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Background: Obesity rates in Hispanic women residing in the United States (U.S.) are disproportionately high, increasing the risk of obesity-related disease and mortality. The effectiveness of interventions targeting weight loss in this population remains largely unknown., Purpose: The purpose of this review was to systematically evaluate the evidence related to the effectiveness of weight loss interventions conducted among U.S. Hispanic women and provide guidance for future research., Methods: Bibliographic databases ( n  = 10, from each database's inception to July 2, 2019) were searched using the PRISMA guidelines for systematic reviews. Randomized controlled trials (RCTs) and quasi-experimental studies with weight change outcomes were included. Results were described in a narrative synthesis., Results: 5,423 articles were assessed for eligibility based on inclusion criteria; 15 studies were included in the final review. Nine trials were RCTs and six were quasi-experimental studies; all but six were pilot studies. Most studies recruited overweight or obese women with no existing medical conditions and did not follow participants beyond the intervention. All trials were delivered in-person. Intervention strategies and content and weight change outcomes were highly variable., Conclusions: RCTs with statistically powered sample sizes are needed to robustly test the effects of weight loss interventions in this population., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2021 Kristin E. Morrill et al.)

Differences in obesity and body fat distribution across gender and race/ethnicity have been extensively described. We sought to replicate these differences and evaluate newly emerging data from the All of Us Research Program (AoU). We compared body mass index (BMI), waist circumference, and waist-to-hip ratio from the baseline physical examination, and alanine aminotransferase (ALT) from the electronic health record in up to 88,195 Non-Hispanic White (NHW), 40,770 Non-Hispanic Black (NHB), 35,640 Hispanic, and 5,648 Asian participants. We compared AoU sociodemographic variable distribution to National Health and Nutrition Examination Survey (NHANES) data and applied the pseudo-weighting method for adjusting selection biases of AoU recruitment. Our findings replicate previous observations with respect to gender differences in BMI. In particular, we replicate the large gender disparity in obesity rates among NHB participants, in which obesity and mean BMI are much higher in NHB women than NHB men (33.34 kg/m2 versus 28.40 kg/m2 respectively; p<2.22x10-308). The overall age-adjusted obesity prevalence in AoU participants is similar overall but lower than the prevalence found in NHANES for NHW participants. ALT was higher in men than women, and lower among NHB participants compared to other racial/ethnic groups, consistent with previous findings. Our data suggest consistency of AoU with national averages related to obesity and suggest this resource is likely to be a major source of scientific inquiry and discovery in diverse populations., Competing Interests: The authors have declared that no competing interests exist.

Background: We conducted a Mendelian randomisation (MR) study to investigate whether physical activity (PA) causes a reduction of colorectal cancer risk and to understand the contributions of effects mediated through changes in body fat., Methods: Common genetic variants associated with self-reported moderate-to-vigorous PA (MVPA), acceleration vector magnitude PA (AMPA) and sedentary time were used as instrumental variables. To control for confounding effects of obesity, we included instrumental variables for body mass index (BMI), body fat percentage, waist circumference and arm, trunk and leg fat ratios. We analysed the effect of these instrumental variables in a colorectal cancer genome-wide association study comprising 31,197 cases and 61,770 controls of European ancestry by applying two-sample and multivariable MR study designs., Results: We found decreased colorectal cancer risk for genetically represented measures of MVPA and AMPA that were additional to effects mediated through genetic measures of obesity. Odds ratio and 95% confidence interval (CI) per standard deviation increase in MVPA and AMPA was 0.56 (0.31, 1.01) and 0.60 (0.41, 0.88), respectively. No association has been found between sedentary time and colorectal cancer risk. The proportion of effect mediated through BMI was 2% (95% CI: 0, 14) and 32% (95% CI: 12, 46) for MVPA and AMPA, respectively., Conclusion: These findings provide strong evidence to reinforce public health measures on preventing colorectal cancer that promote PA at a population level regardless of body fatness.

Background: In the U.S., Hispanic women experience a disproportionate rate of obesity and obesity-related chronic diseases. At the same time, Hispanic women remain considerably underrepresented in behavioral weight loss interventions. The purpose of this review is to systematically evaluate the evidence related to the effectiveness of weight loss interventions among Hispanic women in the U.S. This review will identify elements of successful weight loss interventions as well as areas for future research., Methods/design: The following databases will be searched to identify all relevant articles (from inception onwards): PubMed, Embase, Scopus, Web of Science (Science Citation Index and Social Sciences Citation Index), PsycINFO, CINAHL, Chicano Database, SPORTDiscus, CAB Abstracts, and Google Scholar. We will include randomized controlled trials and quasi-experimental studies of adult women (> 18 years) from Hispanic/Latino background living in the United States. Eligible interventions will target weight-related behaviors (including diet, physical activity, behavior modification and/or their combinations). The review's primary outcome will be weight change (expressed as change in lbs/kg or body mass index (BMI) (kg/m 2 )). Three reviewers will independently screen and select data and two will extract data. The methodological quality (or risk of bias) of individual studies will be appraised using the Effective Public Health Practice Project Quality Assessment Tool. A narrative synthesis will describe quality and content of the evidence., Discussion: The aim of this systematic review is to critically examine existing weight loss interventions for Hispanic women in the U.S. and provide quality evidence for the effectiveness of these interventions on weight loss. Further, this review seeks to identify characteristics of effective interventions and suggest future directions for research efforts targeting weight loss in this population. This review will inform the development of future weight loss interventions for this population., Systematic Review Registration: PROSPERO CRD42019119094.

Scope: n-3 polyunsaturated fatty acid (n-3 PUFA) intake is associated with protection from obesity; however, the mechanisms of protection remain poorly characterized. The stearoyl CoA desaturase (SCD), insulin-sensitive glucose transporter (SLC2A4), and sterol regulatory element binding protein (SREBF1) genes are transcriptionally regulated by n-3 PUFA intake and harbor polymorphisms associated with obesity. The present study investigated how consumption of n-3 PUFA modifies associations between SCD, SLC2A4, and SREBF1 polymorphisms and anthropometric variables and metabolic phenotypes., Materials and Methods: Anthropometric variables and metabolic phenotypes were measured in a cross-sectional sample of Yup'ik individuals (n = 1135) and 33 polymorphisms were tested for main effects and interactions using linear models that account for familial correlations. n-3 PUFA intake was estimated using red blood cell nitrogen stable isotope ratios. SCD polymorphisms were associated with ApoA1 concentration and n-3 PUFA interactions with SCD polymorphisms were associated with reduced fasting cholesterol levels and waist-to-hip ratio. SLC2A4 polymorphisms were associated with hip circumference, high-density lipoprotein and ApoA1 concentrations. SREBF1 polymorphisms were associated with low-density lipoprotein and HOMA-IR and n-3 PUFA interactions were associated with reduced fasting insulin and HOMA-IR levels., Conclusion: The results suggest that an individual's genotype may interact with dietary n-3 PUFAs in ways that are associated with protection from obesity-related diseases in Yup'ik people., (© 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Genome-wide Association Studies (GWAS) have resulted in many discovered risk variants for several obesity-related traits. However, before clinical relevance of these discoveries can be achieved, molecular or physiological mechanisms of these risk variants needs to be discovered. One strategy is to perform data mining of phenotypically-rich data sources such as those present in dbGAP (database of Genotypes and Phenotypes) for hypothesis generation. Here we propose a technique that combines the power of existing Bayesian Network (BN) learning algorithms with the statistical rigour of Structural Equation Modelling (SEM) to produce an overall phenotypic network discovery system with optimal properties. We illustrate our method using the analysis of a candidate SNP data set from the AMERICO sample, a multi-ethnic cross-sectional cohort of roughly 300 children with detailed obesity-related phenotypes. We demonstrate our approach by showing genetic mechanisms for three obesity-related SNPs.

Background and Aims: Genome-wide association studies (GWAS) have identified several loci that are associated with body mass index (BMI = kg/m(2)). However, little is known regarding whether the genetic basis of BMI differs among children of diverse racial/ethnic backgrounds, how the cumulative effect of these genes influences weight, or the contribution of these variants to body composition. This study examined the association between 17 GWAS-identified loci located in 16 genes and body-composition phenotypes in a multiethnic pediatric sample and evaluated the association of a composite genetic risk score with these phenotypes., Methods: Anthropometric measures of BMI, waist circumference and waist-to-hip ratio were obtained in a sample of 298 children. Lean and fat mass were obtained from dual-energy X-ray absorptiometry (DXA). Genotypes of 17 single nucleotide polymorphisms (SNPs) were tested for association with the phenotypic measures, adjusted by standard covariates and estimates of genetic admixture., Results: Both SNPs rs8050136 and rs9939609 in FTO were associated with BMI and waist circumference in a direction opposite to that observed among adults, and an inverse association was detected between the risk variant in MC4R and total lean body mass. Lean body mass mediated the association between TMEM18 and BMI. The association between the genetic risk score and body composition differed according to ethnic/racial classification., Conclusions: Our findings suggest that genetic associations with BMI among children are different from those in adults, that some loci may operate through lean body mass, and that genetic risk scores will not have universal applicability across ethnic/racial groups., (Copyright © 2011 IMSS. Published by Elsevier Inc. All rights reserved.)

A dramatic rise in obesity has occurred among humans within the last several decades. Little is known about whether similar increases in obesity have occurred in animals inhabiting human-influenced environments. We examined samples collectively consisting of over 20 000 animals from 24 populations (12 divided separately into males and females) of animals representing eight species living with or around humans in industrialized societies. In all populations, the estimated coefficient for the trend of body weight over time was positive (i.e. increasing). The probability of all trends being in the same direction by chance is 1.2 × 10(-7). Surprisingly, we find that over the past several decades, average mid-life body weights have risen among primates and rodents living in research colonies, as well as among feral rodents and domestic dogs and cats. The consistency of these findings among animals living in varying environments, suggests the intriguing possibility that the aetiology of increasing body weight may involve several as-of-yet unidentified and/or poorly understood factors (e.g. viral pathogens, epigenetic factors). This finding may eventually enhance the discovery and fuller elucidation of other factors that have contributed to the recent rise in obesity rates.

Different populations suffer from different rates of obesity and type-2 diabetes (T2D). Little is known about the genetic or adaptive component, if any, that underlies these differences. Given the cultural, geographic, and dietary variation that accumulated among humans over the last 60,000 years, we examined whether loci identified by genome-wide association studies for these traits have been subject to recent selection pressures. Using genome-wide SNP data on 938 individuals in 53 populations from the Human Genome Diversity Panel, we compare population differentiation and haplotype patterns at these loci to the rest of the genome. Using an "expanding window" approach (100-1,600 kb) for the individual loci as well as the loci as ensembles, we find a high degree of differentiation for the ensemble of T2D loci. This differentiation is most pronounced for East Asians and sub-Saharan Africans, suggesting that these groups experienced natural selection at loci associated with T2D. Haplotype analysis suggests an excess of obesity loci with evidence of recent positive selection among South Asians and Europeans, compared to sub-Saharan Africans and Native Americans. We also identify individual loci that may have been subjected to natural selection, such as the T2D locus, HHEX, which displays both elevated differentiation and extended haplotype homozygosity in comparisons of East Asians with other groups. Our findings suggest that there is an evolutionary genetic basis for population differences in these traits, and we have identified potential group-specific genetic risk factors.

IntroductionNational obesity prevention strategies may benefit from precision health approaches involving diverse participants in population health studies. We used cohort data from the National Institutes of Health All of Us Research Program (All of Us) Researcher Workbench to estimate population-level obesity prevalence.MethodsTo estimate state-level obesity prevalence we used data from physical measurements made during All of Us enrollment visits and data from participant electronic health records (EHRs) where available. Prevalence estimates were calculated and mapped by state for 2 categories of body mass index (BMI) (kg/m2): obesity (BMI >30) and severe obesity (BMI >35). We calculated and mapped prevalence by state, excluding states with fewer than 100 All of Us participants.ResultsData on height and weight were available for 244,504 All of Us participants from 33 states, and corresponding EHR data were available for 88,840 of these participants. The median and IQR of BMI taken from physical measurements data was 28.4 (24.4- 33.7) and 28.5 (24.5-33.6) from EHR data, where available. Overall obesity prevalence based on physical measurements data was 41.5% (95% CI, 41.3%-41.7%); prevalence of severe obesity was 20.7% (95% CI, 20.6-20.9), with large geographic variations observed across states. Prevalence estimates from states with greater numbers of All of Us participants were more similar to national population-based estimates than states with fewer participants.ConclusionAll of Us participants had a high prevalence of obesity, with state-level geographic variation mirroring national trends. The diversity among All of Us participants may support future investigations on obesity prevention and treatment in diverse populations.

Central obesity is a leading health concern with a great burden carried by ethnic minority populations, especially Hispanics/Latinos. Genetic factors contribute to the obesity burden overall and to inter-population differences. We aimed to identify the loci associated with central adiposity measured as waist-to-hip ratio (WHR), waist circumference (WC) and hip circumference (HIP) adjusted for body mass index (adjBMI) by using the Hispanic Community Health Study/Study of Latinos (HCHS/SOL); determine if differences in associations differ by background group within HCHS/SOL and determine whether previously reported associations generalize to HCHS/SOL. Our analyses included 7472 women and 5200 men of mainland (Mexican, Central and South American) and Caribbean (Puerto Rican, Cuban and Dominican) background residing in the USA. We performed genome-wide association analyses stratified and combined across sexes using linear mixed-model regression. We identified 16 variants for waist-to-hip ratio adjusted for body mass index (WHRadjBMI), 22 for waist circumference adjusted for body mass index (WCadjBMI) and 28 for hip circumference adjusted for body mass index (HIPadjBMI), which reached suggestive significance (P

BackgroundGenome-wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) associated with type 2 diabetes (T2D), mainly among individuals of European ancestry. In the present study, we examined the frequency of these SNPs and their association with T2D-related traits in an Alaska Native study population with a historically low prevalence of T2D. We also investigated whether dietary characteristics that may protect against T2D, such as n-3 polyunsaturated fatty acid (PUFA) intake, modify these associations.MethodsIn 1144 Yup'ik people, we examined 17 SNPs repeatedly identified in GWAS for individual and cumulative associations with T2D-related traits. Cumulative associations were evaluated using a genetic risk score (GRS) calculated by summing risk alleles. Associations were tested for interactions with sex, body mass index (BMI), and n-3 PUFA intake.ResultsThe rs7754840 SNP in CDKAL1 is significantly associated with HbA1c (P = 0.00091). The rs5015480 SNP near HHEX is significantly associated (in opposite direction to that in Europeans) with a combined fasting glucose (FG) and HbA1c measure (P = 0.00046) and with homeostatic model assessment of β-cell function (HOMA-B; P = 0.0014). The GRS is significantly associated with FG and combined FG and HbA1c only when the HHEX SNP is dropped from the GRS. Associations are not modified by BMI or n-3 PUFA intake.ConclusionOur results highlight the potential importance of CDKAL1 and HHEX in glucose homeostasis in this Alaska Native population with a low prevalence of T2D, and suggest that these loci should be examined in greater detail in this population.

Objectives To determine whether the relationship between anthropometric measurements of obesity and mortality varies according to age, race, and ethnicity in older women. Design Prospective cohort study of multiethnic postmenopausal women. Setting Women's Health Initiative ( WHI) observational study and clinical trials in 40 clinics. Participants Postmenopausal women aged 50-79 participating in WHI (N = 161,808). Measurements Baseline height, weight, and waist circumference ( WC) were measured, and body mass index ( BMI) was calculated based on height and weight. Demographic, health, and lifestyle data from a baseline questionnaire were used as covariates. The outcome was adjudicated death (n = 18,320) during a mean follow-up of 11.4 ± 3.2 years. Results Hazard ratios ( HRs) and 95% confidence intervals (95% CIs) indicated that ethnicity and age modified ( P < .01) the relationship between obesity and mortality. Underweight was associated with higher mortality, but overweight or slight obesity was not a risk factor for mortality in most ethnic groups except for Hispanic women in the obesity I category ( HR = 1.42, 95% CI = 1.04-1.95). BMI was not or was only weakly associated with mortality in individuals aged 70-79 ( HR = 0.90, 95% CI = 0.85-0.95 for overweight; HR = 0.98, 95 CI = 0.92-1.06 for obese I; HR = 1.11, 95% CI = 1.00-1.23 for obese II; HR = 1.08, 95% CI = 0.92-1.26 for obese III). In contrast, higher central obesity measured using WC was consistently associated with higher mortality in all groups. Conclusion Underweight is a significant risk factor for mortality in older women, and healthy BMI ranges may need to be specific for age, race, and ethnicity. The findings support a consistent relationship between central obesity and mortality. [ABSTRACT FROM AUTHOR]

Over 80% of African-American (AA) women are overweight or obese. A large racial disparity between AA and European-Americans (EA) in obesity rates exists among women, but curiously not among men. Although socio-economic and/or cultural factors may partly account for this race-by-sex interaction, the potential involvement of genetic factors has not yet been investigated. Among 2814 self-identified AA in the Atherosclerosis Risk in Communities study, we estimated each individual's degree of West-African genetic ancestry using 3437 ancestry informative markers. We then tested whether sex modifies the association between West-African genetic ancestry and body mass index (BMI), waist-circumference (WC), and waist-to-hip ratio (WHR), adjusting for income and education levels, and examined associations of ancestry with the phenotypes separately in males and females. We replicated our findings in the Multi-Ethnic Study of Atherosclerosis (n = 1611 AA). In both studies, we find that West-African ancestry is negatively associated with obesity, especially central obesity, among AA men, but not among AA women (p -5 interaction = 4.14 ? 10-5 in pooled analysis of WHR). In conclusion, our results suggest that the combination of male gender and West-African genetic ancestry is associated with protection against central adiposity, and suggest that the large racial disparity that exists among women, but not men, may be at least partly attributed to genetic factors. [ABSTRACT FROM AUTHOR]

Type 2 Diabetes (T2D) is a chronic disease arising from the development of insulin absence or resistance within the body, and a complex interplay of environmental and genetic factors. The incidence of T2D has increased throughout the last few decades, together with the occurrence of the obesity epidemic. The consideration of variants identified by GenomeWide Association Studies (GWAS) into risk assessment models for T2D could aid in the identification of at-risk patients who could benefit from preventive medicine. In this study, we build several risk assessment models, evaluated with two different classification approaches (Logistic Regression and Neural Networks), to measure the effect of including genetic information in the prediction of T2D. We used data from to the Original and the Offspring cohorts of the Framingham Heart Study, which provides phenotypic and genetic information for 5245 subjects (4306 controls and 939 cases). Models were built by using several covariates: gender, exposure time, cohort, body mass index (BMI), and 65 SNPs associated to T2D. We fitted Logistic Regressions and Bayesian Regularized Neural Networks and then assessed their predictive ability by using a ten-fold cross validation. We found that the inclusion of genetic information into the risk assessment models increased the predictive ability by 2%, when compared to the baseline model. Furthermore, the models that included BMI at the onset of diabetes as a possible effector, gave an improvement of 6% in the area under the curve derived from the ROC analysis. The highest AUC achieved (0.75) belonged to the model that included BMI, and a genetic score based on the 65 established T2D-associated SNPs. Finally, the inclusion of SNPs and BMI raised predictive ability in all models as expected; however, results from the AUC in Neural Networks and Logistic Regression did not differ significantly in their prediction accuracy. [ABSTRACT FROM AUTHOR]

Syndecans are a family of type-I transmembrane proteins that are involved in cell-matrix adhesion, migration, neuronal development, and inflammation. Previous quantitative genetic studies pinpointed Drosophila Syndecan (dSdc) as a positional candidate gene affecting variation in fat storage between two Drosophila melanogaster strains. Here, we first used quantitative complementation tests with dSdc mutants to confirm that natural variation in this gene affects variability in Drosophila fat storage. Next, we examined the effects of a viable dSdc mutant on Drosophila whole-body energy metabolism and associated traits. We observed that young flies homozygous for the dSdc mutation had reduced fat storage and slept longer than homozygous wild-type flies. They also displayed significantly reduced metabolic rate, lower expression of spargel (the Drosophila homologue of PGC-1), and reduced mitochondrial respiration. Compared to control flies, dSdc mutants had lower expression of brain insulin-like peptides, were less fecund, more sensitive to starvation, and had reduced life span. Finally, we tested for association between single nucleotide polymorphisms (SNPs) in the human SDC4 gene and variation in body composition, metabolism, glucose homeostasis, and sleep traits in a cohort of healthy early pubertal children. We found that SNP rs4599 was significantly associated with resting energy expenditure (P = 0.001 after Bonferroni correction) and nominally associated with fasting glucose levels (P = 0.01) and sleep duration (P = 0.044). On average, children homozygous for the minor allele had lower levels of glucose, higher resting energy expenditure, and slept shorter than children homozygous for the common allele. We also observed that SNP rs1981429 was nominally associated with lean tissue mass (P = 0.035) and intra-abdominal fat (P = 0.049), and SNP rs2267871 with insulin sensitivity (P = 0.037). Collectively, our results in Drosophila and humans argue that syndecan family members play a key role in the regulation of body metabolism. [ABSTRACT FROM AUTHOR]

Air pollution has consistently been associated with cardiometabolic outcomes, although associations with obesity have only been recently reported. Studies of air pollution and adiposity have mostly relied on body mass index (BMI) rather than body fat percentage (BF%), and most have not accounted for noise as a possible confounder. Additionally, it is unknown whether genetic predisposition for obesity increases susceptibility to the obesogenic effects of air pollution. To help fill these gaps, we used the UK Biobank, a large, prospective cohort study in the United Kingdom, to explore the relationship between air pollution and adiposity, and modification by a polygenic risk score for BMI. We used 2010 annual averages of air pollution estimates from land use regression (NO 2 , NO X , PM 2.5 , PM 2.5absorbance , PM 2.5-10 , PM 10), traffic intensity (TI), inverse distance to road (IDTR), along with examiner-measured BMI, waist-hip-ratio (WHR), and impedance measures of BF%, which were collected at enrollment (2006–2010, n = 473,026) and at follow-up (2012–2013, n = 19,518). We estimated associations of air pollution with BMI, WHR, and BF% at enrollment and follow-up, and with obesity, abdominal obesity, and BF%-obesity at enrollment and follow-up. We used linear and logistic regression and controlled for noise and other covariates. We also assessed interactions of air pollution with a polygenic risk score for BMI. On average, participants at enrollment were 56 years of age, 54% were female, and 32% had completed college or a higher degree. Almost all participants (~95%) were white. All air pollution measures except IDTR were positively associated with at least one continuous measure of adiposity at enrollment. However, NO 2 was negatively associated with BMI but positively associated with WHR at enrollment, and IDTR was also negatively associated with BMI. At follow-up (controlling for enrollment adiposity), we observed positive associations for PM 2.5-10 with BMI, PM 10 with BF%, and TI with BF% and BMI. Associations were similar for binary measures of adiposity, with minor differences for some pollutants. Associations of NO X , NO 2 , PM 2.5absorbance , PM 2.5 and PM 10 , with BMI at enrollment, but not at follow-up, were stronger among individuals with higher BMI polygenic risk scores (interaction p <0.05). In this large, prospective cohort, air pollution was associated with several measures of adiposity at enrollment and follow-up, and associations with adiposity at enrollment were modified by a polygenic risk score for obesity. [ABSTRACT FROM AUTHOR]