ID 308 -
Cynk
PL: Cynk
EN: Zink
Pdf: zinc
1. Charakterystyka żywności / składnika
The food constituent that is the subject of the claims is zinc, which is a well recognized nutrient and is measurable in foods by established methods. Zinc occurs naturally in foods and is authorised for addition to foods (Annex I of the Regulation (EC) No 1925/20064 and Annex I of Directive 2002/46/EC5). This evaluation applies to zinc naturally present in foods and those forms authorised for addition to foods (Annex II of the Regulation (EC) No 1925/2006 and Annex II of Directive 2002/46/EC).
The Panel considers that the food constituent, zinc, which is the subject of the health claims, is sufficiently characterised.
2.13. Funkcjonowanie tarczycy (ID 308)
The claim effect is “thyroid health”. The Panel assumes that the target population is the general population.
The Panel considers that normal thyroid function is beneficial to human health.
3. Naukowe uzasadnienia wpływu na zdrowie człowieka -
Zinc is present in all tissues. It has essential structural, regulatory or catalytic roles in many enzymes. It maintains the configuration of a number of non-enzymatic proteins such as pre-secretory granules of insulin, some mammalian gene transcription proteins and thymulin. It facilitates hormone and receptor binding at membrane and nuclear levels, and it may maintain integrity of biomembranes. Consequently zinc participates in gene expression and in the mechanisms and control of major metabolic pathways involving proteins, carbohydrates, nucleic acids and lipids (SCF, 1993; DoH, 1991). Human zinc deficiency symptoms include retarded growth, depressed immune function, skin lesions, skeletal abnormalities, impaired reproductive ability and behavioural abnormalities such as changes in mood, loss of affect and emotional lability, anorexia, dysfunction of smell and taste, irritability and depression (SCF, 2003; EVM, 2002, Cousins, 2006).
3.12. Funkcjonowanie tarczycy (ID 308)
The major secretory product of the thyroid gland is thyroxine (T4), which is converted to the active thyroid hormone triiodo-L-thyronine (T3) within cells by deiodinases. T3 actions in its target tissues are initiated by binding of the hormone to specific thyroid hormone receptor proteins within the nucleus. T3 receptors are included among the nuclear zinc-binding proteins. Thus it appears that lack of zinc might impair thyroid hormone signalling by reducing the ability of the thyroid hormone receptor to bind to DNA and thereby influence target gene transcription (Freake, 2006; Freake et al., 2001).
A total of 7 references were cited for the substantiation of the claimed effect, including one opinion of a scientific body, one review paper, one human study and four in vivo studies.
In the review (Christianson, 1991) and the opinion of the scientific body (SCF 2003) the claimed effect was not stated. One in vivo study dealt with the effect of zinc deficiency on metabolic rate (Evans, 2004) which is unrelated to the claimed effect. The Panel notes that these references did not provide any scientific data that could be used to substantiate the claimed effect
In a 75 days metabolic study of low zinc intakes in six men, Wada and King (1986) reported that circulating TSH, total T4 and free T4 tended to decrease during the zinc depletion phase, returning to control concentrations after zinc repletion, but only the decrease in free T4 was considered to be significant. The Panel notes that limited conclusions can be drawn from this small study on the claimed effect.
In zinc deficient rats, reduced plasma T4 and T3 concentrations were observed (Lukaski et al., 1992; Freake et al., 2001). In zinc deficient guinea pigs, thyroid glands were smaller in size and showed histopathological changes of atrophy and degeneration in the follicles. They concluded that thyroid lesions were related to the depletion in serum T3 and T4 which was, in turn, owing to zinc deficiency (Gupta et al., 1997). The Panel considers that the evidence provided in animals does not predict an effect of zinc intake on thyroid function in humans.
The Panel concludes that the evidence provided is insufficient to establish a cause and effect relationship between the dietary intake of zinc and normal thyroid 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 zinc as per Annex to Regulation (EC) No 1924/2006. The target population is the general population. Such amounts can be easily consumed as part of a balanced diet. Tolerable Upper Intake Levels (UL) have been established for zinc as 25 mg/day in adults and to pregnant and lactating woman. For children and adolescents UL was established as 7 mg/day for 1-3 years, 10 mg/day for 4-6 years, 13 mg/day for 7-10 years, 18 mg/day for 11-14 years and 22 mg/day for 15-17 years (SCF 2003).
Warunki i możliwe ograniczenia stosowania oświadczenia
3-6 mg of zinc
Must meet minimum requirements for use of the claim "source of [name of vitamin/s] and/or [name of mineral/s]" as per Annex to Regulation 1924/2006.
Agency guidance for supplements is that products containing >25 mg of Zinc should carry the label advisory statement "Long term intake [of this amount of zinc] may lead to anaemia"
