2.1. Redukcja masy ciała (ID 854, 1556, 3725)

The claimed effects are “weight management” and “contributes to weight management”. The Panel assumes that the target population is overweight individuals.
In the context of the proposed wordings, the Panel assumes that the claimed effects refer to the reduction of body weight.
Weight loss in overweight subjects, even without achieving a normal body weight, is considered to be a beneficial physiological effect.
The Panel considers that reduction of body weight is a beneficial physiological effect for overweight individuals.

2.2. Zmniejszenie stężenia glukozy we krwi po posiłku (ID 1559)

The claimed effect is “reduction of glycaemic response”. The Panel assumes that the target population is individuals 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 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 and hyperinsulinaemia are common in the general population of adults.
The Panel considers that the reduction of post-prandial glycaemic responses may be a beneficial physiological effect.

2.3. Utrzymanie prawidłowego stężenia glukozy we krwi (ID 835, 3724)

The claimed effects are “glycaemic control” and “contributes to maintain a healthy blood sugar level”. 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 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.

2.4. Utrzymanie prawidłowego stężenia cholesterolu we krwi na czczo (ID 3217)

The claimed effect is “helps to maintain physiological lipid levels in the blood”. 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 (fasting) blood concentrations of triglycerides.
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.

2.6. Utrzymanie prawidłowego funkcjonowania jelit (ID 834, 1557, 3901)

The claimed effects are “bowel functions”, “intestinal health/bowel function” and “bowel function/colonic function”. 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 of normal bowel function by promoting intestinal regularity and reducing intestinal transit time.
Changes in bowel habits within the normal range, e.g. reduced intestinal transit time and increased frequency of bowel movements, might be considered as maintenance of normal bowel function.
The Panel considers that maintenance of normal bowel function in the context of a reduction in intestinal transit time and an increase in the frequency of bowel movements within the normal range might be a beneficial physiological effect.

2.7. Zmniejszenie ilości potencjalnie patogennych mikroorganizmów przewodu pokarmowego (ID 1558)

The claimed effect is “prebiotic action/bifidogenic action”. The Panel assumes that the target population is the general population.
In the context of the proposed wording, the Panel assumes that the claimed effect refers to the capacity of food(s)/food constituent(s) to increase the numbers of bacteria considered to be beneficial. The numbers/proportions of bacterial groups that would constitute a “beneficial” colon/intestinal flora have not been established. Increasing the number of any group of microorganisms, including bifidobacteria, is not in itself considered as a beneficial physiological effect. The Panel considers that the evidence provided does not establish that increasing numbers of gastro-intestinal microorganisms is a beneficial physiological effect.
The Panel considers that decreasing potentially pathogenic gastro-intestinal microorganisms might be a beneficial physiological effect.

3.1. Redukcja masy ciała (ID 854, 1556, 3725)

A total of 45 references were cited for the scientific substantiation of this claim. Among them, six reported on intervention studies in humans investigating the effects of glucomannan on body weight (Birketvedt et al., 2005; Cairella and Marchini, 1995; Vido et al., 1993; Vita et al., 1992; Vuksan et al., 1999; Walsh et al., 1984). Also, the Panel identified three additional references cited in relation to other claims on glucomannan as being pertinent to this claim (Wood et al., 2007; Chen et al., 2003; Vuksan et al., 2001).
Walsh et al. (1984) conducted an eight-week double-blind, placebo-controlled, randomised trial in 20 obese subjects, who were randomly assigned to consume either glucomannan or placebo (starch) administered as 1 g doses (two capsules of 500 mg each) with 8 oz of water three times per day (before each meal) for eight weeks in the context of usual dietary patterns and levels of physical
exercise. Body weight loss during the study was significantly higher in the glucomannan group
(-5.5 1.5 kg) than in the placebo group (1.5 1.5 kg; difference between groups 7.0 1.4 kg, p<0.005).
In a double-blind, placebo-controlled randomised intervention study (Cairella and Marchini, 1995), 30 overweight women (BMI=25-30 kg/m2) were treated for 60 days with a 1,200 kcal/d (5,040 kJ/d) diet plus either placebo (n=15) or glucomannan (n=15). A total of four capsules of glucomannan or placebo were given daily with 1-2 glasses of water 30-60 minutes prior to the two main meals (appr. 4 g per day). Body weight loss during the study was statistically significantly (p=0.0017) higher in the glucomannan group (-4.3 kg) than in the placebo group (-2.7 kg, mean difference 1.6 kg, 95%CI=0.7-2.5).
In a double-blind, placebo-controlled randomised intervention study (Birketvedt et al., 2005), healthy overweight subjects were randomly assigned to consume either glucomannan (n=23) or placebo (n=29) for five weeks in the context of an energy-reduced diet providing 1,200 kcal per day. Glucomannan (1.24 g per day) and placebo were administered in tablets (n=6) with 250 mL of water 15 minutes before each meal (three times daily) and at 3 pm (n=4 tablets). Weight loss during the
intervention was significantly higher in the glucomannan group (-3.8 0.9) than in the placebo group
(-2.5 0.5, p<0.01).
In the study by Vita et al. (1992), 50 obese subjects (15 males) were randomly assigned to consume a hypocaloric diet (1,000 kcal/d or 4,200 kJ/d for women and 1,300 kcal or 5,460 kJ/d for men) either alone (control, n=25, 8 males) or together with glucomannan supplements (2+3+3 capsules with 300 mL water before meals, appr. 4 g per day in three doses) for three months. The authors reported a greater weight loss in the glucomannan group compared to controls at the end of the study (p<0.02) expressed as percentage of initial body weight from baseline. Mean changes are given as a histogram (approx. -25 % versus -20 % of initial body weight in the glucomannan and placebo groups respectively) and SD are not reported.
In a double-blind, placebo-controlled randomised intervention study (Vido et al., 1993), 60 overweight children under the age of 15 (mean age 11.2 years) were randomised to consume glucomannan (two capsules with two glasses of water one hour prior to each meal, 2 g/d, n=30) or placebo (n=30) for two months in the context of a normocaloric diet. The percentage of children being overweight significantly decreased during the study in both the intervention and the placebo groups with no significant differences between groups. No differences between groups in body weight changes were observed at the end of the study.
In a cross-over randomised controlled trial (RTC), 11 non diabetic, mildly hypertensive, free-living subjects with the insulin resistance syndrome (out of 278 subjects screened) consumed, in random order, test biscuits with glucomannan (0.5 g of glucomannan per 100 kcal of dietary intake, 8-13 g per day) or wheat bran fibre control biscuits for three weeks each separated by a 2-week washout (Vuksan et al., 2000). No statistically significant differences in body weight changes were observed between the glucomannan and the wheat bran fibre (control) interventions. In another study by the same authors with identical design, no statistically significant differences in body weight changes were observed between the glucomannan and the wheat bran fibre (control) interventions in a group of 11 type 2 diabetic subjects (Vuksan et al., 1999). The Panel notes the small number of subjects included in these studies, the short study duration, and that glucomannan was not given as pre-load before the meals but was rather consumed with the meals.
In a parallel-arm, double-blind, placebo-controlled intervention study by Wood et al., (2007), 30 overweight and obese men were randomly assigned to consume either glucomannan (3 g/d, n=15) or placebo (n=15) for 12 weeks in the context of a carbohydrate restricted diet for weight loss. No statistically significant differences in body weight changes were observed between the glucomannan and the placebo groups.
In the study by Chen et al. (2003), 22 diabetic subjects (12 female) with elevated blood cholesterol concentrations received, following a randomised, double-blind, crossover design, glucomannan and placebo (starch) for 28 days each with no washout period in between. Glucomannan and placebo were administered in gelatine capsules with a glass of water three times daily half an hour prior to meals. The dose of glucomannan increased progressively from 1.2 (for three days), 2.6 (for three days) to 3.6 g per day (for 22 days). No statistically significant differences in body weight changes were observed between the glucomannan and placebo groups. The Panel notes the short duration of the study and the absence of a washout period between interventions.
The Panel notes that no long-term studies (>3 months) on the effects of glucomannan on body weight are available.
The Panel also notes that glucomannan is a soluble-type of fibre which forms a viscous, gel-like mass in the stomach when hydrated, and that this “mass effect” could delay gastric emptying and induce satiety leading to a decrease in subsequent energy intake (Keithley and Swanson, 2005).
In weighing the evidence, the Panel took into account that most of the intervention studies, which were of adequate sample size and duration, found a statistically significant effect of glucomannan on body weight loss in the context of a hypocaloric diet when administered as a pre-load before meals, and that the mechanism by which glucomannan could exert the claimed effect is established.
Panel concludes that a cause and effect relationship has been established between the consumption of glucomannan and the reduction of body weight in the context of an energy-restricted diet.

3.2. Zmniejszenie stężenia glukozy we krwi po posiłku (ID 1559)

A total of 10 references were submitted in relation to this claim. Six were textbooks and consensus opinions in relation to the health effects of dietary fibre in general, one was a narrative review on the health effects of dietary fibre in general, one was a narrative review on the potential health effects of glucomannan and two reported on human intervention studies investigating the effects of glucomannan on health outcomes other than post-prandial glycaemic responses (e.g. fasting plasma and glucose concentrations, long-term blood glucose control). Also, some intervention studies on the effects of glucomannan on post-prandial glycaemic responses in type 2 diabetic subjects under pharmacological treatment for hyperglycaemia have been cited in relation to other claims on glucomannan. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claimed effect.
One reference submitted (Magnati et al., 1984) reported on a randomised, placebo-controlled, cross- over intervention investigating the effects of glucomannan on post-prandial blood glucose responses during an oral glucose tolerance test (OGTT) with 75 g glucose in 24 obese normoglycaemic subjects (19 females). No measures of insulin responses were reported. The Panel considers that no conclusions can be drawn from this study for the scientific substantiation of the claimed effect.
The Panel concludes that a cause and effect relationship has not been established between the consumption of glucomannan and the reduction of post-prandial glycaemic responses.

3.3. Utrzymanie prawidłowego stężenia glukozy we krwi (ID 835, 3724)

A total of 18 references were submitted in relation to this claim. Six were textbooks and monographs not including original data on the effects of glucomannan on blood glucose control, one was a narrative review on the health effects of dietary fibre in general, four were narrative reviews on the potential health effects of glucomannan including diabetes prevention and treatment, and one reported on human intervention studies investigating the effects of glucomannan on health outcomes other than
post-prandial glycaemic responses. In addition, one human intervention study investigating the effects of glucomannan on post-prandial blood glucose responses and four human intervention studies on the effects of glucomannan on medium-term blood glucose concentrations in type 2 diabetic subjects under hypoglycaemic pharmacological treatment were presented. The Panel considers that no conclusions can be drawn from these studies for the scientific substantiation of the claimed effect.
Only one of the references provided was considered by the Panel as pertinent to the claim (Vuksan et al., 2000).
In a cross-over randomised controlled trial (RTC), 11 non diabetic, mildly hypertensive, free-living subjects with the insulin resistance syndrome (out of 278 subjects screened) consumed, in random order, test biscuits with glucomannan (0.5 g of glucomannan per 100 kcal of dietary intake, 8-13 g per day) or wheat bran fibre control biscuits for three weeks each separated by a 2-week washout (Vuksan et al., 2000). A statistically significant decrease in plasma concentrations of fructosamine (a marker of blood glucose control) was observed with glucomannan compared to the wheat bran fibre control (between-group difference = 5.2±1.4 %, p<0.002). Changes in fasting glucose and insulin concentrations were not different between treatments. The Panel notes the small and highly selected sample of subjects recruited for this study, and that no evidence for a sustained effect was provided.
In weighing the evidence, the Panel took into account that only one small intervention study of short duration on a highly selected population sub-group was presented for the substantiation of the claimed effect, and that no evidence on the sustainability of the effect was provided.
The Panel concludes that a cause and effect relationship has not been established between the consumption of glucomannan and the maintenance of normal blood glucose concentrations.

3.4. Utrzymanie prawidłowego stężenia cholesterolu we krwi na czczo (ID 3217)

Among the 22 references cited in the list in relation to this claim, most addressed the effects of food/components other than glucomannan on claimed effects other than blood lipids. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claim.
Seven human studies which reported on the effects of glucomannan intake on blood concentrations of triglycerides have been presented (Vuksan et al., 1999, 2000; Chen et al., 2003; Vido et al., 1993; Walsh et al., 1984; Vita et al., 1992; Wood et al., 2007). The study designs have been described in section 3.1. Only one of the studies (Vita et al., 1992) reported a significant decrease in blood concentrations of triglycerides after consumption of glucomannan compared to placebo at the end of a three-month intervention, whereas five studies did not observe any differences between groups and one study reports a significant increase in the glucomannan group after two months of intervention (Vido et al., 1993).
Two animal studies cited in the list reported on changes in the lipid profile following consumption of glucomannan (Hou et al., 1990; Vorster et al., 1985). The Panel considers that the evidence provided in animal studies is not sufficient to predict the occurrence of an effect of glucomannan consumption on maintenance of normal blood concentrations of triglycerides in humans.
In weighing the evidence, the Panel took into account that only one out of seven studies presented reported a significant decrease in plasma concentrations of triglycerides following consumption of glucomannan.
The Panel concludes that a cause and effect relationship has not been established between the consumption of glucomannan and the maintenance of normal (fasting) blood concentrations of triglycerides.

3.5. Utrzymanie prawidłowego funkcjonowania jelit (ID 834, 1557, 3901)

Among the references provided for the scientific substantiation of the claim were five human intervention studies, three animal studies and several reviews and textbooks.
In all five human studies a commercial glucomannan preparation was studied.
Marzio et al. (1989) evaluated mouth to caecum transit time measured by hydrogen breath test in constipated patients (n=13) after ingestion of glucomannan (daily dose 3 g). The Panel notes the small number of subjects in the study and the fact that the method used to assess transit time has several limitations (Cummings et al., 2004). Subjects with chronic constipation (n=78) participated in the multicentric, open and non-controlled study in which the effect of glucomannan (daily dose 2-3 g) on the frequency of bowel movements and enema use, and on abdominal symptoms, was studied (Passaretti et al., 1991). The Panel considers that no conclusions can be drawn from this uncontrolled study for the scientific substantiation of the claimed effect. In the single-blind sequential study of Chen et al. (2006) glucomannan (daily dose 4.5 g) versus corn starch was given to eight subjects with low dietary fibre intake (<20 g/day). The frequency of defecations (mean number/day±SEM) was 1.1±0.2 in the placebo period and 1.4±0.2 in the glucomannan period (p<0.05). The Panel notes that the study was single-blinded and non-randomised with a small number of subjects. The Panel considers that no conclusions can be drawn from this uncontrolled study for the scientific substantiation of the claimed effect.
Two studies were performed with chronically constipated children (Loening-Baucke et al., 2004; Staiano et al., 2000). Loening-Baucke et al. (2004) evaluated in a double-blind, randomised, cross- over study the effect of glucomannan (100 mg/kg body weight) on the frequency of bowel movements in a group of children with chronic constipation. The Panel notes the high drop out rate (only 31 from 46 children completed the study), the fact that the children continued laxative treatment during the intervention period, and the fact that most of the children suffered also from encopresis accompanying constipation. The Panel considers that no conclusions can be drawn from this study for the scientific substantiation of the claimed effect. In another study, glucomannan was given to a group of children with severe brain damage (Staiano et al., 2000). The Panel considers that the evidence provided does not establish that children with severe brain damage are representative of the general population with regard to the autonomous nervous system and therefore bowel function, nor that results obtained in studies on subjects with severe brain damage can be extrapolated to the general population with regard to normal bowel function.
The Panel notes that no studies were provided from which conclusions could be drawn for the scientific substantiation of the claimed effect.
The Panel concludes that a cause and effect relationship has not been established between the consumption of glucomannan and the maintenance of normal bowel function.

3.6. Zmniejszenie ilości potencjalnie patogennych mikroorganizmów przewodu pokarmowego (ID 1558)

Among the 23 references provided for the scientific substantiation of the claim were five human intervention studies, two animal studies, seven reviews and nine textbooks or guideline opinions.
The human studies provided were related to endpoints not related to the claimed effect (e.g. stool bulk, intestinal transit time, abdominal comfort, number of lactobacilli and bifidobacteria). The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claimed effect.
The Panel concludes that a cause and effect relationship has not been established between the consumption of glucomannan and decreasing potentially pathogenic gastro-intestinal microorganisms.

4.1. Redukcja masy ciała (ID 854, 1556, 3725)

The Panel considers that the following wording reflects the scientific evidence: “Glucomannan contributes to the reduction of body weight in the context of an energy-restricted diet”.

5.1. Redukcja masy ciała (ID 854, 1556, 3725)

The Panel considers that in order to obtain the claimed effect, at least 3 g of glucomannan should be consumed daily in three doses of at least 1 g each, together with 1-2 glasses of water before meals, in the context of an energy-restricted diet. The target population is overweight adults.