2.1. Udział w prawidłowym przebiegu funkcji poznawczych (ID 532)

The claimed effect is “brain function (adult & children)”. The Panel assumes that the target population is the general population.
In the context of the clarifications provided by Member States, the Panel assumes that the claimed effect refers to contribution to normal cognitive function. Cognitive function includes memory,
attention (concentration), learning, intelligence and problem solving, which are well defined constructs and which can be measured by validated psychometric cognitive tests.
The Panel considers that contribution to normal cognitive function is a beneficial physiological effect.

2.2. Utrzymanie prawidłowego stanu kości (ID 642, 697, 1552)

The claimed effect is “bone 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 effect refers to the maintenance of normal bone through the promotion of calcium absorption.
The Panel considers that maintenance of normal bone is a beneficial physiological effect.

3.1. Udział w prawidłowym przebiegu funkcji poznawczych (ID 532)

The references provided to substantiate the claim included narrative reviews on the role of n-3 and n-6 fatty acids in the brain which did not provide original data for the scientific substantiation of the claim. One study investigated correlations between nutrient intake and the lipid profiles of meibomian gland secretions in women with Sjögren's syndrome. Three studies addressed the effects of food constituents other than DHA, EPA and GLA on cognitive-related outcomes (i.e. DHA and arachidonic acid, total n-3 fatty acids). One animal study investigated the effect of an n-3 fatty acid-depleted diet on the brain, retina, and liver fatty acyl composition of rats. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claim.
The Panel notes that no human studies have been provided on the effect of the consumption of a combination of DHA, EPA and GLA on cognitive endpoints.
The Panel concludes that a cause and effect relationship has not been established between the consumption of DHA, EPA and GLA and contribution to normal cognitive function.

3.2. Utrzymanie prawidłowego stanu kości (ID 642, 697, 1552)

A number of narrative reviews on the effects of dietary fats and fatty acids on calcium absorption and excretion, and on bone mass and bone turnover in different population subgroups, which included no original data that could be used for the scientific substantiation of the claim, and human intervention studies on the effects of different fats and combinations of fatty acids on health outcomes (e.g. urolithiasis, calcium absorption, and fatty acid profiles in blood and cells) other than the claimed effect, were provided. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claim.
In a pilot randomised controlled intervention (Kruger et al., 1998), 66 elderly women (mean age 79.5 years) living in nursing homes, and with a clinical diagnosis of osteopenia or osteoporosis, were assigned to consume 6 g of a mixture of evening primrose oil and fish oil (60 % linoleic acid (LA), 8 % GLA, 4 % EPA and 3 % DHA) or 6 g of a control oil (coconut oil, 97 % saturated fatty acids, 0.2 % LA) for 18 months. A total of 21 women consumed the evening primrose and fish oil mixture for an additional 18 months, irrespective of the study group to which they were randomised. All women received 600 mg of calcium carbonate daily. The Panel notes that the follow-up is an open label, uncontrolled phase of the study, and considers that no conclusions can be drawn from this
follow-up for the scientific substantiation of the claim. The oils were supplied in 500 mg capsules, and four capsules were consumed three times daily. Bone mineral density (BMD), markers of bone turnover, and plasma and urinary calcium, potassium, creatinine and phosphate were assessed at baseline, and at 6, 12 and 18 months. No significant differences in any of these variables were observed between the intervention and control groups during the study. The Panel notes that this study does not show an effect of the food constituents on the maintenance of bone.
Bassey et al. (2000) reported on one RCT in which 43 pre-menopausal women (age range 25-40 years) and 42 post-menopausal women (age range 50-65 years) were randomly assigned to consume capsules (10 daily) each providing 4 g of evening primrose oil and 440 mg of marine fish oil plus one gram of calcium, or one gram of calcium only (control), for 12 months. The Panel assumes that the composition of the evening primrose oil plus marine fish oil mixture is the same as in the study by Kruger et al. (1998). Randomisation and data analysis were performed separately for pre- and post-menopausal women. BMD (primary outcome) and markers of bone turnover were assessed at the beginning and end of the study. No significant differences between intervention and control groups were observed with respect to any of these variables during the study. The Panel notes that this study does not show an effect of the food constituents on the maintenance of bone.
A randomised controlled intervention study on the effects of evening primrose oil, fish oil, a mixture of evening primrose and fish oil, and olive oil (placebo) given for 16 weeks on calcium absorption and excretion, and on markers of bone turnover, was provided (van Papendorp et al., 1995). BMD was not assessed in this study. The Panel notes that acute changes in markers of bone turnover do not predict the occurrence of an effect on bone mineral density and/or mass, and considers that no conclusions can be drawn from this study for the scientific substantiation of the claim.
Several studies on the effects of different fats and fatty acids on bone loss, bone mass, BMD and bone turnover in different animal models of post-menopausal osteoporosis (e.g. ovariectomised rats), and a series of in vitro studies which used osteoblast/osteoclast cell lines, were provided. The Panel considers that evidence provided in animal and in vitro studies is not sufficient to predict the occurrence of an effect of the consumption of DHA, EPA and GLA on the maintenance of bone in vivo in humans.
In weighing the evidence, the Panel took into account that two of the human intervention studies from which conclusions could be drawn for the scientific substantiation of the claim did not show an effect of the food constituents on bone mineral density, that in a third study acute changes in markers of bone turnover do not predict the occurrence of an effect on bone mineral density and/or mass, and that evidence provided in animal and in vitro studies is not sufficient to predict the occurrence of an effect of the consumption of DHA, EPA and GLA on the maintenance of bone in vivo in humans.
The Panel concludes that a cause and effect relationship has not been established between the consumption of DHA, EPA and GLA and maintenance of normal bone.