Environmental components of childhood obesity prevention interventions: an overview of systematic reviews.

Childhood obesity has a complex multi-factorial aetiology grounded in environmental and individual level factors that affect behaviour and outcomes. An ecological, systems-based approach to addressing childhood obesity is increasingly being advocated. The primary aim of this review is to summarize the evidence reported in systematic reviews on the effectiveness of population-level childhood obesity prevention interventions that have an environmental component. We conducted a systematic review of reviews published since 1995, employing a standardized search strategy in nine databases. Inclusion criteria required that reviews be systematic and evaluated at least one population-level, environmental intervention in any setting aimed at preventing or reducing obesity in children (5-18 years). Sixty-three reviews were included, ten of which were of high quality. Results show modest impact of a broad range of environmental strategies on anthropometric outcomes. Systematic reviews vary in methodological quality, and not all relevant primary studies may be included in each review. To ensure relevance of our findings to practice, we also report on relevant underlying primary studies, providing policy-relevant recommendations based on the evidence reviewed. Greater standardization of review methods and reporting structures will benefit policymakers and public health professionals seeking informed decision-making

Childhood obesity in Malta: contributions of the obesogenic environment.

Background. There is a high prevalence of childhood obesity in Malta. The aim of this research is to gain insight into the environmental drivers of childhood obesity in Malta, and identify opportunities for an environmental approach to obesity prevention. Methods. This thesis comprises: (i) a contextual analysis of childhood obesity and the policy response in Malta; (ii) an overview of systematic reviews to identify environmental components of effective prevention interventions; (iii) an assessment of Maltese television advertising; (iv) an environmental audit of the food and built environment; (v) semi-structured interviews and focus groups with key informants; and (vi) microsimulation modelling to forecast the future health and economic burden of obesity in Malta. Results. Numerous environmental factors at multiple levels deter healthy dietary and physical activity behaviour among Maltese children. These include an obesogenic built environment that provides few opportunities for play or active transport, and a food environment characterised by easy access to, and heavy promotion of, energy-dense foods and beverages. The contextual analysis and environmental audit revealed several obesogenic aspects of the environment in Malta, such as substantial promotion of food high in fat, sugar and salt to children on local TV channels and a price premium for certain healthy food options in grocery stores. Thematic analysis of qualitative data revealed numerous barriers to healthy behaviours for Maltese children, including parental concerns about traffic hazard leading to restricted physical activity, and familal dietary patterns which encourage over-consumption of food. Interviews with food industry and public health actors also highlighted ‘framings’ of obesity that closely matched those described in the international literature. Microsimulation modelling illustrated the substantial financial savings and reductions in noncommunicable disease incidence if population weight reduction were to be achieved. Conclusions. An obesogenic environment underlies the problem of childhood obesity in Malta. The socio-ecological approach used in this research highlighted key areas for intervention and illustrated the importance of taking context into account when designing national obesity-prevention efforts

Common variants of the TCF7L2 gene are associated with increased risk of type 2 diabetes mellitus in a UK-resident South Asian population

Background Recent studies have implicated variants of the transcription factor 7-like 2 (TCF7L2) gene in genetic susceptibility to type 2 diabetes mellitus in several different populations. The aim of this study was to determine whether variants of this gene are also risk factors for type 2 diabetes development in a UK-resident South Asian cohort of Punjabi ancestry. Methods We genotyped four single nucleotide polymorphisms (SNPs) of TCF7L2 (rs7901695, rs7903146, rs11196205 and rs12255372) in 831 subjects with diabetes and 437 control subjects. Results The minor allele of each variant was significantly associated with type 2 diabetes; the greatest risk of developing the disease was conferred by rs7903146, with an allelic odds ratio (OR) of 1.31 (95% CI: 1.11 – 1.56, p = 1.96 × 10-3). For each variant, disease risk associated with homozygosity for the minor allele was greater than that for heterozygotes, with the exception of rs12255372. To determine the effect on the observed associations of including young control subjects in our data set, we reanalysed the data using subsets of the control group defined by different minimum age thresholds. Increasing the minimum age of our control subjects resulted in a corresponding increase in OR for all variants of the gene (p ≤ 1.04 × 10-7). Conclusion Our results support recent findings that TCF7L2 is an important genetic risk factor for the development of type 2 diabetes in multiple ethnic groups

Contribution of type 2 diabetes associated loci in the Arabic population from Tunisia: a case-control study

<p>Abstract</p> <p>Background</p> <p>Candidate gene and genome-wide association studies have both reproducibly identified several common Single Nucleotide Polymorphisms (SNPs) that confer type 2 diabetes (T2D) risk in European populations. Our aim was to evaluate the contribution to T2D of five of these established T2D-associated loci in the Arabic population from Tunisia.</p> <p>Methods</p> <p>A case-control design comprising 884 type 2 diabetic patients and 513 control subjects living in the East-Center of Tunisia was used to analyze the contribution to T2D of the following SNPs: E23K in <it>KCNJ11/Kir6.2</it>, K121Q in <it>ENPP1</it>, the -30G/A variant in the pancreatic β-cell specific promoter of Glucokinase, rs7903146 in <it>TCF7L2 </it>encoding transcription factor 7-like2, and rs7923837 in <it>HHEX </it>encoding the homeobox, hematopoietically expressed transcription factor.</p> <p>Results</p> <p><it>TCF7L2</it>-rs7903146 T allele increased susceptibility to T2D (OR = 1.25 [1.06–1.47], <it>P </it>= 0.006) in our study population. This risk was 56% higher among subjects carrying the TT genotype in comparison to those carrying the CC genotype (OR = 1.56 [1.13–2.16], <it>P </it>= 0.002). No allelic or genotypic association with T2D was detected for the other studied polymorphisms.</p> <p>Conclusion</p> <p>In the Tunisian population, <it>TCF7L2</it>-rs7903146 T allele confers an increased risk of developing T2D as previously reported in the European population and many other ethnic groups. In contrast, none of the other tested SNPs that influence T2D risk in the European population was associated with T2D in the Tunisian Arabic population. An insufficient power to detect minor allelic contributions or genetic heterogeneity of T2D between different ethnic groups can explain these findings.</p

TCF7L2 variant genotypes and type 2 diabetes risk in Brazil: significant association, but not a significant tool for risk stratification in the general population

<p>Abstract</p> <p>Background</p> <p>Genetic polymorphisms of the <it>TCF7L2 </it>gene are strongly associated with large increments in type 2 diabetes risk in different populations worldwide. In this study, we aimed to confirm the effect of the <it>TCF7L2 </it>polymorphism <it>rs7903146 </it>on diabetes risk in a Brazilian population and to assess the use of this genetic marker in improving diabetes risk prediction in the general population.</p> <p>Methods</p> <p>We genotyped the single nucleotide polymorphisms (SNP) rs7903146 of the <it>TCF7L2 </it>gene in 560 patients with known coronary disease enrolled in the MASS II (Medicine, Angioplasty, or Surgery Study) Trial and in 1,449 residents of Vitoria, in Southeast Brazil. The associations of this gene variant to diabetes risk and metabolic characteristics in these two different populations were analyzed. To access the potential benefit of using this marker for diabetes risk prediction in the general population we analyzed the impact of this genetic variant on a validated diabetes risk prediction tool based on clinical characteristics developed for the Brazilian general population.</p> <p>Results</p> <p>SNP rs7903146 of the <it>TCF7L2 </it>gene was significantly associated with type 2 diabetes in the MASS-II population (OR = 1.57 per T allele, p = 0.0032), confirming, in the Brazilian population, previous reports of the literature. Addition of this polymorphism to an established clinical risk prediction score did not increased model accuracy (both area under ROC curve equal to 0.776).</p> <p>Conclusion</p> <p><it>TCF7L2 </it>rs7903146 T allele is associated with a 1.57 increased risk for type 2 diabetes in a Brazilian cohort of patients with known coronary heart disease. However, the inclusion of this polymorphism in a risk prediction tool developed for the general population resulted in no improvement of performance. This is the first study, to our knowledge, that has confirmed this recent association in a South American population and adds to the great consistency of this finding in studies around the world. Finally, confirming the biological association of a genetic marker does not guarantee improvement on already established screening tools based solely on demographic variables.</p

‘Left behind places’: a geographical etymology

‘Left behind places’ has become the leitmotif of geographical inequalities since the 2008 crisis. Yet, the term’s origins, definition and implications are poorly specified and risk obscuring the differentiated problems and pathways of different kinds of areas. This paper explicates the geographical etymology and spatial imaginary of ‘left behind places’. It argues that the appellation and its spatial expression have modified how geographical inequalities are understood and addressed by recovering a more relational understanding of multiple ‘left behind’ conditions, widening the analytical frame beyond only economic concerns, and opening up interpretations of the ‘development’ of ‘left behind places’ and their predicaments and prospects. While renewing interest in fundamental urban and regional concerns, what needs to endure from the ascendance of the ‘left behind places’ label is the terminology and spatial imaginary of reducing geographical inequalities and enhancing social and spatial justice

'Left behind places': a geographical etymology

'Left behind places' has become the leitmotif of geographical inequalities since the 2008 crisis. Yet, the term's origins, definition and implications are poorly specified and risk obscuring the differentiated problems and pathways of different kinds of areas. This paper explicates the geographical etymology and spatial imaginary of 'left behind places'. It argues that the appellation and its spatial expression have modified how geographical inequalities are understood and addressed by recovering a more relational understanding of multiple 'left behind' conditions, widening the analytical frame beyond only economic concerns, and opening up interpretations of the 'development' of 'left behind places' and their predicaments and prospects. While renewing interest in fundamental urban and regional concerns, what needs to endure from the ascendance of the 'left behind places' label is the terminology and spatial imaginary of reducing geographical inequalities and enhancing social and spatial justice

TCF7L2 rs7903146-macronutrient interaction in obese individuals' responses to a 10-wk randomized hypoenergetic diet

BACKGROUND: Transcription factor 7-like 2 (TCF7L2) rs7903146 associates with type 2 diabetes and may operate via impaired glucagon-like peptide 1 secretion, which is stimulated more by fat than by carbohydrate ingestion. OBJECTIVE: The objective was to examine the interaction between TCF7L2 rs7903146 and dietary fat and carbohydrate [high-fat, low-carbohydrate: 40-45% of energy as fat (HF); compared with low-fat, high-carbohydrate: 20-25% of energy as fat (LF)] in obese individuals' responses to a 10-wk hypoenergetic diet (-600 kcal/d). DESIGN: European, obese participants (n = 771) were randomly assigned to receive an HF or an LF diet. Body weight, fat mass (FM), fat-free mass (FFM), waist circumference (WC), resting energy expenditure (REE), fasting fat oxidation in percentage of REE (FatOx), homeostasis model assessed insulin release (HOMA-beta), and HOMA-insulin resistance (HOMA-IR) were determined at baseline and after the intervention; 739 individuals were genotyped for rs7903146. RESULTS: Average weight loss was 6.9 kg with the LF and 6.6 kg with the HF (difference between diets, NS) diet. Among individuals who were homozygous for the T-risk allele, those in the HF diet group experienced smaller weight losses (Deltaweight) (2.6 kg; P = 0.009; n = 622), smaller DeltaFFM (1.6 kg; P = 0.027; n = 609), smaller DeltaWC (3.3 cm; P = 0.010; n = 608), and a smaller DeltaHOMA-IR (1.3 units; P = 0.004; n = 615) than did the LF diet group. For C allele carriers, there were no differences between the HF and LF diet groups. For the HF diet group, each additional T allele was associated with a reduced loss of FM (0.67 kg; P = 0.019; n = 609). TCF7L2 rs7903146 was not associated with DeltaREE, DeltaFatOx, DeltaHOMA-beta, or dropout. CONCLUSION: Our results suggest that obese individuals who are homozygous for the TCF7L2 rs7903146 T-risk allele are more sensitive to LF than to HF weight-loss diets

The transcription factor 7-like 2 (TCF7L2) polymorphism may be associated with focal arteriolar narrowing in Caucasians with hypertension or without diabetes: the ARIC Study

<p>Abstract</p> <p>Background</p> <p>Transcription factor 7-like 2 (<it>TCF7L2</it>) has emerged as a consistently replicated susceptibility gene for type 2 diabetes, however, whether the <it>TCF7L2 </it>gene also has similar effects on the retinal microvasculature is less clear. We therefore aimed to investigate the association between the transcription factor 7-like 2 (<it>TCF7L2</it>) rs7903146 polymorphism and retinal microvascular phenotypes in the Atherosclerosis Risk in Communities (ARIC) Study (1993-1995).</p> <p>Methods</p> <p>This was a population-based, cross-sectional study of 10,320 middle-aged African American (n = 2,199) and Caucasian (n = 8,121) men and women selected from four United States communities to examine the association between <it>TCF7L2 </it>rs7903146 polymorphism and retinal microvascular signs (retinopathy, focal arteriolar narrowing, arteriovenous nicking, arteriolar and venular calibers). Photographs on one randomly selected eye were graded for presence of retinal microvascular signs and used to measure retinal vessel calibres.</p> <p>Results</p> <p>After adjusting for age, sex, study center, mean arterial blood pressure, total serum cholesterol, triglycerides, and other covariates, few associations of <it>TCF7L2 </it>rs7903146 and retinal microvascular signs were noted. <it>TCF7L2 </it>rs7903146 T risk allele was significantly associated with focal arteriolar narrowing in Caucasians with hypertension [odds ratio (OR)_{CT vs. CC}(95% CI) = 1.25 (1.09-1.44); OR_{TT vs. CC}= 1.56 (1.18-2.06); <it>P </it>= 0.002] and in Caucasians without diabetes [OR _{CT vs. CC}= 1.18 (1.06-1.32); OR _{TT vs. CC}= 1.40 (1.12, 1.75); <it>P </it>= 0.003]. No significant association of the <it>TCF7L2 </it>rs7903146 polymorphism and retinal vascular signs was noted among African American individuals.</p> <p>Conclusions</p> <p><it>TCF7L2 </it>rs7903146 is not consistently associated with retinal microvascular signs. However, we report an association between the <it>TCF7L2 </it>rs7903146 polymorphism and focal arteriolar narrowing in Caucasians with hypertension or without diabetes. Further research in other large, population-based studies is needed to replicate these findings.</p