Showing papers by "Claude Bouchard published in 2011"
TL;DR: It is estimated that daily occupation-related energy expenditure has decreased by more than 100 calories, and this reduction in energy expenditure accounts for a significant portion of the increase in mean U.S. body weights for women and men over the last 50 years.
Abstract: Background The true causes of the obesity epidemic are not well understood and there are few longitudinal population-based data published examining this issue The objective of this analysis was to examine trends in occupational physical activity during the past 5 decades and explore how these trends relate to concurrent changes in body weight in the US Methodology/Principal Findings Analysis of energy expenditure for occupations in US private industry since 1960 using data from the US Bureau of Labor Statistics Mean body weight was derived from the US National Health and Nutrition Examination Surveys (NHANES) In the early 1960's almost half the jobs in private industry in the US required at least moderate intensity physical activity whereas now less than 20% demand this level of energy expenditure Since 1960 the estimated mean daily energy expenditure due to work related physical activity has dropped by more than 100 calories in both women and men Energy balance model predicted weights based on change in occupation-related daily energy expenditure since 1960 for each NHANES examination period closely matched the actual change in weight for 40–50 year old men and women For example from 1960–62 to 2003–06 we estimated that the occupation-related daily energy expenditure decreased by 142 calories in men Given a baseline weight of 769 kg in 1960–02, we estimated that a 142 calories reduction would result in an increase in mean weight to 897 kg, which closely matched the mean NHANES weight of 918 kg in 2003–06 The results were similar for women Conclusion Over the last 50 years in the US we estimate that daily occupation-related energy expenditure has decreased by more than 100 calories, and this reduction in energy expenditure accounts for a significant portion of the increase in mean US body weights for women and men
1,111 citations
TL;DR: Sex differences, and in some instances race differences, in the relationships between anthropometry and fat‐specific depots demonstrate that these characteristics need to be considered when predicting adiposity from WC or BMI.
Abstract: The purpose of this study was to examine sex and race differences in the relationship between anthropometric measurements and adiposity in white and African-American (AA) adults Visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) areas were measured with computed tomography (CT) Fat mass (FM) was measured with dual-energy-X-ray absorptiometry (DXA) Correlation coefficients were used to assess the relationship of waist circumference (WC) and BMI to VAT, SAT, and FM within sex-by-race groups General linear models were used to compare relationships between WC or BMI, and adiposity across sex and race, within age groups (18–39 and 40–64 years) The sample included 1,667 adults (men: 489 white; 120 AA; women: 666 white, 392 AA) WC and BMI correlations were highest for FM and SAT compared to VAT Women had higher FM levels than men regardless of WC, but the sex difference in FM was attenuated in younger AA adults with a high BMI For a given level of WC or BMI, women had higher levels of SAT than men; however, significant interactions indicated that the relationship was not consistent across all levels of BMI and WC Sex and race differences in VAT varied significantly with WC and BMI In general, white adults had higher levels of VAT than AA adults at higher levels of BMI and WC Sex differences, and in some instances race differences, in the relationships between anthropometry and fat-specific depots demonstrate that these characteristics need to be considered when predicting adiposity from WC or BMI
461 citations
Medical Research Council1, Harvard University2, Lund University3, University of Minnesota4, Duke University5, University of Oulu6, Novo Nordisk7, Technische Universität München8, University College London9, University of Lausanne10, University of Eastern Finland11, National University of Singapore12, King's College London13, University of Bristol14, George Washington University15, National Institutes of Health16, University of Bergen17, University of Michigan18, University of North Carolina at Chapel Hill19, University of Groningen20, Utrecht University21, University of Copenhagen22, Erasmus University Rotterdam23, University of Tübingen24, Harokopio University25, Washington University in St. Louis26, University of Maryland, Baltimore27, University of Granada28, Complutense University of Madrid29, University of Turku30, University of Southern Denmark31, Umeå University32, University of Gothenburg33, Laval University34, University of London35, Pennington Biomedical Research Center36, Lille University of Science and Technology37, Newcastle University38, University of Iceland39, Danube University Krems40, Broad Institute41, University of California, Los Angeles42, Hammersmith Hospital43, University of Cambridge44, National Institute for Health and Welfare45
TL;DR: In this paper, a meta-analysis of data from 45 studies of adults and nine studies of children and adolescents was conducted to confirm or refute unambiguously whether physical activity attenuates the association of FTO with obesity risk.
Abstract: Background: The FTO gene harbors the strongest known susceptibility locus for obesity. While many individual studies have suggested that physical activity (PA) may attenuate the effect of FTO on obesity risk, other studies have not been able to confirm this interaction. To confirm or refute unambiguously whether PA attenuates the association of FTO with obesity risk, we meta-analyzed data from 45 studies of adults (n=218,166) and nine studies of children and adolescents (n=19,268). Methods and Findings: All studies identified to have data on the FTO rs9939609 variant (or any proxy [r(2)>0.8]) and PA were invited to participate, regardless of ethnicity or age of the participants. PA was standardized by categorizing it into a dichotomous variable (physically inactive versus active) in each study. Overall, 25% of adults and 13% of children were categorized as inactive. Interaction analyses were performed within each study by including the FTOxPA interaction term in an additive model, adjusting for age and sex. Subsequently, random effects meta-analysis was used to pool the interaction terms. In adults, the minor (A-) allele of rs9939609 increased the odds of obesity by 1.23-fold/allele (95% CI 1.20-1.26), but PA attenuated this effect (p(interaction) = 0.001). More specifically, the minor allele of rs9939609 increased the odds of obesity less in the physically active group (odds ratio = 1.22/allele, 95% CI 1.19-1.25) than in the inactive group (odds ratio = 1.30/allele, 95% CI 1.24-1.36). No such interaction was found in children and adolescents. Conclusions: The association of the FTO risk allele with the odds of obesity is attenuated by 27% in physically active adults, highlighting the importance of PA in particular in those genetically predisposed to obesity.
447 citations
TL;DR: These genomic predictors of the response of Vo(2max) to regular exercise provide new targets for the study of the biology of fitness and its adaptation to regular Exercise.
Abstract: Low cardiorespiratory fitness is a powerful predictor of morbidity and cardiovascular mortality. In 473 sedentary adults, all whites, from 99 families of the Health, Risk Factors, Exercise Training...
360 citations
TL;DR: This analysis provides a comprehensive map of the transcriptomic features important for aerobic exercise-induced improvements in maximal oxygen consumption and found that both the TRT and a homologous subset of the human high responder genes were regulated to a greater degree in high respondser rodent skeletal muscle.
Abstract: The molecular pathways that are activated and contribute to physiological remodeling of skeletal muscle in response to endurance exercise have not been fully characterized. We previously reported that ∼800 gene transcripts are regulated following 6 wk of supervised endurance training in young sedentary males, referred to as the training-responsive transcriptome (TRT) (Timmons JA et al. J Appl Physiol 108: 1487–1496, 2010). Here we utilized this database together with data on biological variation in muscle adaptation to aerobic endurance training in both humans and a novel out-bred rodent model to study the potential regulatory molecules that coordinate this complex network of genes. We identified three DNA sequences representing RUNX1, SOX9, and PAX3 transcription factor binding sites as overrepresented in the TRT. In turn, miRNA profiling indicated that several miRNAs targeting RUNX1, SOX9, and PAX3 were downregulated by endurance training. The TRT was then examined by contrasting subjects who demonstrated the least vs. the greatest improvement in aerobic capacity (low vs. high responders), and at least 100 of the 800 TRT genes were differentially regulated, thus suggesting regulation of these genes may be important for improving aerobic capacity. In high responders, proangiogenic and tissue developmental networks emerged as key candidates for coordinating tissue aerobic adaptation. Beyond RNA-level validation there were several DNA variants that associated with maximal aerobic capacity (Vo2max) trainability in the HERITAGE Family Study but these did not pass conservative Bonferroni adjustment. In addition, in a rat model selected across 10 generations for high aerobic training responsiveness, we found that both the TRT and a homologous subset of the human high responder genes were regulated to a greater degree in high responder rodent skeletal muscle. This analysis provides a comprehensive map of the transcriptomic features important for aerobic exercise-induced improvements in maximal oxygen consumption.
233 citations
TL;DR: The role of genetic variation and gene-exercise interactions in the biology of adaptation to exercise and the ability to identify the favorable responders for given physiological properties to a given exercise regimen are focused on.
Abstract: This article is devoted to the role of genetic variation and gene-exercise interactions in the biology of adaptation to exercise. There is evidence from genetic epidemiology research that DNA sequence differences contribute to human variation in physical activity level, cardiorespiratory fitness in the untrained state, cardiovascular and metabolic response to acute exercise, and responsiveness to regular exercise. Methodological and technological advances have made it possible to undertake the molecular dissection of the genetic component of complex, multifactorial traits, such as those of interest to exercise biology, in terms of tissue expression profile, genes, and allelic variants. The evidence from animal models and human studies is considered. Data on candidate genes, genome-wide linkage results, genome-wide association findings, expression arrays, and combinations of these approaches are reviewed. Combining transcriptomic and genomic technologies has been shown to be more powerful as evidenced by the development of a recent molecular predictor of the ability to increase VO2max with exercise training. For exercise as a behavior and physiological fitness as a state to be major players in public health policies will require that the role of human individuality and the influence of DNA sequence differences be understood. Likewise, progress in the use of exercise in therapeutic medicine will depend to a large extent on our ability to identify the favorable responders for given physiological properties to a given exercise regimen.
141 citations
TL;DR: Having a high disinhibition eating behavior trait significantly increased the risk of overeating and gaining weight in adults characterized by short sleep duration, and might explain the interindividual differences in weight gain associated with shortSleep duration.
Abstract: 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.
100 citations
TL;DR: The optimal BMI and WC thresholds approximated currently used thresholds in men and in white women and there are no apparent ethnic differences in men; however, in AA women the optimal weight and waist circumference values are ∼3 kg/m2 and 5 cm higher than inwhite women.
Abstract: BMI and waist circumference (WC) are used to identify individuals with elevated obesity-related health risks. The current thresholds were derived largely in populations of European origin. This study determined optimal BMI and WC thresholds for the identification of cardiometabolic risk among white and African-American (AA) adults. The sample included 2096 white women, 1789 AA women, 1948 white men, and 643 AA men aged 18-64 years. Elevated cardiometabolic risk was defined as ≥2 risk factors (blood pressure ≥ 130/85 mm Hg; glucose ≥100 mg/dl; triglycerides ≥150 mg/dl; high-density lipoprotein-cholesterol <40 mg/dl (men) or <50 mg/dl (women)). Receiver Operating Characteristic (ROC) curves were used to identify optimal BMI and WC thresholds in each sex-by-ethnicity group. The optimal BMI thresholds were 30 kg/m2 in white women, 32.9 kg/m2 in AA women, 29.1 kg/m2 white men, and 30.4 kg/m2 in AA men, whereas optimal WC thresholds were 91.9 cm in white women, 96.8 cm in AA women, 99.4 in white men, and 99.1 cm in AA men. The sensitivities at the optimal thresholds ranged from 63.5 to 68.5% for BMI and 68.4 to 71.0% for WC and the specificities ranged from 64.2 to 68.8% for BMI and from 68.5 to 71.0% for WC, respectively. In general, the optimal BMI and WC thresholds approximated currently used thresholds in men and in white women. There are no apparent ethnic differences in men; however, in AA women the optimal BMI and WC values are ~3 kg/m2 and 5 cm higher than in white women.
96 citations
TL;DR: No evidence is found that obesity-risk SNPs in FTO or other obesity candidate genes derived from genome-wide association studies are associated with maximum weight loss or weight regain over 6 years of follow-up in bariatric surgery patients.
Abstract: Associations of markers in 11 obesity candidate genes with maximal weight loss and weight regain in the SOS bariatric surgery cases
93 citations
TL;DR: Evidence continues to be strong for a role of gene-exercise interaction effects on the improvement in insulin sensitivity after exposure to regular exercise.
Abstract: This review of the exercise genomics literature emphasizes the strongest articles published in 2010 as defined by sample size, quality of phenotype measurements, quality of the exercise program or physical activity exposure, study design, adjustment for multiple testing, quality of genotyping, and other related study characteristics. One study on voluntary running wheel behavior was performed in 448 mice from 41 inbred strains. Several quantitative trait loci for running distance, speed, and duration were identified. Several studies on the alpha-3 actinin (ACTN3) R577X nonsense polymorphism and the angiotensin-converting enzyme (ACE) I/D polymorphism were reported with no clear evidence for a joint effect, but the studies were generally underpowered. Skeletal muscle RNA abundance at baseline for 29 transcripts and 11 single nucleotide polymorphisms (SNPs) were both found to be predictive of the V?O2max response to exercise training in one report from multiple laboratories. None of the 50 loci associated with adiposity traits are known to influence physical activity behavior. However, physical activity seems to reduce the obesity-promoting effects of at least 12 of these loci. Evidence continues to be strong for a role of gene-exercise interaction effects on the improvement in insulin sensitivity after exposure to regular exercise. SNPs in the cAMP-responsive element binding position 1 (CREB1) gene were associated with training-induced HR response, in the C-reactive protein (CRP) gene with training-induced changes in left ventricular mass, and in the methylenetetrahydrofolate reductase (MTHFR) gene with carotid stiffness in low-fit individuals. We conclude that progress is being made but that high-quality research designs and replication studies with large sample sizes are urgently needed.
81 citations
TL;DR: It is concluded that Ad36 offers a novel tool to understand the pathways to improve hyperglycemia and hepatic steatosis independently of proximal insulin signaling, and despite a HF diet.
Abstract: Drugs that improve chronic hyperglycemia independently of insulin signaling or reduction of adiposity or dietary fat intake may be highly desirable. Ad36, a human adenovirus, promotes glucose uptake in vitro independently of adiposity or proximal insulin signaling. We tested the ability of Ad36 to improve glycemic control in vivo and determined if the natural Ad36 infection in humans is associated with better glycemic control. C57BL/6J mice fed a chow diet or made diabetic with a high-fat (HF) diet were mock infected or infected with Ad36 or adenovirus Ad2 as a control for infection. Postinfection (pi), systemic glycemic control, hepatic lipid content, and cell signaling in tissues pertinent to glucose metabolism were determined. Next, sera of 1,507 adults and children were screened for Ad36 antibodies as an indicator of past natural infection. In chow-fed mice, Ad36 significantly improved glycemic control for 12 wk pi. In HF-fed mice, Ad36 improved glycemic control and hepatic steatosis up to 20 wk pi. In adipose tissue (AT), skeletal muscle (SM), and liver, Ad36 upregulated distal insulin signaling without recruiting the proximal insulin signaling. Cell signaling suggested that Ad36 increases AT and SM glucose uptake and reduces hepatic glucose release. In humans, Ad36 infection predicted better glycemic control and lower hepatic lipid content independently of age, sex, or adiposity. We conclude that Ad36 offers a novel tool to understand the pathways to improve hyperglycemia and hepatic steatosis independently of proximal insulin signaling, and despite a HF diet. This metabolic engineering by Ad36 appears relevant to humans for developing more practical and effective antidiabetic approaches.
TL;DR: The issues of statistical power, the usefulness of hypothesis-free approaches such as in genome-wide association explorations, the necessity of expanding the research beyond common DNA variants, the advantage of combining transcriptomics with genomics, and the complexities inherent to the search for links between genotype and phenotype in exercise genomics research are focused on.
Abstract: This commentary focuses on the issues of statistical power, the usefulness of hypothesis-free approaches such as in genome-wide association explorations, the necessity of expanding the research beyond common DNA variants, the advantage of combining transcriptomics with genomics, and the complexities inherent to the search for links between genotype and phenotype in exercise genomics research.
TL;DR: In contrast with adverse risk with high trunk adiposity, high leg adiposity is associated with a decreased risk of having two or more cardiometabolic risk factors in both African American and white adults.
Abstract: OBJECTIVE To determine contributions of trunk and extremity adiposity to cardiometabolic risk factors (blood pressure, fasting blood glucose, HDL cholesterol, and triglycerides) among white and African American adults. RESEARCH DESIGN AND METHODS The sample consisted of 1,129 white women, 779 African American women, 1,012 white men, and 300 African American men. RESULTS Higher trunk adiposity was significantly associated with an increased risk of having two or more cardiometabolic risk factors among African American and white men and women. After adjustment for trunk and arm adiposity, higher leg adiposity was significantly associated with a decreased risk of having two or more cardiometabolic risk factors among white men and women and African American women. CONCLUSIONS In contrast with adverse risk with high trunk adiposity, high leg adiposity is associated with a decreased risk of having two or more cardiometabolic risk factors in both African American and white adults.
TL;DR: 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, indicating that maintaining a low level of VAT and a high level of CRF are important targets for maintenance of cardiometabolic health.
Abstract: Longitudinal data suggest that individuals who increased their visceral adiposity and who decreased their cardiorespiratory fitness over time experienced the most detrimental changes in their cardiometabolic risk profile.
TL;DR: In this article, the authors investigated whether the relationship between short sleep duration and subsequent body weight gain is influenced by disinhibited eating behavior, and found that having a high disinhibition eating behavior trait significantly increased the risk of overeating and gaining weight.
TL;DR: SNP in the CETP, LIPC, and LPL loci contribute significantly to plasma HDL-C levels in obese individuals, and the associations persist even after considerable weight loss due to bariatric surgery, however, they are not associated with surgery-induced changes in HDL- C levels.
Abstract: Single nucleotide polymorphisms in CETP, LIPC, and LPL contribute to HDL in cholesterol in the obese, even after weight loss, but are not associated with surgery-induced changes in HDL in cholesterol
TL;DR: Individuals with an increased waist circumference had higher exercise systolic blood pressure compared with individuals with low waist circumference, irrespective of their level of insulin resistance or level of cardiorespiratory fitness.
Abstract: Individuals with insulin resistance and low cardiorespiratory fitness are frequently found to have an increased waist circumference and high exercise blood pressure We tested the hypothesis that the relationships among insulin resistance, low cardiorespiratory fitness, and increased exercise blood pressure may be mediated by an elevated waist circumference This study included 317 apparently healthy men and women (mean age: 348±128 years; mean body mass index: 261±52 kg/m 2 ) Exercise blood pressure values were measured using a submaximal ergometer test evaluating physical working capacity Plasma insulin and glucose levels were measured during a 3-hour oral glucose tolerance test Multivariate regression analyses showed that waist circumference accounted for 328% ( P P P P
TL;DR: The evidence that short sleep duration is another determinant of obesity is accumulating and Lack of sleep has been reported to constitute a metabolic stressor, with increased cortisol concentrations as the end product.
Abstract: What is already known about this subject
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The evidence that short sleep duration is another determinant of obesity is accumulating.
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Lack of sleep has been reported to constitute a metabolic stressor, with increased cortisol concentrations as the end product.
What this study adds
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This is the first study to show that short sleep duration is associated with a preferential increase in abdominal adiposity in adults.
Summary
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.
TL;DR: It is concluded that common variants of MSTN and CKM genes do not play a role in attaining high‐level endurance performance in Caucasian populations.
Abstract: Maximal oxygen uptake (VO2max) is one of the most important determinants of elite endurance performance. VO2max is determined by a whole range of genetic and environmental factors. Single nucleotide polymorphisms (SNPs) in muscle myostatin (MSTN) and creatine kinase (CKM) genes are candidates for VO2max and skeletal muscle performance phenotypes. Common MSTN (rs3791783, rs11681628 and rs7570532) and CKM (rs344816, rs10410448, rs432979, rs1133190, rs7260359, rs7260463 and rs4884) SNPs, selected from HapMap CEU data in order to tag the genetic variability of the proteins, were genotyped in 316 male Caucasian elite endurance athletes and 304 sedentary controls from the Genathlete study. Association with elite endurance performance was determined by logistic regression analysis. The P-value for statistical significance was set at <0.01. None of the SNPs or haplotypes showed a significant association with elite endurance status. We conclude that common variants of MSTN and CKM genes do not play a role in attaining high-level endurance performance in Caucasian populations.
TL;DR: Fat-free mass in obese people contributed little to the treadmill performance potential as assessed by the Max(dur), although the contribution of fat-freemass was positive in thinner people.
TL;DR: The data suggest that abdominal SAT is not protective against unfavorable cardiometabolic risk profiles, consistent across ethnic groups.
Abstract: Abdominal adiposity depots are correlates of adverse cardiometabolic risk factors in Caucasian and African-American adults
TL;DR: It is suggested that dietary fat intake may modify the effect of the FASN rs4246444 polymorphism on LDL-PPD, a small, dense LDL phenotype associated with an increased cardiovascular disease risk and a potential therapeutic target for obesity and insulin resistance.
Abstract: Background: The small, dense LDL phenotype is associated with an increased cardiovascular disease risk. A genome-wide scan performed on the Quebec Family Study (QFS) revealed a quantitative trait locus for LDL peak particle diameter (LDL-PPD) on the 17q21 region. A positional candidate gene – the fatty acid synthase gene (FASN) – encodes a key enzyme in the biogenesis of membrane lipids. FASN may play a role in the regulation of feeding and may be a potential therapeutic target for obesity and insulin resistance. Methods: Analyses were performed on 592 subjects of the QFS. Dietary fat was estimated by a 3-day food record. LDL-PPD was measured by gradient gel electrophoresis on polyacrylamide gradient gels. Results: Five single nucleotide polymorphisms were genotyped in FASN gene. FASN rs4246444 was associated with LDL-PPD, but only when fat intake was taken into account (p = 0.001). High and low lipid consumers were defined using a cutoff of 35% of dietary fat intake. Carriers of the variant allele showed smaller LDL-PPD only when consuming a high amount of fat. This association remained significant after adjustments for age, sex, body mass index and plasma triglyceride levels. Conclusion: The results suggest that dietary fat intake may modify the effect of the FASN rs4246444 polymorphism on LDL-PPD.
TL;DR: Results from a large, biethnic sample of men and women found a FM–FFM relationship very close to that originally described by Forbes, absent of significant variability by ethnicity or sex.
Abstract: The model developed by Forbes (1987) of how body fat mass (FM) and fat-free mass (FFM) change during periods of weight loss or gain (Δ body weight (BW)) assumed that they change in relationship to a constant C = 10·4, where ΔFFM/ΔBW = 10·4/(10·4+FM). Forbes derived C based on aggregated, cross-sectional data from a small sample of women. The objective of the present study was to reanalyse the relationship described by Forbes and to explore whether this relationship is consistent across ethnicity and sex groups using cross-sectional data from a large sample of white and African-American men and women. Baseline data from white and African-American men and women aged 18-60 years, who participated in a clinical study at the Pennington Biomedical Research Center since 2001 and who underwent dual-energy X-ray absorptiometry scans, were available for analysis. To overcome differences in BMI distributions among the ethnicity-by-sex groups, a stratified random sample of participants was selected within each group such that numbers in each BMI category ( < 25, 25-29·9, 30-34·9, 35-39·9, 40+ kg/m2) were proportional to those within the group with the smallest sample size, yielding a sample of 1953 individuals. Linear regression models assessed the FM-FFM relationship across the four ethnicity-by-sex groups. The FM-FFM relationship varied little by ethnicity (P = 0·57) or by sex (P = 0·26). The constant describing the FM-FFM relationship was estimated to be 9·7 (95 % CI 9·0, 10·3). In conclusion, results from our large, biethnic sample of men and women found a FM-FFM relationship very close to that originally described by Forbes, absent of significant variability by ethnicity or sex.
TL;DR: It was found that SNPs in these candidate genes did not modify the association between baseline fitness or BMI and risk of hypertension in CARDIA participants.
Abstract: The association of single nucleotide polymorphisms (SNPs) from seven candidate genes, including genotype-by-baseline fitness and genotype-by-baseline body mass index (BMI) interactions, with incident hypertension over 20 years was investigated in 2663 participants (1301 blacks, 1362 whites) of the Coronary Artery Risk Development in Young Adults Study (CARDIA). Baseline cardiorespiratory fitness was determined from duration of a modified Balke treadmill test. A total of 98 SNPs in blacks and 89 SNPs in whites from seven candidate genes were genotyped. Participants that became hypertensive (295 blacks and 146 whites) had significantly higher blood pressure and BMI (both races), and lower fitness (blacks only) at baseline than those who remained normotensive. Markers at the peroxisome proliferative activated receptor gamma coactivator 1α (PPARGC1A) and bradykinin β2 receptor (BDKRB2) genes were nominally associated with greater risk of hypertension, although one marker each at the BDKRB2 and endothelial nitric oxide synthase-3 (NOS3) genes were nominally associated with lower risk. The association of baseline fitness with risk of hypertension was nominally modified by genotype at markers within the angiotensin converting enzyme, angiotensinogen, BDKRB2 and NOS3 genes in blacks and the BDKRB2, endothelin-1 and PPARGC1A genes in whites. BDKRB2 rs4900318 showed nominal interactions with baseline fitness on the risk of hypertension in both races. The association of baseline BMI with risk of hypertension was nominally modified by GNB3 rs2301339 genotype in whites. None of the above associations were statistically significant after correcting for multiple testing. We found that SNPs in these candidate genes did not modify the association between baseline fitness or BMI and risk of hypertension in CARDIA participants.
TL;DR: Adults with elevated metabolic risk have greater IMT than those with normal risk in normal-weight, overweight, low WC, and high WC, but not significant for overweight or moderate WC categories.
Abstract: Background: Carotid artery intima-media thickness (IMT) is greater in adults with elevated metabolic risk profiles. However, the influence of body mass index (BMI) or waist circumference (WC) on the relationship between IMT and metabolic risk is unclear. Methods: Adults from the Bogalusa Heart Study were classified as normal weight, overweight, or obese and into WC categories (men, low <94 cm, moderate 94–101.9 cm, high ≥102 cm; women, low <80 cm, moderate 80–87.9 cm, high ≥88 cm). Elevated metabolic risk was defined by cardiovascular risk factor clustering (≥2 abnormal risk factors or insulin resistance (upper quartile of homeostasis model of insulin resistance). Carotid ultrasound measurements were obtained and mean IMT was calculated. General linear models compared IMT between elevated versus normal metabolic risk groups, adjusting for sex, age, race/ethnicity, and either BMI or WC category. Results: Adults were 24–43 years of age (n = 991) and 41% had elevated metabolic risk (42% male, 28% Af...
TL;DR: It is suggested that LRP8 gene polymorphisms influence plasma cholesterol levels as well as size and composition of LDL particles, which are associated with an increased cardiovascular disease risk.
TL;DR: These studies strongly suggest that genomic markers can be used to identify high- and low-responders to regular exercise, but additional research is needed to confirm these findings, to maximize the predictive power of genomic markers in all ethnic groups, and to develop strategies on how to deal with low- and non- responders before predictive genomic markers are ready for clinical use.
Abstract: Both observational studies and randomized, controlled interventions have shown that regular physical activity provides several health benefits. Although exercise programs improve risk factor profiles on average, a substantial body of evidence indicates that there are considerable inter-individual differences in response to these programs. Ability to predict who will be a high- or low-responder to exercise would be desirable from a physiologic and clinical perspective. The first exercise training studies utilizing objective genome-wide screening methods were published in 2010, and both reports identified a group of genes and DNA sequence variants that explained a considerable portion of variance in VO2max training response. These studies strongly suggest that genomic markers can be used to identify high- and low-responders to regular exercise. However, additional research is needed to confirm these findings, to maximize the predictive power of genomic markers in all ethnic groups, and to develop strategies on how to deal with low- and non-responders before predictive genomic markers are ready for clinical use.
01 Jan 2011