ID 509 - Kwas alfa-linolenowy

PL: Kwas alfa-linolenowy
EN: Alpha-linolenic acid (LNA-Omega 3)
Pdf: various food(s)/food constituent(s) that are referring to children’s development

Oświadczenie (2)

1. Charakterystyka żywności / składnika

The food constituent that is the subject of the health claims is alpha-linolenic acid (ALA).
ALA is an essential n-3 polyunsaturated fatty acid with 18 carbon atoms and three double bonds. ALA is a well recognised nutrient, is well absorbed when consumed in the form of triglycerides, and is measurable in foods by established methods.
The Panel notes that in the conditions of use for flaxseed oil (ID 578, 579, 601, 3182), ALA was identified as the proposed active ingredient.
The Panel considers that the food constituent, ALA, which is the subject of the health claims, is sufficiently characterised.

2.3. Utrzymanie prawidłowego funkcjonowania serca (ID 509, 579)

The claimed effects are “cardiovascular system” and “heart health”. The Panel assumes that the target population is the general population.
In the context of the proposed wordings and the clarifications provided by Member States, the Panel assumes that the claimed effects refer to the maintenance of normal cardiac function.
The Panel considers that maintenance of normal cardiac function is a beneficial physiological effect.

3.1. Utrzymanie prawidłowego funkcjonowania serca (ID 509, 579)

Some of the references provided in relation to the claim reported on fatty acids other than ALA (e.g. DHA and/or EPA), or on health outcomes other than the claimed effect (e.g. blood and tissue lipids, blood coagulation, blood glucose and insulin concentrations, blood pressure, markers of sub- clinical inflammation and endothelial activation). The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claimed effect.
One randomised, single-blind intervention study on the effects of an ALA-rich diet compared to the usual post-infarction diet on secondary prevention of myocardial infarction was provided (de Lorgeril et al., 1994). The Panel notes that the comparison diet (post-infarction diet) and the ALA-rich diet were not controlled for dietary factors other than ALA (e.g. fat and saturated fat), which could have contributed to the claimed effect. The Panel considers that no conclusions can be drawn from this reference for the scientific substantiation of the claimed effect.
Narrative reviews and consensus opinions on the health effects of polyunsaturated fatty acids, including ALA, on various health effects, including atherosclerosis and coronary heart disease, were provided. The Panel notes that although some European countries have based dietary reference values for ALA on the protective effects of ALA intake in relation to coronary heart disease (CHD), which have been reported in some observational studies (e.g. Gezondheidsraad, 2001), most dietary reference values are adequate intake levels derived from observed intakes, and there is currently no consensus on the role of ALA in the prevention of CHD (EFSA Panel on Dietetic Products Nutrition and Allergies (NDA), 2010).
One systematic review and meta-analysis, which included all pertinent studies submitted individually for the scientific substantiation of the claimed effect, was provided in the consolidated list (Brouwer et al., 2004).
In the meta-analysis by Brouwer et al. (2004), three single-blind, randomised controlled interventions in which the investigators were aware of the intervention were considered (de Lorgeril et al., 1994; Singh et al., 1997; Singh et al., 2002). In the study by Singh et al. (1997), only patients in secondary prevention for myocardial infarction were considered and in the studies by de Logeril et al. (1994) and Singh et al., (2002) the dietary treatment involved dietary modifications other than changes in ALA intakes, and no control for dietary factors other than ALA, which could have contributed to the claimed effect, was made. The Panel considers that the evidence provided does not establish that patients under medical (including pharmacological) treatment for secondary prevention of myocardial infarction are representative of the general population with regard to cardiac function. The Panel also considers that no conclusions can be drawn from these references for the scientific substantiation of the claimed effect.
In addition, five prospective cohort studies reporting on ALA intakes and mortality from heart disease were included in the meta-analysis (Ascherio et al., 1996; Dolecek and Granditis, 1991; Oomen et al., 2001; Pietinen et al., 1997). These studies considered a total of 155,503 subjects. Four of these cohorts consisted of men, and one of women (n=76,283) (Hu et al., 1999). All cohorts consisted of subjects who were free of diagnosed cardiovascular disease at baseline. The combined risk estimates of fatal heart disease for a high vs. low intake of ALA were 0.79 (95 % CI: 0.60 to 1.04) when the relative risk (RR) was calculated and adjusted for confounding factors. The mean ALA intake in the highest categories in the individual studies was 2.0 g/day vs. 0.8 g/day in the lowest categories; thus the RR referred to a mean difference in ALA intakes of 1.2 g/day. The Panel notes that this meta- analysis did not show an effect of ALA on the risk of fatal heart disease.
The Panel is aware of another systematic review which assessed the effects of omega-3 fatty acids on cardiovascular disease outcomes in primary and secondary prevention studies (Wang et al., 2006). The Panel considers that the evidence provided does not establish that patients under medical (including pharmacological) treatment for secondary prevention of myocardial infarction are representative of the general population with regard to cardiac function. Three prospective cohort studies conducted in populations with no history of cardiovascular disease and which had estimated ALA intakes (Folsom and Demissie, 2004; Hu et al., 2002; Oomen et al., 2001) and one randomised controlled trial (Natvig et al., 1968) on ALA intake (5.5 g/day vs. 0.14 g/day) were evaluated. The Panel notes that no evidence was found in studies on primary prevention that ALA intakes reduced the rates of cardiac death.
In weighing the evidence, the Panel took into account that most prospective cohort studies and one randomised controlled trial, did not show an effect of ALA intake on the maintenance of normal cardiac function.
The Panel concludes that a cause and effect relationship has not been established between the dietary intake of alpha-linolenic acid and maintenance of normal cardiac function.

Warunki i możliwe ograniczenia stosowania oświadczenia

Minimum 0.3 g per 100g (15% of the 2 g RDI suggested by SCF)