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AbstractCentral body fat distribution has been shown to be related to hyperinsulinemia, insulin resistance, hypertriglyceridemia, and atherosclerosis to a greater degree than general obesity. There are known to be both genetic and environmental effects on all components of this clustering. Whether these genetic effects are due to one set of genes in common to the components or whether genetic influences on insulin resistance and/or general/abdominal fatness 'turn on' other genes that affect other components of the syndrome is not clear. We analyzed data from the Swedish Adoption/Twin Study of Aging (60% female; monozygotic = 116, dizygotic = 202; average age 65 years) to determine whether there were genetic and/or environmental factors shared among general body fat distribution, abdominal body fat distribution, fasting insulin levels and cardiovascular disease. We found additive genetic effects in males to be significantly different from those in females with genetic effects accounting for variance in waist–hip ratio (males = 28%; females = 49%), body mass index (males = 58%; females = 73%), fasting insulin levels (FI) (males = 27%; females = 49%), and cardiovascular disease (CVD) (males = 18%; females = 37%). There were also shared genetic and environmental effects among all the variables except CVD, but a majority of the genetic variance for these measures was trait specific. Twin Research (2000) 3, 43–50.

Purpose. This study was conducted to develop a regression equation that accurately estimates body fat percentage using relatively easy and inexpensive methods that do not require women to remove clothing. Design. A cross-sectional design was employed. Setting. All data were collected at the University. Subjects. Subjects were 200 white women ages 20 to 65 years. The sample was equally distributed across four age groups, 20–29, 30–39, 40–49, and 50–65, and within each age group, one-third of the women were lean, one-third were of average weight, and one-third were obese. Measures. Subjects were hydrostatically weighed and participated in a variety of anthropometric and lifestyle assessments, including skinfolds, circumferences, and questionnaire responses. Results. The full regression model included six measures: hip circumference, triceps skinfold (observed and quadratic), age (quadratic), self-reported physical activity, and calf skinfold (quadratic). This equation accounted for 81 % of the variance in body weight measured by hydrostatic weighing (SEE = 3.5%). A simpler, five-variable equation was also formed that did not include the calf skinfold assessment (R2 = .800, SEE = 3.6%). Conclusions. The prediction equations in this study afford accurate and relatively easy and inexpensive means of estimating body fat percentage in a wide range of white women without having them remove their clothing.

AbstractLeg length in humans is considered to be an indicator of the long-term impact of quality of childhood living conditions and nutritional status. The main objective of this study was to evaluate the magnitude of association of percentage body fat (PBF) with relative subischial leg length (RSLL), adjusting for age, sex and body mass index (BMI), among adolescents and adults in a population of poor socioeconomic background in India. Data were taken from a cross-sectional study conducted in 2010–2014 among the Limbu community of Darjeeling, West Bengal – an indigenous community with poor socioeconomic background, low literacy rate, low income and inadequate living conditions. The study villages were located in the Himalayan and sub-Himalayan regions of Darjeeling. The present study sample comprised 97 adolescents aged 16–19 years (47 boys, 50 girls) and 260 adults aged 20–39 years (135 men, 125 women). Anthropometric measurements of stature/height (cm), weight (kg), sitting height (cm) and skinfold thicknesses (biceps, triceps, subscapular, suprailiac) (mm) were recorded. Derived variables were BMI (kg/m2), subischial leg length (SLL) (cm), RSLL (%), sum of four skinfolds (mm) and PBF (%). Significant sex differences at p<0.05 were observed for all anthropometric characteristics, except for body weight among adolescents and RSLL, subscapular and sum of four skinfolds in adults. The linear regression models adjusting for age and sex showed that RSLL had a negative relationship with PBF (p<0.05) among adolescents and adults. Higher body fat, independent of BMI, was correlated with lower RSLL among both adolescents and adults from the Limbu community, indicating a possible association with poor quality living conditions in childhood. However, this may also have been due to the allometry of total body fat with body proportions – a relatively larger trunk results in more body fat.

A genetic predisposition to higher waist-to-hip ratio adjusted for BMI (WHRadjBMI), a measure of body fat distribution, associates with increased risk for type 2 diabetes. We conducted an exome-wide association study of coding variation in UK Biobank (405,569 individuals) to identify variants that lower WHRadjBMI and protect against type 2 diabetes. We identified four variants in the gene ACVR1C (encoding the activin receptor-like kinase 7 receptor expressed on adipocytes and pancreatic β-cells), which independently associated with reduced WHRadjBMI: Asn150His (-0.09 SD, P = 3.4 × 10-17), Ile195Thr (-0.15 SD, P = 1.0 × 10-9), Ile482Val (-0.019 SD, P = 1.6 × 10-5), and rs72927479 (-0.035 SD, P = 2.6 × 10-12). Carriers of these variants exhibited reduced percent abdominal fat in DEXA imaging. Pooling across all four variants, a 0.2 SD decrease in WHRadjBMI through ACVR1C was associated with a 30% lower risk of type 2 diabetes (odds ratio [OR] 0.70, 95% CI 0.63, 0.77; P = 5.6 × 10-13). In an analysis of exome sequences from 55,516 individuals, carriers of predicted damaging variants in ACVR1C were at 54% lower risk of type 2 diabetes (OR 0.46, 95% CI 0.27, 0.81; P = 0.006). These findings indicate that variants predicted to lead to loss of ACVR1C gene function influence body fat distribution and protect from type 2 diabetes. ; This work was funded by the National Institutes of Health (R01 HL127564 to S.K.), which had no involvement in the design and conduct of the study; the collection, analysis, and interpretation of the data; or the preparation, review, and approval of the manuscript. This project was also conducted using the Type 2 Diabetes Knowledge Portal resource which is funded by the Accelerating Medicines Partnership. REGICOR study was supported by the Spanish Ministry of Economy and Innovation through the Carlos III Health Institute (Red Investigación Cardiovascular RD12/0042, PI09/90506), European Funds for Development (ERDF-FEDER), and by the Catalan Research andTechnology Innovation Interdepartmental Commission (2014SGR240). Samples for the Leicester cohort were collected as part of projects funded by the British Heart Foundation (British Heart Foundation Family Heart Study, RG2000010; UK Aneurysm Growth Study, CS/14/2/30841) and the National Institute for Health Research (NIHR Leicester Cardiovascular Biomedical Research Unit Biomedical Research Informatics Centre for Cardiovascular Science, IS_BRU_0211_20033). NJS is supported by the British Heart Foundation and is a NIHR Senior Investigator. The Munich MI Study is supported by the German Federal Ministry of Education and Research (BMBF) in the context of the e:Med program (e:AtheroSysMed) and the FP7 European Union project CVgenes@target (261123). Additional grants were received from the Fondation Leducq (CADgenomics: Understanding Coronary Artery Disease Genes, 12CVD02).This study was also supported through the Deutsche Forschungsgemeinschaft cluster of excellence Vascular Biology (ATVB) Study was supported by a grant from RFPS-2007-3-644382 and Programma di ricerca Regione-Università 2010-2012 Area 1–Strategic Programmes– Diabetes Page 30 of 53 30 Regione Emilia-Romagna. Funding for the exome-sequencing project (ESP) was provided by RC2 HL103010 (HeartGO), RC2 HL102923 (LungGO), and RC2 HL102924 (WHISP). Exome sequencing was performed through RC2 HL102925 (BroadGO) and RC2 HL102926 (SeattleGO). The JHS is supported by contracts HHSN268201300046C, HHSN268201300047C, HHSN268201300048C, HHSN268201300049C, HHSN268201300050C from the National Heart, Lung, and Blood Institute and the National Institute on Minority Health and Health Disparities. Dr. Wilson is supported by U54GM115428 from the National Institute of General Medical Sciences. Exome sequencing in ATVB, PROCARDIS, Ottawa, PROMIS, Southern German Myocardial Infarction Study, and the Jackson Heart Study was supported by 5U54HG003067 (to Dr. Gabriel).

Ministerio de Ciencia e Innovacion, Grant/Award Number: FJCI-2017-34967; Sixth Framework Programme, Grant/Award Number: 016181 FOOD ; This work was done as part of the IDEFICS study (www.idefics.eu). We gratefully acknowledge the financial support of the European Community within the Sixth RTD Framework Programme Contract No. 016181 (FOOD). ; Background Elevated cardiometabolic risk (CMR) is an important factor for cardiovascular diseases later in life while physical fitness seems to decrease CMR. Objective Thus, the aim of the present study is to assess the association between muscular fitness (MF) and cardiorespiratory fitness (CRF) on CMR in European children, both cross-sectional and longitudinally. Methods A total of 289 children (49.5% males) from eight European countries, aged 6 to 9, with longitudinal information on blood pressure, triglycerides, total cholesterol, HDL-cholesterol, homoeostasis model assessment, body mass index, data on fitness level, objectively measured physical activity (PA), diet quality, and total screen time were included. A CMR score was calculated and dichotomized. MF and CRF were also dichotomized. Cross-sectional and longitudinal multilevel logistic regressions adjusting for lifestyle behaviours were performed. Results Reaching a high level of MF during childhood as well as remaining in that level over-time were associated with an 82% and 62% lower probability of high CMR at follow-up, respectively. Also, children who became top CRF over time, showed a 77% lower probability (P < 0.05) of being in the highest CMR quartile at follow-up, independently of sociodemographic and lifestyle indicators. Conclusions A high MF at early childhood and during childhood reduces the odds of having CMR. Same occurs with the improvement of CRF during childhood. These findings highlight the importance of enhancing fitness to avoid CMR already in children. ; Instituto de Salud Carlos III Spanish Government European Commission FJCI-2017-34967 ; European Commission 016181 FOOD