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Lewis J.L.,Food Standards Australia New Zealand
British Journal of Nutrition

Food regulation aims to protect public health through a safe and nutritious food supply produced by a compliant food industry. Food standards of developed countries generally do not regulate protein content or protein quality because the risk of dietary protein inadequacy in their national populations is very low. Protein is nevertheless regulated for reasons of product quality or protein labelling or to minimise assessed health risks associated with consumption of certain animal- and vegetable-protein foods; analogue products that extend or simulate commonly available animal-protein foods; and special purpose foods such as infant formula and foods, supplementary and medical foods, and foods for weight loss. The extent and approach to protein regulation varies greatly among jurisdictions but where it occurs, it is applied through minimum and sometimes maximum limits on protein content or quality measures or both using an inter-related approach. Protein quality measures range from amino acid profiles and digestibility corrected scores to protein rating, a rat bioassay and reference proteins not further described. Regulatory methods for protein quality determination are referenced to the published scientific literature or developed nationally. Internationally, the Codex Alimentarius regulates the protein content and quality of some foods. The Codex approach varies according to the food but is similar to the approaches used in national and regional food regulation. This paper provides a comparison of the regulation of protein in foods using examples from the food regulations of Australia New Zealand, Canada, the European Union, the United States of America and the Codex Alimentarius. © 2012 The Author. Source

Charlton K.E.,University of Wollongong | Batterham M.J.,University of Wollongong | Buchanan L.M.,University of Wollongong | Mackerras D.,Food Standards Australia New Zealand | Mackerras D.,Charles Darwin University
BMJ Open

Objectives: To determine the effect of adjustment for intraindividual variation on estimations of urinary iodine concentrations (UIC), prevalence of iodine deficiency and population distribution of iodine status. Setting: Community-dwelling older adults from New South Wales, Australia. Participants: 84 healthy men and women aged 60. 95 years were recruited prior to introduction of the mandatory iodine fortification programme. Primary and secondary outcome measures: UIC data were collected from three spot urine samples, each 1 week apart. Repeated measures analysis of variance were determined between-person (sb) and total (sobs) SDs. Adjusted UIC values were calculated as ((person's UIC.group mean)×(sb/s obs))+group mean, and a corrected UIC distribution was calculated. Results: The sb/sobs for using three samples and two samples were 0.83 and 0.79, respectively. Following adjustment for intraindividual variation, the proportion with UIC <50 μg/L reduced from 33% to 19%, while the proportion with UIC ≥100 μg/L changed from 21% to 17%. The 95th centile for UIC decreased from 176 to 136 μg/L. Adjustment by taking averages yielded a lesser degree of contraction in the distribution than the analysis of variance method. Conclusions: The addition of information about intraindividual variability has potential for increasing the interpretability of UIC data collected to monitor the iodine status of a population. Source

Mackerras D.E.M.,Food Standards Australia New Zealand | Mackerras D.E.M.,Charles Darwin University | Singh G.R.,Charles Darwin University | Eastman C.J.,University of Sydney
Medical Journal of Australia

Objective: To determine the iodine status of participants in the Aboriginal Birth Cohort Study who resided in the Darwin Health Region (DHR) in the "Top End" of the Northern Territory prior to the introduction of mandatory iodine fortification of bread. Design, setting and participants: Participants in our study had been recruited at birth and were followed up at a mean age of 17.8 years. Spot urine samples were collected and assessed for iodine concentration at a reference laboratory. The median urinary iodine concentration (MUIC) of residents of the DHR was calculated and compared with international criteria for iodine status. Analyses were conducted for subgroups living in urban areas (Darwin-Palmerston) and remote communities (rural with an Aboriginal council). We collected a repeat sample in a subset of participants to explore the impact of within-person variation on the results. Main outcome measure: MUIC for residents of the DHR. Results: Urine specimens were provided by 376 participants in the DHR. Overall MUIC was 58 μg/L when weighted to the 2006 Census population. Urban boys had higher values (MUIC = 77 μg/L) than urban and remote-dwelling non-pregnant girls (MUIC= 55 μg/L), but all these groups were classified as mildly iodine deficient. Remotedwelling boys had the lowest MUIC (47 μg/L, moderate deficiency). Pregnant girls and those with infants aged less than 6 months also had insufficient iodine status. Correction for within-person variation reduced the spread of the population distribution. Conclusions: Previously, iodine deficiency was thought to occur only in the southeastern states of Australia. This is the first report of iodine deficiency occurring in residents of the NT. It is also the first study of iodine status in a defined Indigenous population. Future follow-up will reassess iodine status in this group after the introduction of iodine fortification of bread. Source

Mulvenna V.,Khan Research Laboratories | Dale K.,Monash University | Priestly B.,Monash University | Mueller U.,Food Standards Australia New Zealand | And 4 more authors.
International Journal of Environmental Research and Public Health

Cyanobacteria (blue-green algae) are abundant in fresh, brackish and marine waters worldwide. When toxins produced by cyanobacteria are present in the aquatic environment, seafood harvested from these waters may present a health hazard to consumers. Toxicity hazards from seafood have been internationally recognised when the source is from marine algae (dinoflagellates and diatoms), but to date few risk assessments for cyanobacterial toxins in seafood have been presented. This paper estimates risk from seafood contaminated by cyanobacterial toxins, and provides guidelines for safe human consumption. © 2012 by the authors; licensee MDPI, Basel, Switzerland. Source

Schulze A.,University of Heidelberg | Mills K.,Food Standards Australia New Zealand | Weiss T.S.,University of Regensburg | Urban S.,University of Heidelberg

Human hepatitis B virus (HBV) is characterized by a high species specificity and a distinct liver tropism. Within the liver, HBV replication occurs in differentiated and polarized hepatocytes. Accordingly, the in vitro HBV infection of primary human hepatocytes (PHHs) and the human hepatoma cell line, HepaRG, is restricted to differentiated, hepatocyte-like cells. Though preparations of PHH contain up to 100% hepatic cells, cultures of differentiated HepaRG cells are a mixture of hepatocyte-like and biliary-like epithelial cells. We used PHH and HepaRG cells and compared the influence of virus inoculation dose, cell differentiation, and polarization on productive HBV infection. At multiplicities of genome equivalents (mge) >8,000, almost 100% of PHHs could be infected. In contrast, only a subset of HepaRG cells stained positive for HBcAg at comparable or even higher mge. Infection predominantly occurred at the edges of islands of hepatocyte-like HepaRG cells. This indicates a limited accessibility of the HBV receptor, possibly as a result of its polar sorting. Multidrug resistance protein 2 (MRP2), a marker selectively transported to the apical (i.e., canalicular) cell membrane, revealed two polarization phenotypes of HepaRG cells. HBV infection within the islands of hepatocyte-like HepaRG cells preferentially occurred in cells that resemble PHH, exhibiting canalicular structures. However, disruption of cell-cell junctions allowed the additional infection of cells that do not display a PHH-like polarization. Conclusion: HBV enters hepatocytes via the basolateral membrane. This model, at least partially, explains the difference of PHH and HepaRG cells in infection efficacy, provides insights into natural HBV infection, and establishes a basis for optimization of the HepaRG infection system. © 2011 American Association for the Study of Liver Diseases. Source

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