Parenting, Eating and Activity for Child Health (PEACH) is a multi-component lifestyle intervention for families with overweight and obese children. PEACH was translated from an efficacious randomised-controlled trial (RCT) and delivered at scale as PEACH Queensland (QLD) in Queensland, Australia. The aim of this study is to explore pre–post changes in parenting, and child-level eating, activity and anthropometry, in the PEACH QLD service delivery project. PEACH QLD enrolled 926 overweight/obese children (817 families). Pre-programme evaluation was completed for 752 children and paired pre–post-programme evaluation data were available for 388 children. At baseline, children with pre–post-programme data were (mean) 8·8 years old, and at follow-up were 9·3 years old, with mean time between pre–post-programme measures of 0·46 years. Outcomes reflected each domain of the PEACH programme: parenting, eating behaviour of the child and activity behaviours (means reported). Parents reported improvements in parenting self-efficacy (3·6 to 3·7, P=0·001). Children had improved eating behaviours: eating more daily serves of vegetables (2·0 to 2·6, P=0·001) and fewer non-milk sweetened beverages (0·9 to 0·6, P=0·001) and discretionary foods (2·2 to 1·5, P=0·001). Children spent more time in moderate-to-vigorous physical activity (86 to 105 min/d, P=0·001) and less time in sedentary screen-based behaviours (190 to 148 min/d, P=0·001). Consequently, there were significant improvements in mean BMIz (−0·112; P<0·001) and weight status (healthy weight/overweight/obese/morbidly obese prevalence from 0/22/33/45 % to 2/27/34/37 %, P<0·001). When delivered at scale, PEACH remains an effective family-based, multi-component, lifestyle weight management programme for overweight and obese children whose families engage in the programme.

The role of vitamin D in supporting the growth and maintenance of the skeleton is robust; with recent research also suggesting a beneficial link between vitamin D and other non-skeletal health outcomes, including immune function, cardiovascular health and cancer. Despite this, vitamin D deficiency remains a global public health issue, with a renewed focus in the UK following the publication of Public Health England's new Dietary Vitamin D Requirements. Natural sources of vitamin D (dietary and UVB exposure) are limited, and thus mechanisms are needed to allow individuals to achieve the new dietary recommendations. Mandatory or voluntary vitamin D food fortification may be one of the mechanisms to increase dietary vitamin D intakes and subsequently improve vitamin D status. However, for the food industry and public to make informed decisions, clarity is needed as to whether vitamins D2 and D3 are equally effective at raising total 25-hydroxyvitamin D (25(OH)D) concentrations as the evidence thus far is inconsistent. This review summarises the evidence to date behind the comparative efficacy of vitamins D2 and D3 at raising 25(OH)D concentrations, and the potential role of vitamin D food fortification as a public health policy to support attainment of dietary recommendations in the UK. The comparative efficacy of vitamins D2 and D3 has been investigated in several intervention trials, with most indicating that vitamin D3 is more effective at raising 25(OH)D concentrations. However, flaws in study designs (predominantly under powering) mean there remains a need for a large, robust randomised-controlled trial to provide conclusive evidence, which the future publication of the D2–D3 Study should provide (BBSRC DRINC funded: BB/I006192/1). This review also highlights outstanding questions and gaps in the research that need to be addressed to ensure the most efficacious and safe vitamin D food fortification practices are put in place. This further research, alongside cost, availability and ethical considerations (vitamin D3 is not suitable for vegans), will be instrumental in supporting government, decision-makers, industry and consumers in making informed choices about potential future vitamin D policy and practice.

The effect of Zn, as an adjunct to antibiotics, on the treatment of severe pneumonia in young children is still under debate; therefore, we performed a meta-analysis to evaluate the therapeutic role of Zn for severe pneumonia in children younger than 5 years. PubMed, Cochrane library and Embase databases were systematically searched from inception until October 2015 for randomised-controlled trials (RCT) that assessed the effect of Zn as an adjunct to antibiotics for severe pneumonia. Random-effects model was used for calculating the pooled estimates, and intention-to-treat principle was also applied. Nine RCT involving 2926 children were included. Overall, the pooled results showed that adjunct treatment with Zn failed to reduce the time to recovery from severe pneumonia (hazard ratios (HR)=1·04; 95 % CI 0·90, 1·19; I2=39 %; P=0·58), hospital length of stay (HR=1·04; 95 % CI 0·83, 1·33; I2=57 %; P=0·74), treatment failure (relative risk (RR)=0·95; 95 % CI 0·79, 1·14; I2=20 %; P=0·58) or change of antibiotics (RR=1·07; 95 % CI 0·79, 1·45; I2=44 %; P=0·67). In addition, continuous outcomes were consistent while meta-analysed with standard mean difference, and all outcomes remained stable in intention-to-treat analysis. No significant differences were observed in the two groups between death rate, adverse events or recovery times of severe pneumonia indicators. Our results suggested that adjunct treatment with Zn failed to benefit young children in the treatment of severe pneumonia. Considering the clinical heterogeneity, baseline characteristics of children, definition of severe pneumonia and Zn supplement way should be taken into consideration in future research. This study was registered at PRESPERO as CRD42015019798.

Concern has been expressed recently that Se may increase the risk of type 2 diabetes, but this has not been tested in a randomised-controlled trial (RCT) in pregnant women. We took advantage of having stored plasma samples from the Se in Pregnancy Intervention (SPRINT) RCT of Se supplementation in pregnancy to test the effect of Se supplementation on a marker of insulin resistance in UK pregnant women. Because our blood samples were not fasted, we measured plasma adiponectin concentration, a recognised marker of insulin resistance that gives valid measurements in non-fasted samples, as diurnal variability is minor and there is no noticeable effect of food intake. In SPRINT, 230 primiparous UK women were randomised to treatment with Se (60 μg/d) or placebo from 12 weeks of gestation until delivery. We hypothesised that supplementation with Se at a nutritional level would not exacerbate the fall in adiponectin concentration that occurs in normal pregnancy, indicating the lack of an adverse effect on insulin resistance. Indeed, there was no significant difference between the two groups in the change in adiponectin from 12 to 35 weeks (P=0·938), nor when the analysis was restricted to the bottom or top quartiles of baseline whole-blood Se (P=0·515 and 0·858, respectively). Cross-sectionally, adiponectin concentration was not associated with any parameter of Se status, either at 12 or 35 weeks. It is reassuring that a nutritional dose of Se had no adverse effect on the concentration of adiponectin, a biomarker of insulin resistance, in pregnant women of modest Se status.