ID 182 - Witamina E

PL: Witamina E
EN: Vitamin E
Pdf:

Oświadczenie (2)

1. Charakterystyka żywności / składnika

The food constituent that is the subject of the health claims is vitamin E, which is a well recognised nutrient and is measurable in foods by established methods.
Vitamin E is authorised for addition to foods (Annex I of the Regulation (EC) No 1925/20066 and Annex I of Directive 2002/46/EC7). This evaluation applies to vitamin E naturally present in foods and those forms authorised for addition to foods (Annex II of Regulation (EC) No 1925/2006 and Annex II of Directive 2002/46/EC).
The Panel considers that the food constituent, vitamin E, which is the subject of the health claims, is sufficiently characterised.

2.10. Udział w prawidłowym przebiegu procesów poznawczych (ID 182, 183)

The claimed effects are “antioxidant activity and cognitive function”, and “mental state and performance”. The Panel assumes that the target population is the general population.
Cognitive function includes memory, attention (concentration), learning, intelligence and problem solving. These are well defined constructs and can be measured by validated psychometric cognitive tests.
The Panel considers that contribution to normal cognitive function is a beneficial physiological effect.

3. Naukowe uzasadnienia wpływu na zdrowie człowieka

The evidence provided by opinions/reports from authoritative bodies and reviews shows that there is good consensus on the role of vitamin E in the body (Berdanier et al., 2002; EVM, 2002; Gibney et al., 2002; IoM, 2000; NNR, 2004; Sadler et al., 1999; SCF, 2003; Shils et al., 2006). Vitamin E is fat-soluble and is transported in plasma lipoproteins and partitions into membranes and fat-storage sites where it has the unique role of protecting polyunsaturated fatty acids from peroxidation. Plasma
-tocopherol is regulated by the liver -tocopherol transfer protein ( -TTP). In humans, a genetic
defect in -TTP results in severe vitamin E deficiency (Shils et al., 2006).
A major vitamin E deficiency symptom in humans is peripheral neuropathy characterised by the degeneration of the large calibre axons in the sensory neurons (IoM, 2000). Vitamin E deficiency as a result of inadequate intake of vitamin E is uncommon. Vitamin E deficiency can occur as a result of
genetic abnormalities in -TTP and as a result of various fat malabsorption syndromes. Vitamin E supplementation halts the progression of the neurological abnormalities caused by inadequate nerve
tissue -tocopherol and, in some cases, has reversed these abnormalities. Other vitamin E deficiency symptoms observed in humans include spinocerebellar ataxia, skeleton myopathy, pigmented retinopathy (IoM, 2000), loss of deep tendon reflexes, unsteady gait, restriction of upward gaze and visual field loss (Sadler et al., 1999).

3.10. Udział w prawidłowym przebiegu procesów poznawczych (ID 182, 183)

A total of seven references were provided to substantiate the claimed effect. Three references did not address relevant endpoints (cardiovascular efficacy, safety of high vitamin E intake). The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claimed effect. The narrative review provided discussed the use of antioxidants, including vitamin E, in prevention and treatment of Alzheimer disease. This reference did not contain any primary data that could be used to substantiate the claimed effect.
Three articles reported on observational human studies.
One of these, a large (n=3,385) longitudinal cohort study of healthy men aged 71-90 years, investigated associations between the use of both vitamin E and vitamin C supplements and cognitive performance assessed two years later using the Cognitive Abilities Screening Instrument (Masaki et al., 2000). The Panel notes that findings from this study cannot be used for the scientific substantiation of the claimed effect as the study investigated the association of two vitamins rather than vitamin E alone.
The two other studies were a prospective cohort study, which evaluated the association between dietary intake of antioxidants (including vitamin E) and risk of Alzheimer disease (Engelhart et al., 2002) and a cross-sectional study, which examined associations between dietary intake of nutrients (including vitamin E) and cognitive performance in 260 elderly people, aged 65-90 years, who were free of significant cognitive impairment (Ortega et al., 1997). The Panel notes that no conclusions on a causal relationship between the dietary intake of vitamin E and cognitive function can be drawn from these studies because confounding by other dietary and lifestyle factors inherent to the observational study design cannot be excluded.
The Panel concludes that a cause and effect relationship has not been established between the dietary intake of vitamin E and contribution to normal cognitive function.

5. Warunki i możliwe ograniczenia stosowania oświadczenia

The Panel considers that in order to bear the claim a food should be at least a source of Vitamin E as per Annex to Regulation (EC) No 1924/2006. Such amounts can be easily consumed as part of a balanced diet. The target population is the general population. Tolerable Upper Intake Levels (UL) have been established for vitamin E in children, adolescents and adults (SCF, 2003).

Warunki i możliwe ograniczenia stosowania oświadczenia

See above;