2.1. Zwiększenie sytości (ID 790)

The claimed effect is “weight management, obesity and satiety”. The Panel assumes that the target population is individuals who need to control their energy intake.
Satiety understood as the decrease in motivation to eat after consumption of food varies in magnitude and duration and may include only changes in appetite ratings (hunger, fullness, satiety, and desire to eat) or also a reduction in subsequent energy intake. The effect may persist up to several hours, may change energy intake either at the next meal or across the day and, if sustained, may lead to a reduction in body weight. In the context of this opinion, satiety is interpreted as the decrease in the motivation to eat after consumption of food leading to a reduction in energy intake.
The Panel considers that an increase in satiety might be a beneficial physiological effect.

2.2. Osiąganie lub utrzymywanie prawidłowej masy ciała (ID 790)

The claimed effect is “weight management, obesity and satiety”. The Panel assumes that the target population is the general population.
Weight management can be interpreted as the contribution to maintenance of a normal body weight. In this context, weight loss in overweight subjects without achieving a normal body weight is considered beneficial to health.
The Panel considers that maintenance or achievement of a normal body weight is a beneficial physiological effect.

2.3. Utrzymanie prawidłowego stężenia trójglicerydów we krwi (ID 793, 816)

The claimed effects are “lipid management” and “heart health/cholesterol maintenance”. 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 maintenance of normal (fasting) blood concentrations of triglycerides and of normal blood cholesterol concentrations. The latter is addressed in section 2.4.
Triglycerides in plasma are either derived from dietary fats or synthesised in the body from other energy sources like carbohydrates. In fasting conditions, serum triglycerides are mainly transported in very-low-density lipoproteins (VLDL) synthesised in the liver. Excess calorie intake with a meal is converted to triglyceride and transported to the adipose tissue for storage. Hormones regulate the release of triglycerides from adipose tissue in order to meet energy needs between meals. Normal values for blood concentrations of triglycerides have been defined.
The Panel considers that maintenance of normal (fasting) blood concentrations of triglycerides may be a beneficial physiological effect.

2.4. Utrzymanie prawidłowego stężenia cholesterolu we krwi (ID 793, 816)

The claimed effects are “lipid management” and “heart health/cholesterol maintenance”. 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 maintenance of normal (fasting) blood concentrations of triglycerides and of normal blood cholesterol concentrations. The former is addressed in section 2.3.
Low-density lipoproteins (LDL) carry cholesterol from the liver to peripheral tissues, including the arteries. Elevated LDL-cholesterol, by convention >160 mg/dL, may compromise the normal structure and function of the arteries.
The Panel considers that maintaining normal blood cholesterol concentrations is a beneficial physiological effect.

2.5. Zmniejszenie stężenia glukozy we krwi po posiłku (ID 789, 2932)

The claimed effects are “glycaemic response” and “postprandial blood glucose”. The Panel assumes that the target population is subjects willing to reduce their post-prandial glycaemic responses.
In the context of the proposed wording “contributes to lower the glycaemic response”, the Panel notes that the claimed effect relates 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 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.

2.6. Utrzymanie prawidłowego stężenia glukozy we krwi (ID 792)

The claimed effect is “energy and vitality”. 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 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. Zwiększenie sytości (ID 790)

The references provided included studies on the effects of food/constituents other than PHGG (e.g., guar gum) on health outcomes other than satiety (e.g., insulin and glucose responses), and studies on the stimulation of glucagon-like peptide-1 release by different food components or test meals. The Panel considers that no scientific conclusions can be drawn from these references for the substantiation of the claim.
Among the references provided assessing appetite ratings, four intervention studies were performed with guar gum (French and Read, 1994; Adam and Westerterp-Plantenga, 2005a and 2005b; Lavin and Read 1995). The Panel considers that no scientific conclusions can be drawn from these references for the substantiation of the claim. Two (Kovacs et al., 2001 and 2002) described the test product as modified guar gum and Wolf et al. (2003) utilise a novel low-viscosity guar gum beverage. Whereas it is uncertain how “modified” guar gum relates to PHGG, the Panel assumes that low- viscosity guar gum refers to PHGG. The three additional articles were cited in the two review articles provided and all refer specifically to PHGG (Pasman et al., 1997; Heini et al., 1998; Van de Ven et al., 1994).
Three of the studies presented assessed the effects of PHGG on appetite ratings during 7-11 days of supplementation (Kovacs et al., 2001; Pasman et al., 1997; Heini et al., 1998) and one additional study investigated the effects of PHGG on appetite ratings after a single meal (Wolf et al., 2003). None of these studies addressed the effects of PHGG on subsequent energy intake. The Panel considers that no sientific conclusions can be drawn form these studies for the substantiation of the claimed effect.
Three of the studies presented assessed the effects of PHGG on appetite ratings and subsequent energy intake.
Pasman et al. (1997) reported a lack of effect of one week of PHGG supplementation (40 g per day) on hunger and satiety in 17 obese women despite a significant reduction in energy intake over the last three days of the week compared to normal (non-supplemented) conditions. However, energy intake was assessed under free-living conditions using self-reported measures, the validity of which is questionable. The Panel considers that this weakness of the study greatly limits the conclusions that can be drawn for the substantiation of the claimed effect.
Van de Ven et al. (1994) reported a reduction in food intake in 15 healthy women following consumption of a fructose/PHGG (3%) preload either 30 or 60 minutes before a test meal compared to placebo. Hunger was also reduced after the preload and for up to 5 h after the test meal in the fructose/PHGG (3%) preload compared to placebo. However, when the energy content of the preload was taken into account, energy intake was higher for the fructose/PHGG (3%) preload plus the meal than for placebo plus the meal.
Kovacs et al. (2002), following a randomised cross-over design, observed an effect of modified guar gum supplementation (2.5g) to a semi-solid meal (compared to an unsupplemented semi-solid meal and to a solid meal) on appetite ratings but not on total energy intake or meal pattern assessed in the laboratory on the last day of each 2-week intervention period in 15 overweight males.
In weighing the evidence, the Panel took into account that the two studies presented showed no effect of PHGG consumption on appetite ratings leading to a reduction in energy intake when the energy content of the test meal was taken into account.
The Panel considers that a cause and effect relationship has not been established between the consumption of PHGG and increased satiety.

3.2. Osiąganie lub utrzymywanie prawidłowej masy ciała (ID 790)

Twenty four references were presented in relation to this claim. Of these, 21 did not address the influence of PHGG manipulations on measures of body weight, one book chapter only reported on the general health effects of dietary fibre, and one review did not refer to any additional pertinent studies than the one described below. The Panel considers that no scientific conclusions can be drawn from these references for the substantiation of the claim.
Kovacs et al. (2001) examined the effect of addition of modified guar gum to a low-energy semi-solid meal on appetite and body weight loss in 28 overweight male volunteers (aged 19-56 years). The study involved three treatment periods of two weeks with a low-energy diet containing a semi-solid meal either with or without modified guar gum or a solid meal. The modified guar gum-supplemented meal prevented the increase in hunger, desire to eat. However, and despite some variability in the effect on weight loss induced by the order of treatments (any intervention was more effective on weight loss when it took place during the first intervention period), no significant differences were observed between the interventions with respect to weight loss.
The Panel considers that a cause and effect relationship has not been established between the consumption of PHGG and maintenance or achievement of a normal body weight.

3.3. Utrzymanie prawidłowego stężenia trójglicerydów we krwi (ID 793, 816)

The references provided included studies on the effects of food/food constituents other than PHGG (e.g., guar gum), on health outcomes other than fasting concentrations of triglycerides (e.g. faecal output, acute post-prandial concentrations of triglycerides). The Panel considers that no scientific conclusions can be drawn from these references for the substantiation of the claim.
Only two of the references provided directly assessed the effects of PHGG on fasting serum concentrations of triglycerides in humans (Takahashi et al., 1993; Yamatoya et al., 1997). In the study by Takahashi et al. (1993), a very high dose of PHGG (108 g per day) was administered to eight male subjects after a control, PHGG-free diet, for four weeks. The Panel notes the small number of subjects, the absence of a control group, and that the dose of PHGG used is several times higher than the amount proposed in the conditions of use to obtain the claimed effect. In the study by Yamatoya et
al. (1997), 15 women with total cholesterol concentrations 190 mg/dL (4.91 mmol/L) were assigned to consume either 5 g per day (n=9) or 15 g per day (n=6) of PHGG for two consecutive weeks. The Panel notes the small number of subjects, the absence of a control group, and the short period of the intervention.
The Panel considers that no conclusions can be drawn from these small, non-controlled studies for the substantiation of the claimed effect.
The Panel concludes that a cause and effect relationship has not been established between the consumption of PHGG and maintenance of normal (fasting) blood concentrations of triglycerides.

3.4. Utrzymanie prawidłowego stężenia cholesterolu we krwi (ID 793, 816)

The references provided included studies on the effects of food/food constituents other than PHGG (e.g., guar gum) on health outcomes other than blood cholesterol (e.g., faecal output, post-prandial concentrations of triglycerides). The Panel considers that no scientific conclusions can be drawn from these references for the substantiation of the claim.
Only two of the references provided directly assessed the effects of PHGG on total serum cholesterol concentrations in humans (Takahashi et al., 1993; Yamatoya et al., 1997). In the study by Takahashi et al. (1993), a very high dose of PHGG (108 g per day) was administered to eight male subjects after a control, PHGG-free diet, for four weeks. The Panel notes the small number of subjects, the absence of a control group, and that the dose of PHGG used is several times higher than the amount proposed in the conditions of use to obtain the claimed effect. In the study by Yamatoya et al. (1997),
15 women with total cholesterol concentrations 190 mg/dL (4.91 mmol/L) were assigned to consume either 5 g per day (n=9) or 15 g per day (n=6) of PHGG for two consecutive weeks. The Panel notes the small number of subjects, the absence of a control group, and the short period of the intervention.
The Panel considers that no conclusions can be drawn from these small, non-controlled studies for the substantiation of the claimed effect.
The Panel concludes that a cause and effect relationship has not been established between the consumption of PHGG and maintenance of normal blood cholesterol concentrations at the proposed conditions of use.

3.5. Zmniejszenie stężenia glukozy we krwi po posiłku (ID 789, 2932)

A total of 14 publications were cited in relation to the proposed claims. The references provided included one animal feeding study (Suzuki and Hara, 2004) along with intervention studies and reviews on the health effects of dietary fibre in general, on the health effects of specific fibres other than PHGG (e.g., guar gum), on the health effects of foods with a low glycaemic index, and on the effects of PHGG on health outcomes unrelated to the reduction of post-prandial responses (e.g., blood lipids). The Panel considers that no scientific conclusions can be drawn from these references for the substantiation of the claim. The text of one article was only available in Chinese (Gu et al., 2003) and the English translation was not available to the Panel.
Only two of the studies cited investigated the effects of PHGG on post-prandial glycaemic responses. Golay et al. (1995) examined the effect of PHGG in combination with fructose incorporated into a liquid meal on post-prandial glucose and insulin concentrations in six type 2 diabetic patients. The Panel notes that four of the subjects were treated with oral anti-diabetic therapy. The Panel considers that results from pharmacologically treated type 2 diabetic subjects cannot be extrapolated to the general population.
In the randomised cross over intervention study by Trinidad (2004), eleven healthy subjects and nine type 2 diabetic subjects under dietetic management consumed as a reference 50 g of available carbohydrate from white bread (100 g) and on separate occasions increasing amounts of PHGG (3, 5, 10 and 15 g) either in white bread, added to rice or dissolved in 250 mL water and taken as a drink with white bread. Capillary blood samples were taken before and 15, 30, 45, 60, 90 and 120 minutes after consumption of the test products in normal subjects or before and 30, 60, 90, 120, 150 and 180 minutes after consumption of the test products in diabetic subjects. Whilst increasing amounts of PHGG significantly decreased the area under the plasma glucose curve in a dose-dependent manner in
diabetic subjects, it was not reduced significantly in non-diabetic subjects. The Panel notes the lack of control for a volume effect (it was not reported whether 250 mL of water was consumed in all conditions) and that insulin responses were not assessed. The Panel considers that no scientific conclusions can be drawn from this study in relation to the claimed effect.
In weighing the evidence, the Panel took into account that no conclusions could be drawn for the substantiation of the claim from any of the cited studies which examined the effect of PHGG on post- prandial glycaemic responses.
The Panel concludes that a cause and effect relationship has not been established between the consumption of PHGG and reduction of post-prandial glycaemic responses.

3.6. Utrzymanie prawidłowego stężenia glukozy we krwi (ID 792)

A total of eight publications were cited in relation to the proposed claim. The references provided include intervention studies and reviews on the health effects of dietary fibre in general, on the health effects of specific fibres other than PHGG (e.g. guar gum) and on the health effects of foods with a low glycaemic index. The Panel considers that no conclusions can be drawn from these references for the substantiation of the claim. The text of one article was only available in Chinese (Gu et al., 2003) and the English translation was not available to the Panel.
Only two of the studies cited examined the effects of PHGG on blood glucose concentrations. However, both studies (Golay et al., 1995; Trinidad et al., 2004) investigated the effects of PHGG on post-prandial glycaemic responses, and no measures of long-term blood glucose control were reported. The Panel considers that no scientific conclusions can be drawn from these studies in relation to the long-term maintenance or achievement of normal blood glucose concentrations.
The Panel concludes that a cause and effect relationship has not been established between the consumption of PHGG and the long-term maintenance of normal blood glucose concentrations.