A Review of Dietary Zinc Recommendations

Background. Large discrepancies exist among the dietary zinc recommendations set by expert groups. Objective. To understand the basis for the differences in the dietary zinc recommendations set by the World Health Organization, the U.S. Institute of Medicine, the International Zinc Nutrition Consultative Group, and the European Food Safety Agency. Methods. We compared the sources of the data, the concepts, and methods used by the four expert groups to set the physiological requirements for absorbed zinc, the dietary zinc requirements (termed estimated and/or average requirements), recommended dietary allowances (or recommended nutrient intakes or population reference intakes), and tolerable upper intake levels for selected age, sex, and life-stage groups. Results. All four expert groups used the factorial approach to estimate the physiological requirements for zinc. These are based on the estimates of absorbed zinc required to offset all obligatory zinc losses plus any additional requirements for absorbed zinc for growth, pregnancy, or lactation. However, discrepancies exist in the reference body weights used, studies selected, approaches to estimate endogenous zinc losses, the adjustments applied to derive dietary zinc requirements that take into account zinc bioavailability in the habitual diets, number of dietary zinc recommendations set, and the nomenclature used to describe them. Conclusions. Estimates for the physiological and dietary requirements varied across the four expert groups. The European Food Safety Agency was the only expert group that set dietary zinc recommendations at four different levels of dietary phytate for adults (but not for children) and as yet no tolerable upper intake level for any life-stage group

Molecular and phenotypical investigation of ciprofloxacin resistance among Campylobacter jejuni strains of human origin: high prevalence of resistance in Turkey

Campylobacteriosis is one of the most frequently reported zoonoses worldwide. The well-documented increase in the ciprofloxacin resistance has increased the importance of rapid detection of the resistance. The incidence of ciprofloxacin resistance was investigated using real-time PCR. Identification of one hundred and fifty-eight strains was performed by PCR. Minimum inhibitory concentration (MIC) of ciprofloxacin was determined by Epsilometer test. Following the confirmation of the efficiencies of singleplex real-time PCR methods using two different probes, a cytosine to thymine point mutation at codon 86 was detected by allelic discrimination. Of the 158 strains, 114 (72.2%) were determined to be resistant to ciprofloxacin. The MIC50 and the MIC90 of ciprofloxacin were found to be 8 and >= 32 mg/L, respectively. By real-time PCR, the presence of the mutation was confirmed in all, but one, resistant strains and the absence of the mutation was demonstrated in all, but one, susceptible strains. The rate of resistance is high among C. jejuni strains and ciprofloxacin should not be used in the treatment of such infections in Turkey. A cytosine to thymine mutation is the most frequently detected mechanism for the resistance. Real-time PCR can be used for the quick screening of the resistance

Scientific Opinion on the re-evaluation of Quinoline Yellow (E 104) as a food additive:Question No EFSA-Q-2008-223

The Panel on Food Additives and Nutrient Sources added to Food provides a scientific opinion re-evaluating the safety of Quinoline Yellow (E 104). Quinoline Yellow has been previously evaluated by the Joint FAO/WHO Expert Committee on Food Additives (JECFA) in 1975, 1978 and 1984, and the EU Scientific Committee for Food (SCF) in 1984. Both committees established an Acceptable Daily Intake (ADI) of 0-10 mg/kg body weight (bw). Studies not evaluated by JECFA and the SCF included a chronic toxicity and carcinogenicity study with a reproductive toxicity phase in rats and a study on behaviour in children by McCann et al. from 2007. The latter study concluded that exposure to a mixture of colours including Quinoline Yellow resulted in increased hyperactivity in 8- to 9-years old children. The Panel concurs with the conclusion from a previous EFSA opinion on the McCann et al. study that the findings of the study cannot be used as a basis for altering the ADI. The Panel notes that Quinoline Yellow was negative in in vitro genotoxicity as well as in long term carcinogenicity studies. The Panel concludes that the currently available database on semi-chronic, reproductive, developmental and long-term toxicity of Quinoline Yellow, including a study in rats not apparently taken into consideration by JECFA or the SCF, provides a rationale for re-definition of the ADI. Using the NOAEL of 50 mg/kg bw/day provided by the chronic toxicity and carcinogenicity study with a reproductive toxicity phase carried out in rats and applying an uncertainty factor of 100 to this NOAEL, the Panel establishes an ADI of 0.5 mg/kg bw/day. The Panel notes that at the maximum levels of use of Quinoline Yellow, refined intake estimates are generally well over the ADI of 0.5 mg/kg bw/day

EFSA CEF Penal (EFSA Panel on Food Contact Materials, Enzymes, Flavourings and Processing Aids), 2014. Scientific Opinion on Flavouring Group Evaluation 212, Revision 2 (FGE.212Rev2): α,β-Unsaturated alicyclic ketones and precursors from chemical subgroup 2.6 of FGE.19

International audienc

EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA); Scientific Opinion on Dietary Reference Values for protein

This opinion of the EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA) deals with the setting of Dietary Reference Values (DRVs) for protein. The Panel concludes that a Population Reference Intake (PRI) can be derived from nitrogen balance studies. Several health outcomes possibly associated with protein intake were also considered but data were found to be insufficient to establish DRVs. For healthy adults of both sexes, the average requirement (AR) is 0.66 g protein/kg body weight per day based on nitrogen balance data. Considering the 97.5th percentile of the distribution of the requirement and assuming an efficiency of utilisation of dietary protein for maintenance of 47 %, the PRI for adults of all ages was estimated to be 0.83 g protein/kg body weight per day and is applicable both to high quality protein and to protein in mixed diets. For children from six months onwards, age-dependent requirements for growth estimated from average daily rates of protein deposition and adjusted by a protein efficiency for growth of 58 % were added to the requirement for maintenance of 0.66 g/kg body weight per day. The PRI was estimated based on the average requirement plus 1.96 SD using a combined SD for growth and maintenance.For pregnancy, an intake of 1, 9 and 28 g/d in the first, second and third trimesters, respectively, is proposed in addition to the PRI for non-pregnant women. For lactation, a protein intake of 19 g/d during the first six months, and of 13 g/d after six months, is proposed in addition to the PRI for non-lactating women. Data are insufficient to establish a Tolerable Upper Intake Level (UL) for protein. Intakes up to twice the PRI are regularly consumed from mixed diets by some physically active and healthy adults in Europe and are considered safe

Causes of genome instability: the effect of low dose chemical exposures in modern society.

Genome instability is a prerequisite for the development of cancer. It occurs when genome maintenance systems fail to safeguard the genome's integrity, whether as a consequence of inherited defects or induced via exposure to environmental agents (chemicals, biological agents and radiation). Thus, genome instability can be defined as an enhanced tendency for the genome to acquire mutations; ranging from changes to the nucleotide sequence to chromosomal gain, rearrangements or loss. This review raises the hypothesis that in addition to known human carcinogens, exposure to low dose of other chemicals present in our modern society could contribute to carcinogenesis by indirectly affecting genome stability. The selected chemicals with their mechanisms of action proposed to indirectly contribute to genome instability are: heavy metals (DNA repair, epigenetic modification, DNA damage signaling, telomere length), acrylamide (DNA repair, chromosome segregation), bisphenol A (epigenetic modification, DNA damage signaling, mitochondrial function, chromosome segregation), benomyl (chromosome segregation), quinones (epigenetic modification) and nano-sized particles (epigenetic pathways, mitochondrial function, chromosome segregation, telomere length). The purpose of this review is to describe the crucial aspects of genome instability, to outline the ways in which environmental chemicals can affect this cancer hallmark and to identify candidate chemicals for further study. The overall aim is to make scientists aware of the increasing need to unravel the underlying mechanisms via which chemicals at low doses can induce genome instability and thus promote carcinogenesis