Absence of Adolescent Obesity in Grenada: Is This a Generational Effect?

Background: Low- and middle-income countries are affected disproportionately by the ongoing global obesity pandemic. Representing a middle income country, the high prevalence of obesity among Grenadian adults as compared to US adults is expected as part of global obesity trends. The objective of this study was to determine if Grenadian adolescents have a higher prevalence of overweight compared to their US counterparts, and if a disparity exists between urban and rural adolescents.Methods: Using a subcohort of participants in the Grenadian Nutrition Student Survey, diet quality and anthropometric measures were collected from 55% of the classrooms of first year secondary students in Grenada (n = 639). Rural or urban designations were given to each school. Body Mass Index (BMI) was calculated and categorized as overweight or obese for each student following CDC classification cutoffs. A standardized BMI (BMIz) was calculated for each school. Sex-specific BMI and overall BMIz were compared to a 1980s US cohort. Multilevel models, overall and stratified by sex, of students nested within schools were conducted to determine if BMIz differed by rural or urban locality, gender, and diet quality.Results: The mean age of this cohort was 12.7 (SD = 0.8) years with 83.8% of the cohort identifying as Afro-Caribbean. Females had nearly twice the prevalence of overweight when compared to males (22.7 vs. 12.2%) but a similar prevalence of obesity (8.2 vs. 6.8%). Grenadian adolescents had lower prevalence of overweight (females: 22.7 vs. 44.7%; males: 12.2 vs. 38.8%, respectively) as compared to US counterparts. Eating a traditional diet was negatively associated with BMIz score among females (β^ = −0.395; SE = 0.123) in a stratified, multilevel analysis. BMIz scores did not differ significantly by rural or urban school designation.Conclusions: Among Grenadian adolescents, this study identified a lower overweight prevalence compared to US counterparts and no difference in overweight prevalence by urban or rural location. We hypothesize that the late introduction of processed foods to Grenada protected this cohort from obesogenic promoters due to a lack of fetal overnutrition. However, further research in subsequent birth cohorts is needed to determine if adolescent obesity will increase due to a generational effect

Associations of Body Size and Composition with Physical Activity in Adolescent Girls

To examine whether components of body composition (size, fat mass, and fat-free mass) were related to physical activity

Validity of self-reported leisure-time sedentary behavior in adolescents

<p>Abstract</p> <p>Background</p> <p>To evaluate the concordance between leisure-time sedentary behavior in adolescents assessed by an activity-based questionnaire and accelerometry.</p> <p>A convenience sample of 128 girls and 73 boys, 11-15 years of age (12.6 ± 1.1 years) from six states across the United States examined as part of the feasibility studies for the Trial of Activity in Adolescent Girls (TAAG). Three days of self-reported time spent watching TV/videos, using computers, playing video/computer games, and talking on the phone was assessed using a modified version of the Self-Administered Physical Activity Checklist (SAPAC). Criterion measure of sedentary behavior was via accelerometry over three days using a cut point of < 50 counts · 30 sec^-1epoch. Comparisons between sedentary behavior by the two instruments were made.</p> <p>Results</p> <p>Adolescents generally underestimated minutes of sedentary behavior compared to accelerometry-measured minutes. The overall correlation between minutes of sedentary behavior by self-report and accelerometry was weak (Spearman r = 0.14; 95% CI 0.05, 0.23). Adjustment of sedentary minutes of behavior for total minutes assessed using either percentages or the residuals method tended to increase correlations slightly. However, regression analyses showed no significant association between self-reported sedentary behavior and minutes of sedentary behavior captured via accelerometry.</p> <p>Discussion</p> <p>These findings suggest that the modified 3-day Self-Administered Physical Activity Checklist is not a reliable method for assessing sedentary behavior. It is recommended that until validation studies for self-report instruments of sedentary behavior demonstrate validity, objective measures should be used.</p

Role of Nicotine Dependence on the Relationship between Variants in the Nicotinic Receptor Genes and Risk of Lung Adenocarcinoma

<div><p>Several variations in the nicotinic receptor genes have been identified to be associated with both lung cancer risk and smoking in the genome-wide association (GWA) studies. However, the relationships among these three factors (genetic variants, nicotine dependence, and lung cancer) remain unclear. In an attempt to elucidate these relationships, we applied mediation analysis to quantify the impact of nicotine dependence on the association between the nicotinic receptor genetic variants and lung adenocarcinoma risk. We evaluated 23 single nucleotide polymorphisms (SNPs) in the five nicotinic receptor related genes (<i>CHRNB3, CHRNA6, and CHRNA5/A3/B4</i>) previously reported to be associated with lung cancer risk and smoking behavior and 14 SNPs in the four ‘control’ genes (<i>TERT</i>, <i>CLPTM1L, CYP1A1</i>, and <i>TP53</i>), which were not reported in the smoking GWA studies. A total of 661 lung adenocarcinoma cases and 1,347 controls with a smoking history, obtained from the Environment and Genetics in Lung Cancer Etiology case-control study, were included in the study. Results show that nicotine dependence is a mediator of the association between lung adenocarcinoma and gene variations in the regions of <i>CHRNA5/A3/B4</i> and accounts for approximately 15% of this relationship. The top two <i>CHRNA3</i> SNPs associated with the risk for lung adenocarcinoma were rs1051730 and rs12914385 (p-value = 1.9×10⁻¹⁰ and 1.1×10⁻¹⁰, respectively). Also, these two SNPs had significant indirect effects on lung adenocarcinoma risk through nicotine dependence (p = 0.003 and 0.007). Gene variations rs2736100 and rs2853676 in <i>TERT</i> and rs401681 and rs31489 in <i>CLPTM1L</i> had significant direct associations on lung adenocarcinoma without indirect effects through nicotine dependence. Our findings suggest that nicotine dependence plays an important role between genetic variants in the <i>CHRNA5/A3/B4</i> region, especially <i>CHRNA3,</i> and lung adenocarcinoma. This may provide valuable information for understanding the pathogenesis of lung adenocarcinoma and for conducting personalized smoking cessation interventions.</p></div

Participants’ characteristics by disease status.

1<p>t-test for continuous variables and chi-square test for categorical variables.</p>2<p>measured using the Fagerstrom Test, with a score range of 0 to 10. Higher scores indicated greater nicotine dependence. SD: standard deviation.</p><p>Participants’ characteristics by disease status.</p

Role of nicotine dependence on the association between SNPs and lung adenocarcinoma (ADC) risk.

<p>The SNP associated with lung ADC risk are (1a) total effect without mediator, (1b) indirect-only effect, and (1c) with mediator. <b><i>a</i></b> is the logistic regression coefficient of nicotine dependence on an SNP. <b><i>b</i></b> is the coefficient on nicotine dependence, and <b><i>c</i></b><b>′</b> denotes a direct effect, which is the coefficient on the SNP in a logistic regression of lung ADC with nicotine dependence and a given SNP. <b>c</b>, is the total effect, which is the logistic regression coefficient of lung ADC on a given SNP without controlling nicotine dependence. <b>a</b>×<b>b</b> denotes an indirect effect.</p