2.1. Rozwój mózgu i układu nerwowego (ID 491)

The claimed effect is “brain development and maturation of neurosensorial functions.” Brain and neurological development is interpreted by the Panel as children's development.
The Panel notes that claims related to children's development and health are outside the scope of Article 13 of Regulation (EC) No 1924/2006.
A claim on ALA and contribution to brain development pursuant to Article 14 has already been assessed with a favourable outcome (EFSA, 2009).

2.2. Prekursor cząsteczek regulujących funkcjonowanie komórek (prostaglandyn, leukotrienów) (ID 492, 4671)

The claimed effect is “molecule precursors regulating cell functions (prostaglandins, leucotrienes)”. The Panel assumes that the target population is the general population.
The claimed effect is not sufficiently defined, and neither the wording nor the references cited provided further clarification.
The Panel considers that the claimed effect is general and non specific, and does not refer to any specific health claim as required by Regulation (EC) No 1924/2006.

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.

2.4. Funkcje i interakcje składników odżywczych (ID 576)

The claimed effect is “nutrient tasks and interactions”. The Panel assumes that the target population is the general population.
The claimed effect is not sufficiently defined. The Panel notes that different health outcomes were mentioned in the information provided, and that it was not possible to establish which specific effect is the target for the claim.
The Panel considers that the claimed effect is general and non specific, and does not refer to any specific health claim as required by Regulation (EC) No 1924/2006.

2.5. Utrzymanie prawidłowego ciśnienia tętniczego (ID 575)

The claimed effect is “cardiovascular system, nervous system”. 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 blood pressure.
A claim on ALA and maintenance of normal blood pressure has already been assessed with an unfavourable outcome (EFSA Panel on Dietetic Products Nutrition and Allergies (NDA), 2009). The references cited for this claim did not provide any additional scientific data which could be used to substantiate the claim.

2.6. Poprawa nastroju (ID 578, 601, 3182)

The claimed effects are “mental state and performance”, and “emotional health”. 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 enhancement of mood. Mood is a well defined psychological construct and can be measured by validated tests.
The Panel considers that enhancement of mood might be 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.

3.2. Poprawa nastroju (ID 578, 601, 3182)

Among the publications provided for the scientific substantiation of the claimed effect were textbooks, a publication from a government body which did not specifically mention the claimed effect, and references on outcomes unrelated to the claimed effect, such as the composition of nerve membranes, enzymatic activity, amplitude of electrophysiological parameters, resistance to poisons, performance of learning tasks, n-3 fatty acids and brain function during ageing, a case-report of human ALA deficiency reporting symptoms not related to mood, and a narrative review on the effects of various nutrients (including n-3 fatty acids) on the structure and function of the nervous system including the brain. Other references were narrative reviews and a general publication on the effects of n-3 fatty acids on various outcomes or diseases (mood modulation, stress, toxicomania, dyslexia, autism, depression, cognitive deficits, dementias, schizophrenia, bipolar disorder and post-partum depression) which did not provide any original data for the scientific substantiation of the claimed effect. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claimed effect.
One study examined the effects of supplementation with flax oil and vitamin C on blood fatty acid composition, and behaviour, in children with Attention Deficit Hyperactivity Disorder (ADHD) (Joshi et al., 2006). One study undertaken in students reported on the effects of a mixture of ALA and linoleic acid on behavioural variables associated with anxiety (mood, appetite, mental concentration, fatigue, academic organisation and poor sleep) with respect to tests and examinations (Yehuda et al., 2005). The Panel considers that no conclusions can be drawn from studies on a fixed combination for the substantiation of a claim on ALA alone.
One reference (Ross et al., 2007) was a systematic review of double-blind, placebo-controlled clinical trials published prior to April 2007 on the use of n-3 fatty acids in the treatment of patients diagnosed with mental illness (e.g. schizophrenia, personality disorders, depressive disorder and bipolar disorder). The Panel notes that no evidence has been provided to indicate that results from studies on enhancement of mood in these patients can be extrapolated to the general population.
Another systematic review carried out by Schachter et al. (2005) for the Agency for Healthcare Research and Quality addressed, inter alia, the question of the protective value of n-3 fatty acids with regard to mental health. Addressing the question of whether n-3 fatty acid intake is associated with the onset, continuation or recurrence of depression, the authors identified three intervention studies, six observational studies, and three cross-national ecological studies which met their inclusion
criteria, and which were therefore included in the review. Only one of these studies assessed the effects of ALA intake (Edwards et al., 1998). This study used the Beck Depression Inventory (BDI) in 10 depressed patients and 14 matched controls to assess the effect of diet on depressive symptoms. The Panel notes that no evidence was presented to indicate that results from studies on enhancement of mood in these patients can be extrapolated to the general population.
The Panel concludes that a cause and effect relationship has not been established between the dietary intake of alpha-linolenic acid and enhancement of mood.