Until quite recently, there has been a widespread belief in the popular media and scientific literature that the prevalence of childhood obesity is rapidly increasing. However, high quality evidence has emerged from several countries suggesting that the rise in the prevalence has slowed appreciably, or even plateaued. This review brings together such data from nine countries (Australia, China, England, France, Netherlands, New Zealand, Sweden, Switzerland and USA), with data from 467,294 children aged 2-19 years. The mean unweighted rate of change in prevalence of overweight and obesity was +0.00 (0.49)% per year across all age ×sex groups and all countries between 1995 and 2008. For overweight alone, the figure was +0.01 (0.56)%, and for obesity alone -0.01 (0.24)%. Rates of change differed by sex, age, socioeconomic status and ethnicity. While the prevalence of overweight and obesity appears to be stabilizing at different levels in different countries, it remains high, and a significant public health issue. Possible reasons for the apparent flattening are hypothesised.

Although the median urinary iodine concentration (UIC) is a good indicator of iodine status in populations, there is no established biomarker for individual iodine status. If the UIC were to be used to assess individuals, it is unclear how many repeat urine collections would be needed and if the collections should be spot samples or 24-h samples. In a prospective, longitudinal, 15-mo study, healthy Swiss women (n = 22) aged 52-77 y collected repeated 24-h urine samples (total n = 341) and corresponding fasting, second-void, morning spot urine samples (n = 177). From the UIC in spot samples, 24-h urinary iodine excretion (UIE) was extrapolated based on the age- and sex-adjusted iodine:creatinine ratio. Measured UIE in 24-h samples, estimated 24-h UIE, and UIC in spot samples were (geometric mean ± SD) 103 ± 28 μg/24 h, 86 ± 33 μg/24 h, and 68 ± 28 μg/L, respectively, with no seasonal differences. Intra-individual variation (mean CV) was comparable for measured UIE (32%) and estimated UIE (33%). The CV tended to be higher for the spot UIC (38%) than for the estimated 24-h UIE (33%) (P = 0.12). In this population, 10 spot urine samples or 24-h urine samples were needed to assess individual iodine status with 20% precision. Spot samples would likely be preferable because of their ease of collection. However, the large number of repeated urine samples needed to estimate individual iodine status is a major limitation and emphasizes the need for further investigation of more practical biomarkers of individual iodine status.

The present data show potentially harmful effects of low to moderate consumption of SSBs on markers of cardiovascular risk such as LDL particles, fasting glucose, and hs-CRP within just 3 wk in healthy young men, which is of particular significance for young consumers. This trial was registered at clinicaltrials.gov as NCT01021969.

Background: Obesity increases the risk for iron deficiency, but the underlying mechanism is unclear. It is possible that overweight individuals may have lower dietary iron intake and/or bioavailability. Alternatively, obesity-related inflammation may increase hepcidin concentrations and reduce iron availability. Circulating hepcidin levels have not been compared in normal weight vs overweight individuals. Objective: The objective of this study was to compare iron status, dietary iron intake and bioavailability, as well as circulating levels of hepcidin, leptin and interleukin-6 (IL-6), in overweight vs normal weight children. Design: In 6-14-year-old normal and overweight children (n ¼ 121), we measured dietary iron intake, estimated iron bioavailability and determined body mass index s.d. scores (BMI-SDS). In all children (n ¼ 121), we measured fasting serum ferritin, soluble transferrin receptor (sTfR), C-reactive protein (CRP) and leptin; in a subsample, we measured IL-6 (n ¼ 68) and serum hepcidin (n ¼ 30). Results: There were no significant differences in dietary iron intake or bioavailability comparing normal and overweight children. The prevalence of iron-deficient erythropoiesis (an increased sTfR concentration) was significantly higher in the overweight than in the normal weight children (20 vs 6%, P ¼ 0.022, with sTfR concentrations of 4.40 ± 0.77 and 3.94 ± 0.88 mg l À1 , respectively, P ¼ 0.010). Serum hepcidin levels were significantly higher in the overweight children (P ¼ 0.001). BMI-SDS significantly correlated with sTfR (P ¼ 0.009), serum hepcidin (P ¼ 0.005) and the three measures of subclinical inflammation, namely CRP (Po0.001), IL-6 (Po0.001) and leptin (Po0.001). In a multiple regression model, serum hepcidin was correlated with BMI-SDS (P ¼ 0.020) and body iron (P ¼ 0.029), but not with the inflammatory markers. Conclusion: Our findings indicate that there is reduced iron availability for erythropoiesis in overweight children and that this is unlikely due to low dietary iron supply but rather due to hepcidin-mediated reduced iron absorption and/or increased iron sequestration.