Dietary Digital Diaries: Documenting Adolescents' Obesogenic Environment.
Ontology highlight
ABSTRACT:
SUBMITTER: Staiano AE
PROVIDER: S-EPMC3505082 | biostudies-literature | 2012 Sep
REPOSITORIES: biostudies-literature
Publications
Dietary Digital Diaries: Documenting Adolescents' Obesogenic Environment.
Staiano Amanda E AE Baker Christina M CM Calvert Sandra L SL
Environment and behavior 20110330 5
Obesogenic built environments may contribute to excessive eating and obesity. Twenty-three 12- to 17-year-old low-income African American adolescents created digital diaries by photographing their lunchtime food environment in a summer academic program. Digitally depicted foods were classified as appearing on the platescape (student's or others' plate) or the tablescape (food buffet). Height, weight, BMI percentile, and waist-to-hip ratio were calculated at baseline and week 4. Adolescents digit ...[more]
Similar Datasets
Project description:BackgroundPrevious studies have suggested that modern obesogenic environments accentuate the genetic risk of obesity. However, these studies have proven controversial as to which, if any, measures of the environment accentuate genetic susceptibility to high body mass index (BMI).MethodsWe used up to 120 000 adults from the UK Biobank study to test the hypothesis that high-risk obesogenic environments and behaviours accentuate genetic susceptibility to obesity. We used BMI as the outcome and a 69-variant genetic risk score (GRS) for obesity and 12 measures of the obesogenic environment as exposures. These measures included Townsend deprivation index (TDI) as a measure of socio-economic position, TV watching, a 'Westernized' diet and physical activity. We performed several negative control tests, including randomly selecting groups of different average BMIs, using a simulated environment and including sun-protection use as an environment.ResultsWe found gene-environment interactions with TDI (Pinteraction = 3 × 10 -10 ), self-reported TV watching (Pinteraction = 7 × 10 -5 ) and self-reported physical activity (Pinteraction = 5 × 10 -6 ). Within the group of 50% living in the most relatively deprived situations, carrying 10 additional BMI-raising alleles was associated with approximately 3.8 kg extra weight in someone 1.73 m tall. In contrast, within the group of 50% living in the least deprivation, carrying 10 additional BMI-raising alleles was associated with approximately 2.9 kg extra weight. The interactions were weaker, but present, with the negative controls, including sun-protection use, indicating that residual confounding is likely.ConclusionsOur findings suggest that the obesogenic environment accentuates the risk of obesity in genetically susceptible adults. Of the factors we tested, relative social deprivation best captures the aspects of the obesogenic environment responsible.
| S-EPMC5837271 | biostudies-literature
Project description:BackgroundObesity is associated with risk of aggressive prostate cancer. It is not known whether neighborhood obesogenic factors are independently associated with prostate cancer risk.MethodsNeighborhood socioeconomic status (nSES) and four neighborhood obesogenic environment factors (urbanicity, mixed-land development, unhealthy food environment, and parks) were assessed for associations with prostate cancer risk among 41,563 African American, Japanese American, Latino, and White males in the Multiethnic Cohort (MEC) Study, California site. Multivariable Cox proportional hazards regression was used to estimate HRs and 95% confidence intervals (CI) for nonaggressive and aggressive prostate cancer, adjusting for individual-level sociodemographic, behavioral, and prostate cancer risk factors. Analyses were stratified by race, ethnicity, and, among Latino males, nativity.ResultsMales residing in low-SES, compared with high-SES, neighborhoods had lower risk of nonaggressive prostate cancer [lowest vs. highest quintile HR = 0.81; 95% confidence interval (CI) = 0.68-0.95, Ptrend 0.024], driven by a similar trend among foreign-born Latino males. Foreign-born Latino males in neighborhoods with low mixed-land development had increased risk of non-aggressive disease (lowest vs. highest quintile HR = 1.49; 95% CI = 1.07-2.09). For aggressive disease, the only association noted was between lower mixed-land development and lower risk among White males (Ptrend = 0.040).ConclusionsnSES and obesogenic environment factors were independently associated with prostate cancer risk; associations varied by race, ethnicity, nativity, and disease aggressiveness.ImpactUpstream structural and social determinants of health that contribute to neighborhood obesogenic characteristics likely impact prostate cancer risk differently across groups defined by race, ethnicity, and nativity and by disease aggressiveness.
| S-EPMC9074096 | biostudies-literature
Project description:Aims/hypothesisIn this study, we used an immunodeficient mouse model to explore, in vivo, the longitudinal adaptation of human islets to an obesogenic environment.MethodsNon-diabetic Rag2 (-/-) mice (n = 61) were transplanted with human islets (400 islet equivalents [IEQ]) from six pancreases: four non-diabetic and two with overt metabolic dysfunction (older, high HbA(lc) or history of diabetes). Animals were fed for 12 weeks with a control or high-fat diet (HFD), and followed for weight, serum triacylglycerol, fasting blood glucose and human C-peptide. After the mice were killed, human grafts and the endogenous pancreas were analysed for endocrine volume, distribution of beta and alpha cells, and proliferation.ResultsTransplanted mice on an HFD gained significantly more weight (p < 0.001) and had higher fasting glycaemia (2-12 weeks; p = 0.0002) and consistently higher fasting human C-peptide levels (2-12 weeks; p = 0.04) compared with those on the control diet. Histology demonstrated doubling of human islet graft volume at 12 weeks in animals on the HFD and increased beta cell volume (p < 0.001), but no change in alpha cell volume. Human islet function (hyperbolic product HOMA2%BS) at 12 weeks was four times lower in HFD animals (p < 0.001 vs controls) because of insufficient beta cell adaptation to decreased (70%) sensitivity (HOMA%S). Human islets obtained from donors with metabolic dysfunction failed to adapt to the HFD.Conclusions/interpretationThis longitudinal study provides direct evidence that human islets adapt both endocrine and beta cell mass, function and gene expression to obesity in vivo. The present model will facilitate the identification of mechanisms by which human islets adapt to obesity in vivo and the cell type(s) responsible, and factors predisposing human beta cells to decompensation.
| S-EPMC3536990 | biostudies-literature
Project description:Various measures of the obesogenic environment have been proposed and used in childhood obesity research. The variety of measures poses methodological challenges to designing new research because methodological characteristics integral to developing the measures vary across studies. A systematic review has been conducted to examine the associations between different levels of obesogenic environmental measures (objective or perceived) and childhood obesity. The review includes all articles published in the Cochrane Library, PubMed, Web of Science and Scopus by 31 December 2018. A total of 339 associations in 101 studies have been identified from 18 countries, of which 78 are cross-sectional. Overall, null associations are predominant. Among studies with non-null associations, negative relationships between healthy food outlets in residential neighbourhoods and childhood obesity is found in seven studies; positive associations between unhealthy food outlets and childhood obesity are found in eight studies, whereas negative associations are found in three studies. Measures of recreational or physical activity facilities around the participants' home are also negatively correlated to childhood obesity in nine out of 15 studies. Results differ by the types of measurement, environmental indicators and geographic units used to characterize obesogenic environments in residential and school neighbourhoods. To improve the study quality and compare reported findings, a reporting standard for spatial epidemiological research should be adopted.
| S-EPMC7988549 | biostudies-literature
Project description:BackgroundDespite a large volume of research on the impact of other digital screens (eg, televisions) on eating behavior, little is known about the nature and impact of mealtime smartphone use.ObjectiveWe investigated how smartphones are used in everyday meals, whether phone users differ according to mealtime phone use patterns, and whether specific phone functions (particularly food photography) would affect the amount and enjoyment of food eaten.MethodsAcross 2 studies, we used the experience sampling method to track 1780 meals in situ. In study 1, a total 137 young adults reported on their mealtime smartphone use 3 times per day over 7 consecutive days. This corresponded to each main meal, with participants recording whether they used their phones and what phone functions they engaged in while eating. In study 2, a total of 71 young adults were similarly tracked for 3 meals per day over 7 days. Across the week, participants' meals were randomized to 1 of 3 smartphone conditions: food photography while eating, nonfood photography while eating, or no phone use. As the outcome measures, participants reported on the amount and enjoyment of food they ate.ResultsDuring the week-long tracking, most participants (110/129, 85.3%) recorded at least one instance of mealtime smartphone use, with an average frequency of 1 in 3 meals where phones were used (27.1%; 95% CI 23.6-30.6). Unlike traditional digital screens, mealtime phone use encompassed a wide range of social and nonsocial activities. Further, specific forms of phone use behaviors influenced food intake in different ways. Specifically, in study 2, participants showed the typical pattern of increased food intake across the day when they engaged in nonfood photography during a meal (P<.001); however, this pattern was disrupted when they engaged in food photography (P=.73).ConclusionsOur findings underscore the prevalence and multifaceted nature of mealtime phone use, distinguishing mobile phones from traditional forms of digital screens.Trial registrationClinicalTrials.gov NCT03299075; https://www.clinicaltrials.gov/ct2/show/NCT03299075 and ClinicalTrials.gov NCT03346785; https://clinicaltrials.gov/ct2/show/NCT03346785.
| S-EPMC8138713 | biostudies-literature
Project description:In spite of several studies relating dietary patterns to breast cancer risk, evidence so far remains inconsistent. This study aimed to investigate associations of dietary patterns derived with three different methods with breast cancer risk.The Mediterranean Diet Score (MDS), principal components analyses (PCA) and reduced rank regression (RRR) were used to derive dietary patterns in a case-control study of 610 breast cancer cases and 1891 matched controls within four UK cohort studies. Dietary intakes were collected prospectively using 4- to 7-day food diaries and resulting food consumption data were grouped into 42 food groups. Conditional logistic regression models were used to estimate odds ratios (ORs) for associations between pattern scores and breast cancer risk adjusting for relevant covariates. A separate model was fitted for post-menopausal women only.The MDS was not associated with breast cancer risk (OR comparing first tertile with third 1.20 (95% CI 0.92; 1.56)), nor the first PCA-derived dietary pattern, explaining 2.7% of variation of diet and characterized by cheese, crisps and savoury snacks, legumes, nuts and seeds (OR 1.18 (95% CI 0.91; 1.53)). The first RRR-derived pattern, a 'high-alcohol' pattern, was associated with a higher risk of breast cancer (OR 1.27; 95% CI 1.00; 1.62), which was most pronounced in post-menopausal women (OR 1.46 (95% CI 1.08; 1.98)).A 'high-alcohol' dietary pattern derived with RRR was associated with an increased breast cancer risk; no evidence of associations of other dietary patterns with breast cancer risk was observed in this study.
| S-EPMC4340564 | biostudies-literature
Project description:Research has shown that if a mother experiences a transitory perturbation to her environment during pregnancy or lactation, there are transgenerational consequences often involving a disordered metabolic phenotype in first generation offspring with recovery across subsequent generations. In contrast, little is known about the nature of the transgenerational response of offspring when a mother experiences a perturbation that is not transitory but instead persists across generations. Our study, using a rat model, subjected the parental generation to a change in environment and concomitant shift from a grain-based to obesogenic diets to generate an adipose phenotype in first generation offspring emulating a common scenario in human urbanisation and migration. We then investigated whether the obese phenotype was stable across generations when maintained in the transitioned environment, and whether dietary macronutrient balance affected the response. We found that second and third generation offspring had a reduced body fat to lean mass ratio and a reduced appetite relative to first generation offspring, irrespective of dietary macronutrient balance. The trajectory of this response is suggestive of a reduction in chronic disease risk across generations. This is one of the first studies, to our knowledge, to investigate the transgenerational response following parental transition to a persistent obesogenic environment, and to demonstrate that successive generations respond differently to this constant environment.
| S-EPMC4488537 | biostudies-literature
Project description:ImportanceThe early obesogenic home environment is consistently identified as a key influence on child weight trajectories, but little research has examined the mechanisms of that influence. Such research is essential for the effective prevention and treatment of overweight and obesity.ObjectiveTo test behavioral susceptibility theory's hypothesis that the heritability of body mass index (BMI) is higher among children who live in more obesogenic home environments.Design, setting, and participantsThis study was a gene-environment interaction twin study that used cross-sectional data from 925 families (1850 twins) in the Gemini cohort (a population-based prospective cohort of twins born in England and Wales between March and December 2007). Data were analyzed from July to October 2013 and in June 2018.ExposuresParents completed the Home Environment Interview, a comprehensive measure of the obesogenic home environment in early childhood. Three standardized composite scores were created to capture food, physical activity, and media-related influences in the home; these were summed to create an overall obesogenic risk score. The 4 composite scores were split on the mean, reflecting higher-risk and lower-risk home environments.Main outcomes and measuresQuantitative genetic model fitting was used to estimate heritability of age-adjusted and sex-adjusted BMI (BMI SD score, estimated using British 1990 growth reference data) for children living in lower-risk and higher-risk home environments.ResultsAmong 1850 twins (915 [49.5%] male and 935 [50.5%] female; mean [SD] age, 4.1 [0.4] years), the heritability of BMI SD score was significantly higher among children living in overall higher-risk home environments (86%; 95% CI, 68%-89%) compared with those living in overall lower-risk home environments (39%; 95% CI, 21%-57%). The findings were similar when examining the heritability of BMI in the separate food and physical activity environment domains.Conclusions and relevanceThese findings support the hypothesis that obesity-related genes are more strongly associated with BMI in more obesogenic home environments. Modifying the early home environment to prevent weight gain may be particularly important for children genetically at risk for obesity.
| S-EPMC6396810 | biostudies-literature
Project description:To test whether exposure to violence is associated with same-day increases in obesogenic behaviors among young adolescents, including unhealthy food and beverage consumption, poor quality sleep, and lack of physical activity.Young at-risk adolescents between 12 and 15 years of age were recruited via telephone screening from low-income neighborhoods. Adolescents and their parents completed in-person assessments, followed by Ecological Momentary Assessment (EMA) delivered to 151 adolescents' mobile phones three times a day for 30 days (4329 person days). Three obesogenic behaviors - unhealthy food consumption, poor sleep quality, and lack of physical activity - and violence exposure were assessed daily. Adolescents' body mass index (BMI) was assessed prior to the EMA and 18 months later. A replication was performed among 395 adolescents from a population-representative sample (with 5276 EMA person days).On days that at-risk adolescents were exposed versus not exposed to violence, they were more likely to consume unhealthy foods and beverages (b = 0.12, p = 0.01), report feeling tired the next morning (OR = 1.58, p < 0.01), and to be active (OR = 1.61, p < 0.01). At-risk adolescents who reported higher consumption of soda and caffeinated beverages during the 30-day EMA were more likely to experience increases in BMI in later adolescence. Findings related to sleep and activity were supported in the population-based replication sample; however, no significant same-day associations were found between violence exposure and unhealthy dietary consumption.This study provides evidence that exposure to violence is associated with same-day unhealthy dietary consumption among at-risk adolescents and next-day tiredness related to sleep quality among adolescents from both at-risk and normative populations. Findings also point to unhealthy soda consumption during early adolescence as an important predictor of weight gain among at-risk adolescents.
| S-EPMC5907915 | biostudies-literature
Project description:Obesity is closely associated with adipose tissue inflammation and insulin resistance. Dysglycemia and type 2 diabetes results when islet β cells fail to maintain appropriate insulin secretion in the face of insulin resistance. To clarify the early transcriptional events leading to β-cell failure in the setting of obesity, we fed male C57BL/6J mice an obesogenic, high-fat diet (60% kcal from fat) or a control diet (10% kcal from fat) for one week, and islets from these mice (from four high-fat- and three control-fed mice) were subjected to single-cell RNA sequencing (sc-RNAseq) analysis. Islet endocrine cell types (α cells, β cells, δ cells, PP cells) and other resident cell types (macrophages, T cells) were annotated by transcript profiles and visualized using Uniform Manifold Approximation and Projection for Dimension Reduction (UMAP) plots. UMAP analysis revealed distinct cell clusters (11 for β cells, 5 for α cells, 3 for δ cells, PP cells, ductal cells, endothelial cells), emphasizing the heterogeneity of cell populations in the islet. Collectively, the clusters containing the majority of β cells showed the fewest gene expression changes, whereas clusters harboring the minority of β cells showed the most changes. We identified that distinct β-cell clusters downregulate genes associated with the endoplasmic reticulum stress response and upregulate genes associated with insulin secretion, whereas others upregulate genes that impair insulin secretion, cell proliferation, and cell survival. Moreover, all β-cell clusters negatively regulate genes associated with immune response activation. Glucagon-producing α cells exhibited patterns similar to β cells but, again, in clusters containing the minority of α cells. Our data indicate that an early transcriptional response in islets to an obesogenic diet reflects an attempt by distinct populations of β cells to augment or impair cellular function and/or reduce inflammatory responses as possible harbingers of ensuing insulin resistance.
| S-EPMC7765825 | biostudies-literature