2.1. Zmniejszenie stężenia glukozy we krwi po posiłku (ID 842, 1977)

The claimed effect is “blood glucose control”. The Panel assumes that the target population is subjects willing 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 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). The evidence provided does not establish that decreasing post-prandial glycaemic responses in subjects with normal glucose tolerance is a beneficial physiological effect. However, it may be beneficial to the health of subjects with 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 the reduction of post-prandial glycaemic responses may be a beneficial physiological effect.

2.2. Utrzymanie prawidłowego stężenia glukozy we krwi (ID 842, 1977)

The claimed effect is “blood glucose control”. The Panel assumes the target population is the general population.
In the context of the proposed wordings, the Panel assumes that the claimed effect refers to the long- term maintenance or achievement of normal blood glucose concentrations.
The Panel considers that long-term maintenance of normal blood glucose concentrations is a beneficial physiological effect.

3.1. Zmniejszenie stężenia glukozy we krwi po posiłku (ID 842, 1977)

A total of five publications were cited in relation to this claim. One was an animal study (Gee et al., 1995) not reporting on measures of blood glucose and four reported on human intervention studies on the effects of acacia gum on post-prandial glycaemic responses (Sharma, 1985; Meance et al., 2004; Frémont, 2005; Castellani, 2005). The Panel considers that no scientific conclusions can be drawn from these references for the substantiation of the claimed effect.
A narrative review of the effects of acacia gum on the glycaemic index (Castellani, 2005) referred to an unpublished cross-over intervention study in 18 healthy males who received 100 g sucrose plus 0,5 or 10 g acacia gum in 300 mL of water. However, details of this unpublished study were not available to the Panel, and therefore no scientific conclusions could be drawn for the substantiation of the claimed effect. In the study by Meance et al. (2004), 14 diabetic women consumed as reference 50 g of available carbohydrate from white bread (100 g) and seven days later, the same reference plus either 15 g of acacia gum (n = 7) or 15 g acacia gum plus “one galactomannan” for increased viscosity (n=7) both diluted in 180 mL of water. The Panel notes the lack of control for a time effect (all subjects in the acacia gum groups received the control bread first), the lack of control for a volume effect (it was not reported whether 180 mL of water were consumed as well during the control white bread testing), that insulin responses were not assessed, and that the mean time of diabetes duration in the acacia gum and acacia gum plus one galactomannan groups was 10 and 7.7 years respectively. Moreover, no information was provided on concomitant hypoglycaemic treatment. The Panel considers that no scientific conclusions can be drawn from this study for the substantiation of the claimed effect.
Results from a randomised test meal study were provided in poster form only (Frémont, 2005). A total of 12 healthy subjects (six females, age 18-45 years and an average body mass index 21.6 kg/m2) consumed 50 g of available carbohydrates either as a reference food (glucose) or as crispbread with three different acacia gum contents (acacia gum was added to the standard crispbread formula before baking): bread 1 (control) contained 4.1 g of fibre, 0% acacia gum; bread 2 contained 7.7 g fibre, 6% acacia gum; and bread 3 containing 9.6 g fibre, 11% acacia gum. Post-prandial glycaemic and insulinaemic responses were expressed as glycaemic and insulinaemic indices, respectively. The Panel notes that insufficient information was provided on the methods used in the study (e.g., details on recruitment of subjects, on the biochemical analysis of both biological and food samples, and on the statistical analysis of data were not reported, and no measures of statistical dispersion for food analyses and outcome variables were provided). The Panel considers that no scientific conclusions can be drawn from this study for the substantiation of the claimed effect.
One paper reports on a study in 12 healthy males (30-50 years) where the effects of 100 g of glucose or 100 g of glucose plus 20 g of acacia gum (both dissolved in 250 mL water) on postprandial glucose and insulin responses were measured using a randomised cross-over design (Sharma, 1985). Blood samples were taken before and 30, 60, 90, 120 and 150 minutes after consumption of the glucose load. Areas under the plasma glucose (-18.6%) and insulin (-12.4%) curves significantly decreased when acacia gum was added to the glucose solution. The Panel notes that the dose of acacia gum administered was four times (or twice, if 50 g available carbohydrates is considered as a serving) higher than proposed in the conditions of use in order to obtain the claimed effect. The Panel considers that no scientific conclusions can be drawn from this study for the substantiation of the claimed effect at the proposed conditions of use.
In weighing the evidence, the Panel took into account that no studies were presented which tested the effects of acacia gum on post-prandial blood glucose responses at the proposed conditions of use in the target population and from which scientific conclusions could be drawn for the substantiation of the claimed effect.
The Panel concludes that a cause and effect relationship has not been established between the consumption of acacia gum and the reduction of post-prandial blood glucose responses.

3.2. Utrzymanie prawidłowego stężenia glukozy we krwi (ID 842, 1977)

A total of five publications were cited in relation to this claim (Gee et al., 1995; Sharma, 1985; Meance et al., 2004; Castellani, 2005; Frémont, 2006) and are described in section 3.1.
The Panel notes that no studies have been provided on the long-term effects of acacia gum on measures of blood glucose control.
The Panel concludes that a cause and effect relationship has not been established between the consumption of acacia gum and long-term maintenance of normal blood glucose concentrations.