction of post-prandial glycaemic responses.

4.1. Ograniczenie wzrostu stężenia glukozy (glikemii) po posiłku (ID 821, 824)

The Panel considers that the following wording reflects the scientific evidence: “Consumption of beta-glucans from oats or barley contributes to the reduction of the glucose rise after a meal”.

5.1. Zmniejszenie stężenia glukozy we krwi po posiłku (ID 821, 824)

In order to obtain the claimed effect, 4 g of beta-glucans from oats or barley for each 30 g of available carbohydrates should be consumed per meal. The target population is individuals who wish to reduce their post-prandial glycaemic responses.