Suchergebnisse

Objectives: To assess the extent to which participation in organised physical activity in the school or community outside school hours and neighbourhood play was associated with children's physical activity and sedentary time. Design: Cross-sectional study. Setting: Children were recruited from 47 state-funded primary schools in South West England. Participants: 1223 children aged 8–9 years old. Outcome measures: Accelerometer-assessed moderate-to-vigorous-intensity physical activity (MVPA) and sedentary time. Methods: Children wore an accelerometer, and the mean minutes of MVPA and sedentary time per day were derived. Children reported their attendance at organised physical activity in the school or community outside school hours and neighbourhood play using a piloted questionnaire. Cross-sectional linear and logistic regression were used to examine if attendance frequency at each setting (and all settings combined) was associated with MVPA and sedentary time. Multiple imputation methods were used to account for missing data and increase sample size. Results: Children who attended clubs at school 3–4 days per week obtained an average of 7.58 (95% CI 2.7 to 12.4) more minutes of MVPA per day than children who never attended. Participation in the three other non-school-based activities was similarly associated with MVPA. Evidence for associations with sedentary time was generally weaker. Associations were similar in girls and boys. When the four different contexts were combined, each additional one to two activities participated in per week increased participants' odds (OR: 1.18, 95% CI 1.12 to 1.25) of meeting the government recommendations for 60 min of MVPA per day. Conclusion: Participating in organised physical activity at school and in the community is associated with greater physical activity and reduced sedentary time among both boys and girls. All four types of activity contribute to overall physical activity, which provides parents with a range of settings in which to help their child be active.

Background: Clinical recommendations to limit gestational weight gain (GWG) imply high GWG is causally related to adverse outcomes in mother or offspring, but GWG is the sum of several inter-related complex phenotypes (maternal fat deposition and vascular expansion, placenta, amniotic fluid and fetal growth). Understanding the genetic contribution to GWG could help clarify the potential effect of its different components on maternal and offspring health. Here we explore the genetic contribution to total, early and late GWG. Participants and methods: A genome-wide association study was used to identify maternal and fetal variants contributing to GWG in up to 10 543 mothers and 16 317 offspring of European origin, with replication in 10 660 mothers and 7561 offspring. Additional analyses determined the proportion of variability in GWG from maternal and fetal common genetic variants and the overlap of established genome-wide significant variants for phenotypes relevant to GWG (for example, maternal body mass index (BMI) and glucose, birth weight). Results: Approximately 20% of the variability in GWG was tagged by common maternal genetic variants, and the fetal genome made a surprisingly minor contribution to explain variation in GWG. Variants near the pregnancy-specific beta-1 glycoprotein 5 (PSG5) gene reached genome-wide significance (P=1.71 × 10-8) for total GWG in the offspring genome, but did not replicate. Some established variants associated with increased BMI, fasting glucose and type 2 diabetes were associated with lower early, and higher later GWG. Maternal variants related to higher systolic blood pressure were related to lower late GWG. Established maternal and fetal birth weight variants were largely unrelated to GWG. Conclusions: We found a modest contribution of maternal common variants to GWG and some overlap of maternal BMI, glucose and type 2 diabetes variants with GWG. These findings suggest that associations between GWG and later offspring/maternal outcomes may be due to the relationship of maternal BMI and diabetes with GWG. ; The research leading to these results has received funding from the European Research Council under the European Union's Seventh Framework Programme (FP7/2007-2013)/ERC grant agreement (grant number 669545; DevelopObese), the US National Institute of Health (R01 DK10324), Wellcome Trust (WT088806) and UK Medical Research Council (MC_UU_12013/4 and MC_UU_12013/5).

Background Systematic reviews have highlighted that school-based diet and physical activity (PA) interventions have had limited effects. This study used qualitative methods to examine how the effectiveness of future primary (elementary) school diet and PA interventions could be improved. Methods Data are from the Active For Life Year 5 (AFLY5) study, which was a cluster randomised trial conducted in 60 UK primary schools. Year 5 (8–9 years of age) pupils in the 30 intervention schools received a 12-month intervention. At the end of the intervention period, interviews were conducted with: 28 Year 5 teachers (including 8 teachers from control schools); 10 Headteachers (6 control); 31 parents (15 control). Focus groups were conducted with 70 year 5 pupils (34 control). Topics included how the AFLY5 intervention could have been improved and how school-based diet and PA interventions should optimally be delivered. All interviews and focus groups were transcribed and thematically analysed across participant groups. Results Analysis yielded four themes. Child engagement: Data suggested that programme success is likely to be enhanced if children feel that they have a sense of autonomy over their own behaviour and if the activities are practical. School: Finding a project champion within the school would enhance intervention effectiveness. Embedding diet and physical activity content across the curriculum and encouraging teachers to role model good diet and physical activity behaviours were seen as important. Parents and community: Encouraging parents and community members into the school was deemed likely to enhance the connection between schools, families and communities, and "create a buzz" that was likely to enhance behaviour change. Government/Policy: Data suggested that there was a need to adequately resource health promotion activity in schools and to increase the infrastructure to facilitate diet and physical activity knowledge and practice. Discussion and Conclusions Future primary school diet and PA programmes should find ways to increase child engagement in the programme content, identify programme champions, encourage teachers to work as role models, engage parents and embed diet and PA behaviour change across the curriculum. However, this will require adequate funding and cost-effectiveness will need to be established.

Background: Gestational diabetes and gestational hypertensive disorders are associated with offspring obesity, but the role of maternal adiposity in these associations remains unclear. We aimed to investigate whether these pregnancy complications affect the odds of offspring obesity independently of maternal obesity. Methods: We did an individual participant data (IPD) meta-analysis of mother–offspring pairs from prospective birth cohort studies that had IPD on mothers with singleton liveborn children born from 1989 onwards and had information available about maternal gestational diabetes, gestational hypertension or pre-eclampsia, and childhood body-mass index (BMI). We applied multilevel mixed-effects models to assess associations of gestational diabetes, gestational hypertension, and pre-eclampsia with BMI SD scores and the odds of overweight and obesity throughout childhood, adjusting for lifestyle characteristics (offspring's sex, maternal age, educational level, ethnicity, parity, and smoking during pregnancy). We then explored the extent to which any association was explained by maternal pre-pregnancy or early-pregnancy BMI. Findings: 160 757 mother–offspring pairs from 34 European or North American cohorts were analysed. Compared with uncomplicated pregnancies, gestational diabetes was associated with increased odds of overweight or obesity throughout childhood (odds ratio [OR] 1·59 [95% CI 1·36 to 1·86] for early childhood [age 2·0–4·9 years], 1·41 [1·26 to 1·57] for mid childhood [5·0–9·9 years], and 1·32 [0·97 to 1·78] for late childhood [10·0–17·9 years]); however, these associations attenuated towards the null following adjustment for maternal BMI (OR 1·35 [95% CI 1·15 to 1·58] for early childhood, 1·12 [1·00 to 1·25] for mid childhood, and 0·96 [0·71 to 1·31] for late childhood). Likewise, gestational hypertension was associated with increased odds of overweight throughout childhood (OR 1·19 [95% CI 1·01 to 1·39] for early childhood, 1·23 [1·15 to 1·32] for mid childhood, and 1·49 [1·30 to 1·70] for late childhood), but additional adjustment for maternal BMI largely explained these associations (1·01 [95% CI 0·86 to 1·19] for early childhood, 1·02 [0·95 to 1·10] for mid childhood, and 1·18 [1·03 to 1·36] for late childhood). Pre-eclampsia was associated with decreased BMI in early childhood only (difference in BMI SD score −0·05 SD score [95% CI −0·09 to −0·01]), and this association strengthened following additional adjustment for maternal BMI. Interpretation: Although lowering maternal risk of gestational diabetes, gestational hypertension, and pre-eclampsia is important in relation to maternal and fetal pregnancy outcomes, such interventions are unlikely to have a direct impact on childhood obesity. Preventive strategies for reducing childhood obesity should focus on maternal BMI rather than on pregnancy complications. Funding: EU's Horizon 2020 research and innovation programme (LifeCycle Project). ; This study has received support from the US National Institute of Health (R01 DK10324) and European Research Council under the European Union's Seventh 22 Framework Programme (FP7/2007-2013) / ERC grant agreement no 669545. The Swedish Research Council, The Swedish Heart and Lung Foundation, The Swedish Research Council for Working Life and Social Welfare, the Swedish Asthma and Allergy Association Research Foundation, The Swedish Research Council Formas, Stockholm County Council, and the European Commission's Seventh Framework 29 Program MeDALL under grant agreement No. 261357. This study has received support from the British Heart Foundation (CS/16/4/32482), US National Institute of Health (R01 DK10324) and European Research Council under the European Union's Seventh Framework Programme (FP7/2007-2013) / ERC grant agreement no 669545. The general design of the Generation R Study is made possible by financial support from the Erasmus MC, University Medical Center, Rotterdam, Erasmus University Rotterdam, Netherlands Organization for Health Research and Development (ZonMw), Netherlands Organisation for Scientific Research (NWO), Ministry of Health, Welfare and Sport and Ministry of Youth and Families. Research leading to these results has received funding from the European Union's Seventh Framework Programme (FP7/2007- 2013), project EarlyNutrition under grant agreement n°289346, the European Union's Horizon 2020 research and innovation programme under grant agreement No 633595 (DynaHEALTH) and the European Union's Horizon 2020 research and innovation programme under grant agreement 733206 (LifeCycle Project). European Community's Seventh Framework Programme (FP7/2007-2013) under grant agreements Early Nutrition n° 289346 and by funds from the Norwegian Research Council's MILPAAHEL programme, project No.213148. This study was funded by Grants from UE (FP7-ENV-2011 cod 282957 and HEALTH.2010.2.4.5-1), Spain: ISCIII (G03/176; FIS-FEDER: PI09/02647, PI11/01007, PI11/02591, PI11/02038, PI13/1944, PI13/2032, PI14/00891, PI14/01687, and PI16/1288; Miguel Servet-FEDER CP11/00178, CP15/00025, and CPII16/00051), and Generalitat Valenciana: FISABIO (UGP 15-230, UGP-15-244, and UGP-15-249). The "Rhea" project was financially supported by European projects (EU FP6-2003-Food-3-NewGeneris, EU FP6. STREP Hiwate, EU FP7 ENV.2007.1.2.2.2. Project No 211250 Escape, EU FP7-2008-ENV-28.1.2.1.4 envirogenomarkers, EU FP7-HEALTH-2009- single stage CHICOS, EU FP7 ENV.2008.1.2.1.6. Proposal No 226285 ENRIECO, EU- FP7- HEALTH-2012 Proposal No 308333 HELIX) and the Greek Ministry of Health (Program of Prevention of obesity and neurodevelopmental disorders in preschool children, in Heraklion district, Crete, Greece: 2011-2014; "Rhea Plus": Primary Prevention Program of Environmental Risk Factors for Reproductive Health, and Child Health: 2012-15). ROLO is supported by the Health Research Board Ireland, the Health Research Centre for Health and Diet Research, and the European Union's Seventh Framework Programme (FP7/2007-2013), project EarlyNutrition under grant agreement no. 289346. The SWS is supported by grants from the Medical Research Council, National Institute for Health Research Southampton Biomedical Research Centre, University of Southampton and University Hospital Southampton National Health Service Foundation Trust, and the European Union's Seventh Framework Programme (FP7/2007-2013), project EarlyNutrition (grant 289346). Study participants were drawn from a cohort study funded by the Medical Research Council and the Dunhill Medical Trust.

BACKGROUND: A high circulating concentration of interleukin 6 is associated with increased risk of coronary heart disease. Blockade of the interleukin-6 receptor (IL6R) with a monoclonal antibody (tocilizumab) licensed for treatment of rheumatoid arthritis reduces systemic and articular inflammation. However, whether IL6R blockade also reduces risk of coronary heart disease is unknown. METHODS: Applying the mendelian randomisation principle, we used single nucleotide polymorphisms (SNPs) in the gene IL6R to evaluate the likely efficacy and safety of IL6R inhibition for primary prevention of coronary heart disease. We compared genetic findings with the effects of tocilizumab reported in randomised trials in patients with rheumatoid arthritis. FINDINGS: In 40 studies including up to 133,449 individuals, an IL6R SNP (rs7529229) marking a non-synonymous IL6R variant (rs8192284; p.Asp358Ala) was associated with increased circulating log interleukin-6 concentration (increase per allele 9·45%, 95% CI 8·34-10·57) as well as reduced C-reactive protein (decrease per allele 8·35%, 95% CI 7·31-9·38) and fibrinogen concentrations (decrease per allele 0·85%, 95% CI 0·60-1·10). This pattern of effects was consistent with IL6R blockade from infusions of tocilizumab (4-8 mg/kg every 4 weeks) in patients with rheumatoid arthritis studied in randomised trials. In 25,458 coronary heart disease cases and 100,740 controls, the IL6R rs7529229 SNP was associated with a decreased odds of coronary heart disease events (per allele odds ratio 0·95, 95% CI 0·93-0·97, p=1·53×10(-5)). INTERPRETATION: On the basis of genetic evidence in human beings, IL6R signalling seems to have a causal role in development of coronary heart disease. IL6R blockade could provide a novel therapeutic approach to prevention of coronary heart disease that warrants testing in suitably powered randomised trials. Genetic studies in populations could be used more widely to help to validate and prioritise novel drug targets or to repurpose existing agents and targets for new therapeutic uses. FUNDING: UK Medical Research Council; British Heart Foundation; Rosetrees Trust; US National Heart, Lung, and Blood Institute; Du Pont Pharma; Chest, Heart and Stroke Scotland; Wellcome Trust; Coronary Thrombosis Trust; Northwick Park Institute for Medical Research; UCLH/UCL Comprehensive Medical Research Centre; US National Institute on Aging; Academy of Finland; Netherlands Organisation for Health Research and Development; SANCO; Dutch Ministry of Public Health, Welfare and Sports; World Cancer Research Fund; Agentschap NL; European Commission; Swedish Heart-Lung Foundation; Swedish Research Council; Strategic Cardiovascular Programme of the Karolinska Institutet; Stockholm County Council; US National Institute of Neurological Disorders and Stroke; MedStar Health Research Institute; GlaxoSmithKline; Dutch Kidney Foundation; US National Institutes of Health; Netherlands Interuniversity Cardiology Institute of the Netherlands; Diabetes UK; European Union Seventh Framework Programme; National Institute for Healthy Ageing; Cancer Research UK; MacArthur Foundation.