2.1. Udział w prawidłowym metabolizmie makroskładników (ID 260, 401, 4665, 4666, 4667)

The claimed effects are “chromium has been shown to potentiate insulin action and thereby influences carbohydrate, lipid and protein metabolism”, “chromium is part of enzymes of the carbohydrate and lipid metabolism”, “promotes carbohydrates catabolism by potentiating insulin action and thereby influencing carbohydrates metabolism”, “promotes fat catabolism by potentiating insulin action and thereby influencing lipid metabolism”, and “glucose metabolism”. The Panel assumes that the target population is the general population.
The Panel assumes that the claimed effect refers to macronutrient metabolism.
The Panel considers that contribution to normal macronutrient metabolism is a beneficial physiological effect.

2.2. Utrzymanie prawidłowego stężenia glukozy we krwi (ID 262, 4667)

The claimed effects are “to fulfil increased need during pregnancy and lactation” and “glucose metabolism”. The Panel assumes that the target population is the general population.
In the context of the clarification provided by Member States for ID 262 and in the context of the proposed wordings for ID 4667, the Panel assumes that the claimed effect refers to the maintenance of normal blood glucose concentrations.
The Panel considers that long-term maintenance of normal blood glucose concentrations is a beneficial physiological effect.

2.3. Udział w utrzymaniu lub osiągnięciu prawidłowej masy ciała (ID 339, 4665, 4666)

The claimed effects are “weight control”, “promotes carbohydrates catabolism by potentiating insulin action and thereby influencing carbohydrates metabolism”, and “promotes fat catabolism by potentiating insulin action and thereby influencing lipid metabolism”. 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 body weight control.
Weight control 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 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.

2.4. Zmniejszenie zmęczenia (ID 261)

The claimed effect is “vitamin/mineral supplementation to reduce fatigue and tiredness in situations of inadequate micronutrient status”. The Panel assumes that the target population is the general population.
The Panel considers that reduction of tiredness and fatigue is a beneficial physiological effect.

3.1. Udział w prawidłowym metabolizmie makroskładników (ID 260, 401, 4665, 4666, 4667)

A common feature in all cases of chromium depletion reported in humans is an impaired glucose tolerance and glucose utilisation probably resulting from an increased resistance to the action of insulin (Jeejeebhoy et al., 1977; Freund et al., 1979; Brown et al., 1986). As reported by Jeejeebhoy et al. (1977), these lead to elevated plasma concentrations of fatty acids, increased utilisation of fatty acids as a source of energy, and possibly to abnormalities in nitrogen metabolism, as nitrogen retention increased with the administration of chromium chloride.
Although there is no consensus about the mechanism by which chromium could exert these effects, consensus opinions from authoritative bodies are generally in agreement that chromium facilitates the action of insulin, thus contributing to macronutrient metabolism (SCF, 1993; IoM, 2001; EVM, 2002).
The Panel concludes that a cause and effect relationship has been established between the dietary intake of chromium and contribution to normal macronutrient metabolism. However, the evidence provided does not establish that inadequate intake of chromium leading to impaired macronutrient metabolism occurs in the general EU population.

3.2. Utrzymanie prawidłowego stężenia glukozy we krwi (ID 262, 4667)

Hyperglycaemia is a common feature of chromium depletion in humans, which is reversed by the administration of chromium (Jeejeebhoy et al., 1977; Freund et al., 1979; Brown et al., 1986; SCF, 1993; IoM, 2001; EVM, 2002).
The Panel concludes that a cause and effect relationship has been established between the dietary intake of chromium and the maintenance of normal blood glucose concentrations. However, the evidence provided does not establish that intake of chromium inadequate for the maintenance of normal blood glucose concentrations occurs in the general EU population.

3.3. Udział w utrzymaniu lub osiągnięciu prawidłowej masy ciała (ID 339, 4665, 4666)

Weight loss has been described in one case as a result of chromium depletion in long-term total parenteral nutrition (TPN), which was reversed by the administration of chromium (Jeejeebhoy et al., 1977; Freund et al., 1979; SCF, 1993). However, body weight changes have not been described as a common feature of chromium deficiency.
Among the references provided for the scientific substantiation of this claim, a meta-analysis of double-blind, randomised controlled trials (Pittler et al., 2003) and five intervention studies in humans (Anderson et al., 1983; Grant et al., 1997; Bahadori et al., 1997; Crawford et al., 1999, Rabinovitz et al., 2004) have investigated the effects of different forms of chromium on body weight. The study of
Rabinovitz et al., (2004) was uncontrolled (all subjects received 200 g chromium picolinate (CrPic) twice daily) and therefore the Panel considers that no conclusions can be drawn from this study for the scientific substantiation of the claimed effect.
The meta-analysis by Pittler et al. (2003) investigated the effects of chromium picolinate (CrPic) on body weight by searching and pooling available double-blind, placebo-controlled, randomised trials in humans reporting on body weight, even if body weight was not the primary outcome. Ten trials met the inclusion criteria (Volpe et al., 2001; Kaats et al., 1996; Kaats et al., 1998; Walker et al., 1998; Livolsi et al., 2001; Campbell et al., 1999; Joseph et al., 1999; Hasten et al., 1992; Hallmark et al., 1996; Grant et al., 1997). Fourteen studies were excluded because they were either not randomised, double-blind and placebo controlled, did not test a mono-preparation of CrPic, did not report on body weight or were published in duplicate. Seven other studies reported in six publications (Lee and Reasner, 1994; Anderson et al., 1997; Clancy et al., 1994; Press et al., 1990; Bahadori et al., 1997; Evans, 1989) were also considered but reported data that the authors of the meta-analysis found not
suitable for statistical pooling. Doses of CrPic used in these studies ranged from 188 to 924 g per day, and study duration was from 6 to 12 weeks. No data were available to calculate body mass index (BMI) in five of the studies.
The result of the meta-analysis for body weight suggests a significant reduction in body weight in subjects receiving CrPic compared with subjects receiving placebo (weighted mean difference: -1.1 kg; 95 % CI: -1.8 to -0.4 kg, n = 489). When the six trials (Volpe et al., 2001; Kaats et al., 1996, 1998; Campbell et al., 1999; Joseph et al., 1999; Grant et al., 1997) which included overweight or obese subjects for treatment periods ranging between 6 to 13 weeks were assessed separately, similar results were obtained (weighted mean difference: -1.1 kg; 95 % CI: -1.8 to -0.4 kg, n = 385). Sensitivity analyses performed to test the robustness of the main analysis showed that removing the data of one trial (Kaats et al., 1996) which accounted for 58 % of the overall effect, would alter the direction of the result. The meta-analysis of the remaining nine studies showed no significant effect of CrPic compared to placebo on body weight (weighted mean difference: -0.9 kg; 95 % CI: -2.0 to 0.2 kg, n = 335).
A funnel plot of the mean difference in body weight reduction against trial sample size was consistent with some degree of publication bias.
An additional human intervention study using CrPic and reporting on body weight changes which was published after the meta-analysis by Pittler et al. (2003) was provided in the consolidated list
(Rabinovitz et al., 2004). However, this study lacked a control group (all subjects received 200 g CrPic twice daily) and therefore the Panel considers that no conclusions can be drawn for the scientific substantiation of the claimed effect.
Two additional human intervention studies using CrPic and reporting on body weight with sample sizes of more than 80 subjects, and which were published after the meta-analysis by Pittler et al. (2003), have been identified by the Panel (Lukaski et al., 2007; Yazaki et al., 2010).
In the double-blind, placebo controlled intervention study by Lukaski et al. (2007), 83 women were
randomly assigned to consume CrPic (200 g Cr per day, n = 27), an equivalent amount of picolinic
acid (1720 g, n = 27) or placebo (n = 29) for 12 weeks. All three groups received nutritionally balanced diets controlled for energy and nutrients. No significant differences between groups were observed in body weight changes during the study, suggesting no effect of Cr as CrPic on body weight.
In the randomised, double-blind, placebo-controlled trial by Yazaki et al. (2010), 80 overweight or
obese subjects (40 female) were randomly assigned to consume 1000 g per day of CrPic or placebo (1630 mg per day of dicalcium phosphate) for six months. During the first three months, all subjects were asked to continue with their usual dietary habits and physical activity level, whereas a low- intensity nutrition education and weight loss programme was prescribed to both groups for the remaining three months. Only statistical analyses in completers were performed. Data were available for 67 subjects (35 in the treatment group) at three months and for 58 subjects at six months (30 in the
treatment group). No significant differences between groups were observed in body weight changes (expressed as BMI) during the study at any time point.
The remaining three intervention studies in humans provided in the consolidated list which reported on body weight changes used other forms of chromium, such as chromium chloride (Anderson et al., 1983) or niacin-bound chromium (i.e., chromium nicotinate) (Grant et al., 1997; Crawford et al., 1999).
In a randomised, double-blind cross-over study (Anderson et al., 1983), 76 normal, free-living
subjects (28 females) received supplements of 200 g per day chromium (Cr) in the form of chromium chloride and placebo for three months each in random order. No other dietary or lifestyle changes were advised. No significant differences between chromium and placebo in body weight changes were observed during the study.
Crawford et al. (1999) designed a randomised, double-blinded, placebo-controlled, crossover pilot
study to assess the effects of 600 g per day of niacin-bound chromium on body weight in 20 overweight African-American women undergoing a modest dietary and exercise programme. Placebo and Cr (n=10 verum first) periods were each two months in duration. No significant differences between chromium and placebo in body weight changes were observed during the study. The Panel notes the small number of subjects recruited in this study.
No evidence of a biologically plausible mechanism by which chromium could exert the claimed effect has been provided
In weighing the evidence, the Panel took into account that results from the meta-analysis which assessed the effects of chromium picolinate on body weight were not robust and were possibly clouded by publication bias, that results from the largest intervention studies on the effects of chromium on body weight were inconsistent, that two studies showed a statistically significant effect of chromium on body weight (Kaats et al., 1996, 1998), that three studies (Anderson et al., 1983; Lukaski et al., 2007; Yazaki et al., 2010) showed no effect and that no evidence of a biologically plausible mechanism by which chromium could exert the claimed effect has been provided.
The Panel concludes that the evidence provided is insufficient to establish a cause and effect relationship between the dietary intake of chromium and the contribution to the maintenance or achievement of a normal body weight.

3.4. Zmniejszenie zmęczenia (ID 261)

Five references were provided for the scientific substantiation of this claim. These included two nutrition text books, a consensus opinion on dietary reference intakes for several vitamins and minerals including chromium (IoM, 2001), a general review on the potential effects of chromium including toxicity and an intervention study on the effects of acute chromium supplementation to male runners on a number of biochemical variables but which did not include fatigue as an outcome (Anderson et al., 1984).
Tiredness and fatigue are not among the symptoms observed in the few cases of chromium depletion reported and referred to in the references provided.
The Panel concludes that a cause and effect relationship has not been established between the dietary intake of chromium and reduction of tiredness and fatigue.

4.1. Udział w prawidłowym metabolizmie makroskładników (ID 260, 401, 4665, 4666, 4667)

The Panel considers that the following wording reflects the scientific evidence: “Chromium contributes to normal macronutrient metabolism”.

4.2. Utrzymanie prawidłowego stężenia glukozy we krwi (ID 262, 4667)

The Panel considers that the following wording reflects the scientific evidence: “Chromium contributes to the maintenance of normal blood glucose levels”.