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Background: Recent studies showed that eating behaviors such as disinhibition, emotional and external eating, and snacking mediate genetic susceptibility to obesity. It remains unknown if diet quality and intake of specific food groups also mediate the genetic susceptibility to obesity.Objective: This study aimed to assess if diet quality and intakes of specific food groups mediate the association between a polygenic risk score (PRS) for BMI and BMI and waist circumference (WC). We hypothesized that poor diet quality, high intakes of energy-dense food groups, and low intakes of nutrient-dense food groups mediate the genetic susceptibility to obesity.Methods: This cross-sectional study included 750 participants (56.3% women, aged 41.5 ± 14.9 y, BMI 27.8 ± 7.5 kg/m2) from the Quebec Family Study. A PRSBMI based on >500,000 genetic variants was calculated using LDpred2. Dietary intakes were assessed with a 3-d food record from which a diet quality score (i.e. Nutrient Rich Food Index 6.3) and food groups were derived. Mediation analyses were conducted using a regression-based and bootstrapping approach.Results: The PRSBMI explained 25.7% and 19.8% of the variance in BMI and WC, respectively. The association between PRSBMI and BMI was partly mediated by poor diet quality (β = 0.33 ± 0.12; 95% CI: 0.13, 0.60), high intakes of fat and high-fat foods (β = 0.46 ± 0.16; 95% CI: 0.19, 0.79) and sugar-sweetened beverages (β = 0.25 ± 0.14; 95% CI: 0.05, 0.60), and low intakes of vegetables (β = 0.15 ± 0.08; 95% CI: 0.03, 0.32), fruits (β = 0.37 ± 0.12; 95% CI: 0.17, 0.64), and dairy products (β = 0.17 ± 0.09; 95% CI: 0.02, 0.37). The same trends were observed for WC.Conclusions: The genetic susceptibility to obesity was partly mediated by poor diet quality and intakes of specific food groups. These results suggest that improvement in diet quality may reduce obesity risk among individuals with high genetic susceptibility and emphasize the need to intervene on diet quality among these individuals. [ABSTRACT FROM AUTHOR]

Eating behaviour traits of rigid control and disinhibition have been associated with body weight in both adults and adolescents. Moreover, adults reporting a dieting history have increased levels of unhealthy eating behaviours. Against this background, the present study aimed to examine the relationship between dieting history and eating behaviour traits in adolescents. For the purpose of this research, a total of sixty adolescents (aged 15 (sem 2·4) years) from the Québec Family Study completed the Three-Factor Eating Questionnaire (TFEQ) and a questionnaire regarding eating habits. Self-reported current and past dieting were analysed against eating behaviour traits measured by the TFEQ, including all subscales. As the results revealed, few adolescents reported currently dieting (n 3). Adolescents who reported a dieting history (23·3 %) were older (16·9 v. 14·4 years, P < 0·001), were more likely to be female (78·6 v. 41·3 %, P < 0·05) but did not have a significantly higher BMI z-score (1·5 v. 0·9, P = 0·10), although they were more likely to be either overweight or obese (P < 0·01). After correcting for sex, BMI and age, adolescents who reported a dieting history had higher levels of rigid control and disinhibition (P < 0·05–0·0001) than those reporting no dieting history. A greater proportion of adolescents characterised by high rigid control and high disinhibition were past dieters, compared to those characterised by low levels of both behaviour traits (53 v. 4 %). The study arrived at the following conclusions: as observed in adults, adolescents with a history of dieting present unfavourable eating behaviour traits. These behavioural traits may represent an additional challenge to the long-term regulation of body weight. [ABSTRACT FROM PUBLISHER]

The aim of this study was to determine the independent contribution of previously reported risk factors for adult overweight and obesity. A cross-sectional (n = 537) and a longitudinal (n = 283; 6-year follow-up period) analysis was performed for nine risk factors for overweight and obesity assessed in adult participants (aged 18–64 years) of the Quebec Family Study (QFS). The main outcome measure was overweight/obesity, defined as a BMI ≥25 kg/m2. Using logistic regression analysis adjusted for age, sex, and socioeconomic status, short sleep duration, high disinhibition eating behavior, low dietary calcium intake, high susceptibility to hunger behavior, nonparticipation in high-intensity physical exercise, high dietary restraint behavior, nonconsumption of multivitamin and dietary supplements, high dietary lipid intake, and high alcohol intake were all significantly associated with overweight and obesity in the cross-sectional sample. The analysis of covariance adjusted for age, socioeconomic status, and all other risk factors revealed that only individuals characterized by short sleep duration, high disinhibition eating behavior, and low dietary calcium intake had significantly higher BMI compared to the reference category in both sexes. Over the 6-year follow-up period, short-duration sleepers, low calcium consumers, and those with a high disinhibition and restraint eating behavior score were significantly more likely to gain weight and develop obesity. These results show that excess body weight or weight gain results from a number of obesogenic behaviors that have received considerable attention over the past decade. They also indicate that the four factors, which have the best predictive potential of variations in BMI, be it in a cross-sectional or a longitudinal analytical design, do not have a “caloric value” per se. [ABSTRACT FROM AUTHOR]

OBJECTIVE--A genome-wide association study conducted by the Wellcome Trust Case Control Consortium recently associated single nucleotide polymorphisms (SNPs) in the FTO (fatso/ fat mass and obesity associated) gene with type 2 diabetes. These associations were shown to be mediated by obesity. Other research groups found similar results in Europeans and Hispanics but not African Americans. The mechanism by which FTO influences obesity and type 2 diabetes is currently unknown. The present study investigated the role of two FTO SNPs (rs17817449 and rs1421085) in adiposity, insulin sensitivity, and body weight regulation, including energy intake and expenditure. RESEARCH DESIGN AND METHODS--We genotyped 908 individuals from the Quebec City metropolitan area that participated in the Quebec Family Study, a long-term study of extensively phenotyped individuals designed to investigate factors involved in adiposity. RESULTS--We found significant associations for both SNPs with several obesity-related phenotypes. In particular, rs17817449 was associated with BMI (P = 0.0014), weight (P = 0.0059), and waist circumference (P = 0.0021) under an additive model. In addition, this FTO SNP influenced fasting insulin (P = 0.011), homeostasis model assessment of insulin resistance (P = 0.038), and an insulin sensitivity index derived from an oral glucose tolerance test (P = 0.0091). Associations were also found with resting metabolic rate (RMR) (P = 0.042) and plasma leptin levels (P = 0.036). Adjustment for BMI abolished the associations with insulin sensitivity, RMR, and plasma leptin levels. CONCLUSIONS--These results confirm that genetic variation at the FTO locus contributes to the etiology of obesity, insulin resistance, and increased plasma leptin levels. [ABSTRACT FROM AUTHOR]

The article discusses a study which explored the associations between short sleep duration and reduced leptin levels and increased adiposity in men and women in Québec. The age of the subjects ranges from 21 to 64 years old. The adjusted odds ratio for overweight/obesity among adults who sleep 9 to 10 hours per day was 1.38 and 1.69 for those with 5 to 6 hours of sleep. Short sleep duration may indicate an increased risk of being overweight/obese in adults.

Abstract: Objective: To examine the long-term relationship between sleep duration and type 2 diabetes or impaired glucose tolerance (IGT). Methods: Body composition measurements and self-reported sleep duration were determined in a longitudinal sample of 276 individuals aged 21 to 64 years followed for a mean of 6 years. Risk factors of type 2 diabetes/IGT over the follow-up were determined and relative risks (RRs) calculated for the development of type 2 diabetes/IGT by sleep duration group. Results: Independent risk factors of type 2 diabetes/IGT over the follow-up included age, obesity, sleep duration, and glucose/insulin homeostasis indicators. Using adults with 7-8h of sleep as a reference, the adjusted RR for the development of type 2 diabetes/IGT was 2.78 (1.61-4.12) for those with ⩽6h of sleep and 2.54 (1.42-3.53) for those with ⩾9h of sleep. These elevated RRs remained significant after adjustment for body mass index, waist circumference or percent body fat. Conclusion: Short and long sleeping times are associated with a higher risk of developing type 2 diabetes/IGT, independent of several covariates. These results suggest that sleep duration may represent a novel risk factor for type 2 diabetes/IGT. [Copyright &y& Elsevier]

Abstract: Obesity is a major health problem that can be influenced by eating behaviors. Evidence suggests that the sensory properties of food influence eating behaviors and lead to overeating and overweight. A previous genome-wide linkage scan for eating behavior traits assessed with the Three-Factor Eating Questionnaire (cognitive dietary restraint, disinhibition and hunger) performed in the Quebec Family Study (QFS) revealed a quantitative trait locus for disinhibition on chromosome 19p13. This region encodes a cluster of seven olfactory receptor (OR) genes, including OR7D4, previously associated with odor perceptions. Direct sequencing of the OR7D4 gene revealed 16 sequence variants. Nine OR7D4 sequence variants with minor allele frequency (MAF)>1% as well as 100 SNPs spanning the cluster of OR genes on 19p13 were tested for association with age- and sex-adjusted eating behaviors as well as adiposity traits in 890 subjects. One OR7D4 sequence variant (rs2878329 G>A) showed evidence of association with reduced levels of adiposity (p=0.03), cognitive dietary restraint (p=0.05) and susceptibility to hunger (p=0.008). None of the OR7D4 SNPs was associated with disinhibition, but a SNP (rs2240927) in another OR gene (OR7E24) showed evidence of association (p=0.03). Another SNP in the OR7G3 gene (rs10414255) was also found to be associated with adiposity and eating behaviors. These results are the first to suggest that variations in human olfactory receptor genes can influence eating behaviors and adiposity. The associations reported in the present study should be interpreted with caution considering the number of tests performed and considered as potential new hypotheses about the effects OR polymorphisms on eating behaviors and obesity that need to be further explored in other populations. [Copyright &y& Elsevier]

Abstract: Background. The small, dense LDL phenotype is associated with an increased cardiovascular disease risk. A genome-wide scan performed on 236 nuclear families of the Quebec Family Study (QFS) revealed a QTL for LDL-peak particle size (LDL-PPD) on the 17q21 region. Three positional candidates were identified in this region according to their implication in the phosphoinositide (PI) cycle: the myotubularin-related protein 4 (MTMR4), the phospholipase C, delta 3 (PLCD3), and the diacylglycerol kinase E (DGKE) genes. Objectives. To test the association between MTMR4, PLCD3, and DGKE gene polymorphisms, LDL-PPD and plasma lipid parameters. Methods. Analyses were performed on 680 subjects of QFS. LDL-PPD was measured by gradient gel electrophoresis on non-denaturating 2–16% polyacrylamide gradient gels. Direct sequencing was performed to identify genetic variations within these genes. Results. The c.-754G>C, c.183G>A, and c.579C>A DGKE SNPs were significantly associated with higher plasma triglyceride levels (p =0.029, p =0.008, p =0.001, respectively). The c.508C>G and c.890T>G MTMR4 polymorphisms were associated with plasma total-cholesterol concentrations (p =0.02, p =0.02, respectively), while no association was observed with PLCD3 gene polymorphisms. Conclusion. The c.579C>A DGKE gene polymorphism is associated with plasma triglyceride levels, while MTMR4 SNPs seem to predict variations in plasma cholesterol levels. [Copyright &y& Elsevier]