Quebec Family Study Research Articles

Mechanical efficiency: associations with body composition and glycemic profile in healthy adults.

The aim of this study was to assess the association between net mechanical efficiency (NME) and body composition and glycemic profile, in middle-aged (38.3 ± 14.3years) participants from the Quebec Family Study (QFS). Analyses were completed on a sample of 605 participants (271 males and 334 females) who performed a submaximal exercise test on an ergometer consisting of three consecutive 6-min workloads at increasing intensity during which respiratory gas exchange was assessed. The calculation of NME [power output/ (vO2-vO2seated before exercise)] was based on the values of the last 3min of the first workload at a targeted power output of 30W. Correlations between NME and dependent variables were computed separately in males and females. Associations between NME and body composition and glucose-insulin variables were assessed by comparing groups of subjects categorized in sex-specific tertiles of NME after adjustments for age. Significant negative correlations were observed between NME and body composition and glycemic profile in both sexes. Comparison across tertiles showed that individuals with high NME displayed more favorable adiposity and glycemic profiles. These differences remained significant after further adjustments for participation in vigorous physical activity, cardiorespiratory fitness, and mean exercise respiratory exchange ratio whereas most differences in glucose-insulin variables became non-significant after further adjustment for percent body fat. QFS familial data indicate that the heritability of NME reaches about 30%. In conclusion, the results of this study show that beyond aerobic fitness and physical activity-participation, mechanical efficiency is an additional activity-related variable that is independently associated with variations in body composition and glycemic profile.

Effects of sodium intake and cardiorespiratory fitness on body composition and genetic susceptibility to obesity: results from the Quebec Family Study.

The main aim of this study was to evaluate the effects of Na intake and cardiorespiratory fitness (CRF) on body composition. The study was also intended to assess whether Na intake and/or CRF mediate the genetic susceptibility to obesity. Analyses were performed on a sample of 526 adult participants from the Quebec Family Study for whom a complete data set was available for nutrient and energy intake, CRF and body composition variables. The effects of Na, CRF and their interaction were analysed by comparing sex-specific tertiles using general linear mixed models. In both males and females, we observed a significant effect of Na intake and CRF on all body composition variables. However, in females only, we found that the effect of Na intake on body composition variables varies according to CRF level such that high Na intake was associated with increased body fatness, but only in females with low CRF. This interaction effect remained significant after statistical adjustment for total sugar, fat and energy intake. Using mediation analysis, we also found Na intake and CRF to be significant mediators of the relationship between a polygenic risk score of obesity based on > 500000 genetic variants and BMI or waist circumference. In conclusion, the current study shows that Na intake influences body composition via mechanisms that interact with aerobic fitness, especially in females. Furthermore, both Na intake and CRF seem to be involved in the expression of the genetic susceptibility to obesity.

Dietary Mediators of the Genetic Susceptibility to Obesity—Results from the Quebec Family Study

BackgroundRecent 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. ObjectiveThis 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. MethodsThis 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. ResultsThe 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. ConclusionsThe 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.

The fit-active profile to better reflect the benefits of a lifelong vigorous physical activity participation: mini-review of literature and population data.

Physical activity is favourably considered for its effect on metabolic fitness and body composition. This observation is generally supported by observational studies and is concordant with endurance-trained individuals' metabolic and morphological profiles. However, in some contexts, the measurement of physical activity habits may not provide an adequate representation of its benefits. In this paper, we review relevant literature on the respective effects of fitness and physical activity on anthropometric and metabolic variables and the informative potential of a classification based on aerobic fitness and activity indicators. The relevance to defining a profile based on both fitness and activity is reinforced by data from the Quebec Family Study showing that, in both men and women, "fit-active" individuals displayed a much more favourable morphological and metabolic profile than "unfit-inactive" individuals. Moreover, these benefits seemed to be more related to variations in fitness than in physical activity. In summary, evidence suggests that a profile combining information on aerobic fitness and physical activity may better reflect the lifelong impact of physical activity on body composition and health. Novelty: The fit-active profile better reflects the long-term benefits of vigorous physical activity participation on health. The reported benefits seem to be more related to variations in aerobic fitness than to those in physical activity.

The Challenge of Stratifying Obesity: Attempts in the Quebec Family Study.

Background and aims: Obesity is a major health problem worldwide. Given the heterogeneous obesity phenotype, an optimal obesity stratification would improve clinical management. Since obesity has a strong genetic component, we aimed to develop a polygenic risk score (PRS) to stratify obesity according to the genetic background of the individuals. Methods: A total of 231 single nucleotide polymorphisms (SNP) significantly associated to body mass index (BMI) from 21 genome-wide association studies were genotyped or imputed in 881 subjects from the Quebec Family Study (QFS). The population was randomly split into discovery (80%; n = 704) and validation (20%; n = 177) samples with similar obesity (BMI ≥ 30) prevalence (27.8% and 28.2%, respectively). Family-based associations with obesity were tested for every SNP in the discovery sample and a weighed and continuous PRS231 was constructed. Generalized linear mixed effects models were used to test the association of PRS231 with obesity in the QFS discovery sample and validated in the QFS replication sample. Furthermore, the Fatty Acid Sensor (FAS) Study (n = 141; 27.7% obesity prevalence) was used as an independent sample to replicate the results. Results: The linear trend test demonstrated a significant association of PRS231 with obesity in the QFS discovery sample (ORtrend = 1.19 [95% CI, 1.14-1.24]; P = 2.0x10-16). We also found that the obesity prevalence was significantly greater in the higher PRS231 quintiles compared to the lowest quintile. Significant and consistent results were obtained in the QFS validation sample for both the linear trend test (ORtrend = 1.16 [95% CI, 1.07-1.26]; P = 6.7x10-4), and obesity prevalence across quintiles. These results were partially replicated in the FAS sample (ORtrend = 1.12 [95% CI, 1.02-1.24]; P = 2.2x10-2). PRS231 explained 7.5%, 3.2%, and 1.2% of BMI variance in QFS discovery, QFS validation, and FAS samples, respectively. Conclusions: These results revealed that genetic background in the form of a 231 BMI-associated PRS has a significant impact on obesity, but a limited potential to accurately stratify it. Further studies are encouraged on larger populations.

The role of eating behavior traits in mediating genetic susceptibility to obesity

Genome-wide association studies (GWASs) have identified several genes associated with obesity. The mechanisms through which these genes affect body weight are not fully characterized. Recent studies suggest that eating behavior (EB) traits could be involved, but only a few EB traits were investigated. This study aimed to investigate whether genetic susceptibility to obesity is mediated by EB traits (cognitive restraint, disinhibition, hunger) and their subscales. We hypothesized that EB traits, and their subscales, partly mediate this association. Adult individuals (n=768) who participated in the Quebec Family Study were included in this cross-sectional study. A genetic risk score (GRS) of obesity was calculated based on the 97 genetic variants recently identified in a GWAS meta-analysis of body mass index (BMI). EB traits and their subscales were assessed with the use of the Three-Factor Eating Questionnaire. Regression analyses with age and sex as covariates were used to investigate the associations between GRS, EB traits, BMI, and WC and whether the association between GRS and obesity is mediated by EB traits, which represents the indirect effect of GRS on obesity. The GRS of obesity was positively associated with BMI (β=0.19±0.04, P<0.0001) and WC (β=0.46±0.10, P<0.0001). Regression analyses also revealed that the association between GRS of obesity and BMI was partly mediated by disinhibition and susceptibility to hunger (βindirect=0.09±0.03, P=0.0007, and βindirect=0.04±0.02, P=0.02, respectively). Habitual and situational susceptibility to disinhibition (βindirect=0.08±0.03, P=0.002 and βindirect=0.05±0.02, P=0.003, respectively) as well as internal and external locus of hunger (βindirect=0.03±0.02, P=0.03 for both) were also found to mediate the association between GRS of obesity and BMI. The same trends were observed with WC. The results of this study indicate that the genetic susceptibility to obesity is partly mediated through undesirable EB traits, which suggests that they could be targeted in obesity treatment and prevention. This trial was registered at clinicaltrials.gov as NCT03355729.

Fine Mapping of the Body Fat QTL on Human Chromosome 1q43.

IntroductionEvidence for linkage and association of obesity-related quantitative traits to chromosome 1q43 has been reported in the Quebec Family Study (QFS) and in populations of Caribbean Hispanic ancestries yet no specific candidate locus has been replicated to date.MethodsUsing a set of 1,902 single nucleotide polymorphisms (SNPs) genotyped in 525 African American (AA) and 391 European American (EA) women enrolled in the NIEHS uterine fibroid study (NIEHS-UFS), we generated a fine association map for the body mass index (BMI) across a 2.3 megabase-long interval delimited by RGS7 (regulator of G-protein signaling 7) and PLD5 (Phospholipase D, member 5). Multivariable-adjusted linear regression models were fitted to the data to evaluate the association in race-stratified analyses and meta-analysis.ResultsThe strongest associations were observed in a recessive genetic model and peaked in the 3’ end of RGS7 at intronic rs261802 variant in the AA group (p = 1.0 x 10−4) and in meta-analysis of AA and EA samples (p = 9.0 x 10−5). In the EA group, moderate associations peaked at rs6429264 (p = 2.0 x 10−3) in the 2 Kb upstream sequence of RGS7. In the reference populations for the European ancestry in the 1,000 genomes project, rs6429264 occurs in strong linkage disequilibrium (D’ = 0.94) with rs1341467, the strongest candidate SNP for total body fat in QFS that failed genotyping in the present study. Additionally we report moderate associations at the 3’ end of PLD5 in meta-analysis (3.2 x 10−4 ≤ p ≤ 5.8 x 10−4).ConclusionWe report replication data suggesting that RGS7, a gene abundantly expressed in the brain, might be a putative body fat QTL on human chromosome 1q43. Future genetic and functional studies are required to substantiate our observations and to potentially link them to the neurobehavioral phenotypes associated with the RGS7 region.

Estimating genetic effect sizes under joint disease-endophenotype models in presence of gene-environment interactions.

Effects of genetic variants on the risk of complex diseases estimated from association studies are typically small. Nonetheless, variants may have important effects in presence of specific levels of environmental exposures, and when a trait related to the disease (endophenotype) is either normal or impaired. We propose polytomous and transition models to represent the relationship between disease, endophenotype, genotype and environmental exposure in family studies. Model coefficients were estimated using generalized estimating equations and were used to derive gene-environment interaction effects and genotype effects at specific levels of exposure. In a simulation study, estimates of the effect of a genetic variant were substantially higher when both an endophenotype and an environmental exposure modifying the variant effect were taken into account, particularly under transition models, compared to the alternative of ignoring the endophenotype. Illustration of the proposed modeling with the metabolic syndrome, abdominal obesity, physical activity and polymorphisms in the NOX3 gene in the Quebec Family Study revealed that the positive association of the A allele of rs1375713 with the metabolic syndrome at high levels of physical activity was only detectable in subjects without abdominal obesity, illustrating the importance of taking into account the abdominal obesity endophenotype in this analysis.

Workplace standing time and the incidence of obesity and type 2 diabetes: a longitudinal study in adults.

BackgroundIt is increasingly recognized that standing represents a simple solution to extended periods of sitting. However, it is currently unknown whether workplace standing time is prospectively associated with a lower incidence of chronic diseases. The objective of this study was to examine the association between workplace standing time and the incidence of overweight/obesity (OW/OB) and impaired glucose tolerance/type 2 diabetes (IGT/T2D) in adults.MethodsA longitudinal analysis from the Quebec Family Study (Canada) was conducted on 293 participants, aged 18 to 65 years, followed for a mean of 6 years. Information on self-reported occupational standing time as well as several covariates was collected at both baseline and follow-up. Outcome measures included the development of OW/OB (i.e. body mass index ≥25 kg/m2) and IGT/T2D (i.e. 2-h postload plasma glucose level ≥7.8 mmol/L).ResultsThe incidence rates of OW/OB and IGT/T2D over the 6-year follow-up period were 17.4% and 12.6%, respectively. Significant negative associations were observed between the amount of occupational standing time and the development of outcome measures. However, the associations were no longer significant after adjustment for age, sex, smoking habits, total annual family income, daily caloric intake, and submaximal working capacity. In age- and sex-adjusted logistic regression analysis, significant negative linear trends were observed across levels of standing time and the outcome variables. However, the associations were no longer significant after further adjustment for the other covariates. Finally, we observed that the change in standing time from baseline to year 6 was significantly associated with the development of outcome measures, with higher incidence rates in adults reporting a reduction in standing time at follow-up. However, the associations became non-significant after adjustment for covariates.ConclusionsGreater occupational standing time is not sufficient in and of itself to prevent the development of OW/OB and IGT/T2D in adults. Future efforts are needed to better understand the potential benefits of higher amounts of standing time throughout the day on the prevention of chronic diseases.

Interaction between Common Genetic Variants and Total Fat Intake on Low-Density Lipoprotein Peak Particle Diameter: A Genome-Wide Association Study

Background/Aim: Total fat intake has an important impact on the low-density lipoprotein (LDL) peak particle diameter (LDL-PPD) and may interact with nutrient-sensitive single nucleotide polymorphisms (SNPs). The objective was to examine whether there is suggestive evidence of SNP × dietary fat intake interaction effects influencing the LDL-PPD in the Quebec Family Study (QFS) in order to generate hypotheses to be tested in larger studies. Methods: SNPs from a genome-wide association study (GWAS) using Illumina Human610-Quad BeadChip, total fat intake derived from a 3-day weighted food record, and SNP × total fat intake interaction effects were examined on LDL-PPD in 541 QFS subjects. Results: The GWAS analyses 29 identified independent SNP × total fat intake interaction effects on the LDL-PPD at p < 10^-5, including SNPs in the following genes: ABCG2, CPA3, FNBP1, KCNQ3, NBAS, NCALD, OPRL1, NKAIN2, SH3BGRL2, SOX5, and SUSD4. Conclusions: This observational study suggests that multiple SNPs interact with dietary fat intake to influence variation in the LDL-PPD.

Findings from the Quebec Family Study on the Etiology of Obesity: Genetics and Environmental Highlights

The Quebec Family Study (QFS) was an observational study with three cycles of data collection between 1979 and 2002 in Quebec City, Canada. The cohort is a mixture of random sampling and ascertainment through obese individuals. The study has significantly contributed to our understanding of the determinants of obesity and associated disease risk over the past 35 years. In particular, the QFS cohort was used to investigate the contribution of familial resemblance and genetic effects on body fatness and behaviors related to energy balance. Significant familial aggregation and genetic heritability were reported for total adiposity, fat-free mass, subcutaneous fat distribution, abdominal and visceral fat, resting metabolic rate, physical activity level and other behavioral traits. The resources of QFS were also used to study the contribution of several nontraditional (non-caloric) risk factors as predictors of excess body weight and gains in weight and adiposity over time, including low calcium and micronutrient intake, high disinhibition eating behavior trait, and short sleep duration. An important finding relates to the interactions between dietary macronutrient intake and exercise intensity on body mass and adiposity.Electronic supplementary materialThe online version of this article (doi:10.1007/s13679-013-0086-3) contains supplementary material, which is available to authorized users.

Short sleep duration as a risk factor for the development of the metabolic syndrome in adults

ObjectiveThe objective of this study was to investigate the association between self-reported sleep duration and the incidence of features of the metabolic syndrome in adults. MethodsA longitudinal analysis from the Quebec Family Study (Canada) was conducted on 293 participants, aged 18 to 65years, followed for a mean of 6years (until 2001). Participants were categorized as short (≤6h), adequate (7–8h) or long (≥9h) sleepers. The metabolic syndrome was defined according to the American Heart Association/National Heart, Lung, and Blood Institute's criteria. The hypertriglyceridemic waist phenotype was defined as high waist circumference (≥90cm in men and ≥85cm in women) combined with high fasting triglyceride level (≥2.0mmol/L in men and ≥1.5mmol/L in women). ResultsThe incidence rates of metabolic syndrome and hypertriglyceridemic waist phenotype were 9.9% and 7.5%, respectively. Short sleepers were significantly more at risk of developing the metabolic syndrome (relative risk (RR): 1.74; 95% confidence interval (CI): 1.05–2.72) and the hypertriglyceridemic waist phenotype (RR: 1.82; 95% CI: 1.16–2.79), compared to those sleeping 7 to 8h per night after adjusting for covariates. However, long sleep duration was not associated with an increased risk of developing the metabolic syndrome or the hypertriglyceridemic waist phenotype (either unadjusted or adjusted models). ConclusionShort sleep duration is associated with an increased risk of developing features of the metabolic syndrome in adults.

Seven to Eight Hours of Sleep a Night Is Associated with a Lower Prevalence of the Metabolic Syndrome and Reduced Overall Cardiometabolic Risk in Adults

BackgroundPrevious studies looking at the relationship between sleep duration and the metabolic syndrome have only used a dichotomous approach (presence/absence) and failed to adjust for important confounding factors. The objective of the present study was to examine the association between self-reported sleep duration and features of the metabolic syndrome in adults.MethodsA cross-sectional analysis from the Quebec Family Study (Canada) was conducted on 810 participants aged 18 to 65 years. Participants were categorized as short (≤6 h), adequate (7–8 h) or long (≥9 h) sleepers. The metabolic syndrome was defined according to the American Heart Association/National Heart, Lung, and Blood Institute’s criteria.ResultsOverall, 24.6% of the sample had the metabolic syndrome. A U-shaped relationship between sleep duration and the prevalence of metabolic syndrome (33.3%, 22.0% and 28.8% in short, adequate and long sleepers, respectively) was observed (P<0.01). Only short sleepers had a significant increase in the odds of having the metabolic syndrome (OR = 1.76, 95% CI = 1.08–2.84) compared to adequate sleepers after adjustment for age, sex, smoking habits, highest education level, total annual family income, alcohol consumption, coffee intake, menopausal status, daily caloric intake, and moderate-to-vigorous physical activity. Likewise, the clustered cardiometabolic risk score (i.e. continuous risk score based on the metabolic syndrome components) was significantly higher in short sleepers compared to adequate sleepers after adjustment for covariates (P<0.05).ConclusionSleeping ≤6 h per night is associated with an elevated cardiometabolic risk score and an increase in the odds of having the metabolic syndrome after adjusting for possible confounders. These results strongly suggest that short sleep duration is a risk factor for the metabolic syndrome.

Sedentary Behaviour, Visceral Fat Accumulation and Cardiometabolic Risk in Adults: A 6-Year Longitudinal Study from the Quebec Family Study

BackgroundSedentary behaviour has recently emerged as a unique risk factor for chronic disease morbidity and mortality. One factor that may explain this relationship is visceral adiposity, which is prospectively associated with increased cardiometabolic risk and mortality. The objective of the present study was to determine whether sedentary behaviour was associated with increased accumulation of visceral fat or other deleterious changes in cardiometabolic risk over a 6-year follow-up period among adult participants in the Quebec Family Study.MethodsThe current study included 123 men and 153 women between the ages of 18 and 65. Total sedentary time and physical activity were assessed by self-report questionnaire. Cross-sectional areas of visceral and subcutaneous abdominal adipose tissue were assessed using computed tomography. Cardiometabolic biomarkers including fasting insulin, glucose, blood lipids, HOMA-Insulin Resistance, and oral glucose tolerance were also measured. All variables of interest were collected at both baseline and follow-up.ResultsAfter adjustment for age, sex, baseline BMI, physical activity, energy intake, smoking, education, income and menopausal status, baseline sedentary behaviour was not associated with changes in visceral adiposity or any other marker of cardiometabolic risk. In the longitudinal model which adjusted for all studied covariates, every 15-minute increase in sedentary behaviour from baseline to follow-up was associated with a 0.13 cm increase in waist circumference (95% CI = 0.02, 0.25). However, there was no association between changes in sedentary behaviour and changes in visceral adiposity or other markers of cardiometabolic risk.ConclusionThese results suggest that neither baseline sedentary behaviour nor changes in sedentary behaviour are associated with longitudinal changes in visceral adiposity in adult men and women. With the exception of waist circumference, the present study did not find evidence of a relationship between sedentary behaviour and any marker of cardiometabolic risk in this population.

A variant in the LRRFIP1 gene is associated with adiposity and inflammation

Inflammation is an important factor linking abdominal obesity with insulin resistance and related cardiometabolic risk. A genome-wide association study of adiposity-related traits performed in the Quebec Family Study (QFS) revealed that a single-nucleotide polymorphism (SNP) in the LRRFIP1 gene (rs11680012) was associated with abdominal adiposity (P = 4.6 × 10(-6)). The objective of this study was to assess the relationship between polymorphisms in LRRFIP1 gene and adiposity (BMI, fat mass (FM), waist circumference (WC), and computed tomography-derived areas of total, subcutaneous and visceral abdominal adipose tissue) and markers of inflammation (C-reactive protein (CRP) and interleukin-6 (IL-6)). Using Sequenom, 16 tag SNPs in the LRRFIP1 gene, capturing 78% of the genetic variation, were genotyped in 926 participants of the QFS. Eight SNPs (rs7575941, rs3769053, rs11689421, rs3820808, rs11680012, rs3806505, rs6739130, and rs11686141) showed evidence of association with at least two adiposity phenotypes and plasma levels of one marker of inflammation. The strongest evidence of association was observed with rs11680012, which explained 1.8-3.4% of the variance in areas of abdominal adiposity and 2.0% of the variation in CRP levels. Carriers of the rare allele of rs11680012 had ≈ 30% more abdominal adiposity (P values between 2.7 × 10(-4) and 3.8 × 10(-6)) and 75% higher CRP levels (P = 1.6 × 10(-4)) than the common allele in age and sex adjusted data. Rs11680012 is a G/C SNP converting an arginine into a threonine and this amino acid substitution may potentially alter exonic splicing. This gene may therefore represent a potential interesting target to investigate in further functional studies on adiposity and inflammation.

Association between olfactory receptor genes, eating behavior traits and adiposity: Results from the Quebec Family Study

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.

THE ASSOCIATION BETWEEN SHORT SLEEP DURATION AND WEIGHT GAIN IS DEPENDENT ON DISINHIBITED EATING BEHAVIOR IN ADULTS

STUDY OBJECTIVE To investigate whether the relationship between short sleep duration and subsequent body weight gain is influenced by disinhibited eating behavior. DESIGN Six-year longitudinal study. SETTING Community setting. PARTICIPANTS Two hundred seventy-six adults aged 21 to 64 years from the Quebec Family Study. MEASUREMENTS AND RESULTS Body composition measurements, self-reported sleep duration, and disinhibition eating behavior trait (Three-Factor Eating Questionnaire) were determined at both baseline and after 6 years. For each sleep-duration group (short- [≤6 h] average, [7-8 h], and long- [≥9 h] duration sleepers), differences in weight gain and waist circumference were tested by comparing the lowest (score ≤ 3) versus the highest (score ≥ 6) disinhibition eating behavior tertiles using analysis of covariance, with adjustment for potential confounding factors. Individuals having both short sleep duration and high disinhibition eating behavior were more likely to gain weight and increase their abdominal circumference over time (P<0.05); however, short-duration sleepers having a low disinhibition eating behavior trait were not more likely to increase their adiposity indicators than were average-duration sleepers. Over the 6-year follow-up period, the incidence of overweight/obesity for short-duration sleepers with a high disinhibition eating behavior trait was 2.5 times more frequent than for short-duration sleepers with a low disinhibition eating behavior trait. Energy intake was significantly higher in short-duration sleepers with a high disinhibition eating behavior trait (P<0.05 versus all other groups). CONCLUSIONS We observed that having a high disinhibition eating behavior trait significantly increased the risk of overeating and gaining weight in adults characterized by short sleep duration. This observation is novel and might explain the interindividual differences in weight gain associated with short sleep duration.

Short sleep duration preferentially increases abdominal adiposity in adults: preliminary evidence.

What is already known about this subject • The evidence that short sleep duration is another determinant of obesity is accumulating. • Lack of sleep has been reported to constitute a metabolic stressor, with increased cortisol concentrations as the end product. What this study adds • This is the first study to show that short sleep duration is associated with a preferential increase in abdominal adiposity in adults. The aim of this 6-year longitudinal study was to verify whether short sleep duration preferentially increases abdominal adiposity in adults. A total of 276 adults, aged 18-64 years, from the Quebec Family Study were available for this study. Anthropometric measurements (body mass index and waist circumference), self-reported sleep duration and several covariates were assessed. A regression equation derived from the changes in body mass index and waist circumference of normal- and long-duration sleepers (reference category, ≥ 7 h of sleep per night, n = 233) was used to predict the change in waist circumference of short-duration sleepers (≤6 h of sleep per night, n = 43). Additionally, the influence of sleep duration on waist circumference changes was modelled by using linear regression in both sleep duration groups, adjusting for changes in body mass index and other covariates. We observed that measured (actual) changes in waist circumference were significantly greater than predicted changes (mean ± SEM: 3.41 ± 0.53 vs. 2.69 ± 0.51 cm, respectively, P < 0.05), implying that short-duration sleepers had an excess of abdominal fat accumulation over the 6-year follow-up period. After controlling for the changes in total adiposity as measured by body mass index, only short-duration sleepers gained more abdominal adiposity over 6 years. The present study provides evidence that short sleep duration is associated with preferential increases in abdominal adiposity in adults. This finding is of particular concern because abdominal adiposity is correlated with a number of metabolic anomalies.

Short sleep duration as a cause of obesity: myth or reality?

Short sleep duration as a <i>cause</i> of obesity: myth or reality?

Contributions of Cardiorespiratory Fitness and Visceral Adiposity to Six-Year Changes in Cardiometabolic Risk Markers in Apparently Healthy Men and Women

Both excess visceral adipose tissue (VAT) and low cardiorespiratory fitness (CRF) levels are associated with a deteriorated cardiometabolic risk profile. The aim of the study was to examine the respective contributions of changes in VAT accumulation vs. changes in CRF to 6-yr longitudinal changes in cardiometabolic risk markers. We conducted a prospective, population-based study with an average follow-up of 5.9 ± 0.8 yr. We followed 132 middle-aged participants from the Quebec Family Study (mean age, 35.3 ± 13.9 yr). VAT was measured by computed tomography, whereas the level of CRF was assessed by a submaximal physical working capacity test at baseline and at follow-up. A complete cardiometabolic risk profile, including systolic and diastolic blood pressure, fasting glucose and insulin levels, C-reactive protein (n = 72), as well as a standard lipoprotein-lipid profile, was obtained at baseline and at follow-up. We measured changes in CRF, VAT, and cardiometabolic risk profile over 6 yr. After adjusting for age and sex, 6-yr changes in VAT were negatively correlated with changes in CRF (r = -0.38; P < 0.001). In a multivariate model that included age, sex, changes in VAT, changes in CRF, as well as baseline levels of the above cardiometabolic risk factors, 6-yr changes in VAT were the most important predictor of the change in the metabolic syndrome score (R(2) = 13.2%; P < 0.001). Adding 6-yr changes in CRF levels significantly improved the predictability of the model (R(2) = 19.7%; P = 0.002). Changes in both VAT and CRF levels observed over 6 yr are associated with changes in parameters of the lipoprotein-lipid profile, glucose-insulin homeostasis, and inflammatory markers. Thus, maintaining a low level of VAT and a high level of CRF are important targets for maintenance of cardiometabolic health.