Baseline Correlates of Insulin Resistance in Inner City High‐BMI African‐American Children

To characterize the influence of diet‐, physical activity–, and self‐esteem‐related factors on insulin resistance in 8–10‐year‐old African‐American (AA) children with BMI greater than the 85th percentile who were screened to participate in a community‐based type 2 diabetes mellitus (T2DM) prevention trial. In 165 subjects, fasting glucose‐ and insulin‐derived values for homeostasis model assessment of insulin resistance (HOMA‐IR) assessed insulin resistance. Body fatness was calculated following bioelectrical impedance analysis, and fitness was measured using laps from a 20‐m shuttle run. Child questionnaires assessed physical activity, dietary habits, and self‐esteem. Pubertal staging was assessed using serum levels of sex hormones. Parent questionnaires assessed family demographics, family health, and family food and physical activity habits. Girls had significantly higher percent body fat but similar anthropometric measures compared with boys, whereas boys spent more time in high‐intensity activities than girls. Scores for self‐perceived behavior were higher for girls than for boys; and girls desired a more slender body. Girls had significantly higher insulin resistance (HOMA‐IR), compared with boys (P < 0.01). Adjusting for age, sex, pubertal stage, socioeconomic index (SE index), and family history of diabetes, multivariate regression analysis showed that children with higher waist circumference (WC) (P < 0.001) and lower Harter's scholastic competence (SC) scale (P = 0.044) had higher insulin resistance. WC and selected self‐esteem parameters predicted insulin resistance in high‐BMI AA children. The risk of T2DM may be reduced in these children by targeting these factors.     

BMI and Cervical Cancer Screening among White,African‐American,and Hispanic Women in the United States

Objectives: We examined cervical cancer screening by BMI in white, African‐American, and Hispanic women and explored women's reasons for not undergoing screening. Research Methods and Procedures: We used logistic regression to examine Pap testing in the preceding 3 years across BMI groups for white (n = 6419), African‐American (n = 1715), and Hispanic women (n = 1859) age 18 to 75 years who responded to the 2000 National Health Interview Survey. We used bivariable analyses to describe women's reasons for not undergoing testing and examined whether unscreened women received physician recommendations for screening. Results: Of 12, 170 women, 50% were normal weight, 26% were overweight, and 21% were obese. The proportion who reported Pap testing in the last 3 years was 86% in whites, 88% in African Americans, and 78% in Hispanics. After adjustment for sociodemographics, health care access, and illness burden, severely obese white women (BMI = 40+ kg/m²) were significantly less likely to undergo Pap testing (relative risk, 0.92; 95% CI, 0.83 to 0.99) compared with normal weight women. BMI was not associated with screening in African Americans or Hispanics. A higher proportion of obese white women than normal weight women cited putting off the test or embarrassment or discomfort as the primary reason for not undergoing screening. Among the unscreened, obese women were as likely as normal weight women to receive a physician recommendation to undergo screening. Discussion: Disparities in cervical cancer screening by body weight persist for white women with severe obesity. Disparities were not explained by differences in the rate of physician recommendations for screening, but obese white women may be more likely to delay screening or to find screening painful, uncomfortable, or embarrassing than normal weight white women. Efforts to increase screening among obese women should address women's reservations about screening.     

Common biological networks underlie genetic risk for alcoholism in African‐ and European‐American populations

Alcohol dependence (AD) is a heritable substance addiction with adverse physical and psychological consequences, representing a major health and economic burden on societies worldwide. Genes thus far implicated via linkage, candidate gene and genome‐wide association studies (GWAS) account for only a small fraction of its overall risk, with effects varying across ethnic groups. Here we investigate the genetic architecture of alcoholism and report on the extent to which common, genome‐wide SNPs collectively account for risk of AD in two US populations, African‐Americans (AAs) and European‐Americans (EAs). Analyzing GWAS data for two independent case–control sample sets, we compute polymarker scores that are significantly associated with alcoholism (P = 1.64 × 10^–3 and 2.08 × 10^–4 for EAs and AAs, respectively), reflecting the small individual effects of thousands of variants derived from patterns of allelic architecture that are population specific. Simulations show that disease models based on rare and uncommon causal variants (MAF < 0.05) best fit the observed distribution of polymarker signals. When scoring bins were annotated for gene location and examined for constituent biological networks, gene enrichment is observed for several cellular processes and functions in both EA and AA populations, transcending their underlying allelic differences. Our results reveal key insights into the complex etiology of AD, raising the possibility of an important role for rare and uncommon variants, and identify polygenic mechanisms that encompass a spectrum of disease liability, with some, such as chloride transporters and glycine metabolism genes, displaying subtle, modifying effects that are likely to escape detection in most GWAS designs.     

Genetic variability in IL23R and risk of colorectal adenoma and colorectal cancer

Inflammatory processes, including, specifically, the inflammatory conditions Crohn's disease (CD) and ulcerative colitis (UC) predispose to colorectal cancer. Interleukin-23 is involved in pro-inflammatory signaling; genetic variation in the interleukin-23 receptor (IL23R) has been consistently associated with CD and UC risk. In three case-control studies of colorectal adenoma (n=485 cases/578 controls), colon cancer (n=1424 cases/1780 controls) and rectal cancer (n=583 cases/775 controls), we investigated associations with 18 candidate and tagSNPs in IL23R. The three studies used an identical Illumina GoldenGate assay, allowing thorough investigation across stages and locations of colorectal neoplasia. We further explored associations with molecular cancer subtypes (MSI+, CIMP+, KRAS2mut, TP53mut). In this comprehensive study of genetic variability in IL23R across the spectrum of colorectal carcinogenesis, as well as within colon and rectal tumor molecular subtypes, we observed associations between SNPs in IL23R and risk of rectal cancer: the 88413 C>A (rs10889675) and 69450 C>A (rs7542081) polymorphisms were associated with decreased rectal cancer risk overall (p-trend=0.04 and 0.05 respectively), and specifically with rectal tumors bearing a TP53 mutation (88413 CA/AA vs. CC OR: 0.66; 95% CI: 0.46-94; 69450 CA/AA vs. CC OR: 0.60; 95% CI: 0.37-0.98). However, none of associations remained statistically significant after correction for multiple testing. These data provide some evidence that genetic variability in IL23R may contribute to rectal cancer risk and should be evaluated in additional studies.     

Meat-derived carcinogens,genetic susceptibility and colorectal adenoma risk

Exposure to heterocyclic aromatic amines (HAAs), carcinogens produced when meat is cooked at high temperatures, is an emerging risk factor for colorectal cancer (CRC). In a cross-sectional study of 342 patients undergoing a screening colonoscopy, the role of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) and 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (DiMeIQx), the three most abundant HAAs found in cooked meats, and total mutagenic activity in cooked meats were examined in relation to colorectal adenoma risk. Given that genetic differences in the ability to biotransform HAAs and repair DNA are postulated to modify the HAA–CRC relationship, gene–diet interactions were also examined. Among the total study population, no relationships were observed between dietary HAAs or meat mutagenicity, and colorectal adenoma risk; however, in males, positive associations between dietary HAAs/meat mutagenicity exposures and adenoma risk were suggestive of a relationship. In a separate analysis, polymorphisms in CYP1B1 were found to be associated with colorectal adenoma risk. Additionally, gene–diet interactions were observed for dietary PhIP and polymorphisms in CYP1B1 and XPD, dietary DiMeIQx and XPD polymorphisms, and meat mutagenicity exposure and CYP1B1 polymorphisms. Overall, increased colorectal adenoma risk was observed with higher HAA/meat mutagenicity exposures among those with polymorphisms which confer greater activity to biotransform HAAs and/or lower ability to repair DNA. This research supports the link between dietary HAAs and genetic susceptibility in colorectal adenoma etiology. The vast majority of CRCs arise from colorectal adenomas; thus, the results of this study suggest that changes in meat preparation practices limiting the production of HAAs may be beneficial for CRC prevention.     

Genome-wide association of BMI in African Americans

Recent genome-wide association studies (GWAS) have identified multiple novel loci associated with obesity in Europeans but results in other ethnicities are less convincing. Here, we report a two-stage GWAS of BMI in African Americans. The GWAS was performed using the Affymetrix 6.0 platform in 816 nondiabetic and 899 diabetic nephropathy subjects. 746,626 single-nucleotide polymorphisms (SNPs) were tested for association with BMI after adjustment for age, gender, disease status, and population structure. Sixty high scoring SNPs that showed nominal association in both GWAS cohorts were further replicated in 3,274 additional subjects in four replication cohorts and a meta-analysis was computed. Meta-analysis of 4,989 subjects revealed five SNPs (rs6794092, rs268972, rs2033195, rs815611, and rs6088887) at four loci showing consistent associations in both GWAS (P < 0.0001) and replication cohorts (P < 0.05) with combined P values range from 2.4 × 10(-6) to 5 × 10(-5). These loci are located near PP13439-TMEM212, CDH12, MFAP3-GALNT10, and FER1L4 and had effect sizes between 0.091 and 0.167 s.d. unit (or 0.67-1.24 kg/m(2)) of BMI for each copy of the effect allele. Our findings suggest the presence of novel loci potentially associated with adiposity in African Americans. Further replication and meta-analysis in African Americans and other populations will shed light on the role of these loci in different ethnic populations.     

Colorectal cancer risk factors in the detection of advanced adenoma and colorectal cancer

Several risk factors for colorectal cancer (CRC) have been identified. If individuals with risk factors are more likely to harbor cancer or it precursors screening programs should be targeted toward this population. We evaluated the predictive value of colorectal cancer risk factors for the detection of advanced colorectal adenoma in a population based CRC colonoscopy screening program. Data were collected in a multicenter trial conducted in the Netherlands, in which 6600 asymptomatic men and women between 50 and 75 years were randomly selected from a population registry. They were invited to undergo a screening colonoscopy. Based on a review of the literature CRC risk factors were selected. Information on risk factors was obtained from screening attendees through a questionnaire. For each CRC risk factor, we estimated its odds ratio (OR) relative to the presence of advanced neoplasia as detected at colonoscopy. Of the 1426 screening participants who underwent a colonoscopy, 1236 (86%) completed the risk questionnaire. 110 participants (8.9%) had advanced neoplasia. The following risk factors were significantly associated with advanced neoplasia detected by colonoscopy: age (OR: 1.06 per year; 95% CI: 1.03–1.10), calcium intake (OR: 0.99 per mg; 95% CI: 0.99–1.00), positive CRC family history (OR: 1.55 per first degree family member; 95%CI: 1.11–2.16) and smoking (OR: 1.75; 95%CI: 1.09–2.82). Elderly screening participants, participants with lower calcium intake, a CRC family history, and smokers are at increased risk of harboring detectable advanced colorectal neoplasia at screening colonoscopy.     

Fine Mapping and Identification of BMI Loci in African Americans

Genome-wide association studies (GWASs) primarily performed in European-ancestry (EA) populations have identified numerous loci associated with body mass index (BMI). However, it is still unclear whether these GWAS loci can be generalized to other ethnic groups, such as African Americans (AAs). Furthermore, the putative functional variant or variants in these loci mostly remain under investigation. The overall lower linkage disequilibrium in AA compared to EA populations provides the opportunity to narrow in or fine-map these BMI-related loci. Therefore, we used the Metabochip to densely genotype and evaluate 21 BMI GWAS loci identified in EA studies in 29,151 AAs from the Population Architecture using Genomics and Epidemiology (PAGE) study. Eight of the 21 loci (SEC16B, TMEM18, ETV5, GNPDA2, TFAP2B, BDNF, FTO, and MC4R) were found to be associated with BMI in AAs at 5.8 × 10⁻⁵. Within seven out of these eight loci, we found that, on average, a substantially smaller number of variants was correlated (r² > 0.5) with the most significant SNP in AA than in EA populations (16 versus 55). Conditional analyses revealed GNPDA2 harboring a potential additional independent signal. Moreover, Metabochip-wide discovery analyses revealed two BMI-related loci, BRE (rs116612809, p = 3.6 × 10⁻⁸) and DHX34 (rs4802349, p = 1.2 × 10⁻⁷), which were significant when adjustment was made for the total number of SNPs tested across the chip. These results demonstrate that fine mapping in AAs is a powerful approach for both narrowing in on the underlying causal variants in known loci and discovering BMI-related loci.     

Genome‐wide association study identifies loci associated with liability to alcohol and drug dependence that is associated with variability in reward‐related ventral striatum activity in African‐ and European‐Americans

Genetic influences on alcohol and drug dependence partially overlap, however, specific loci underlying this overlap remain unclear. We conducted a genome‐wide association study (GWAS) of a phenotype representing alcohol or illicit drug dependence (ANYDEP) among 7291 European‐Americans (EA; 2927 cases) and 3132 African‐Americans (AA: 1315 cases) participating in the family‐based Collaborative Study on the Genetics of Alcoholism. ANYDEP was heritable (h ² in EA = 0.60, AA = 0.37). The AA GWAS identified three regions with genome‐wide significant (GWS; P < 5E‐08) single nucleotide polymorphisms (SNPs) on chromosomes 3 (rs34066662, rs58801820) and 13 (rs75168521, rs78886294), and an insertion‐deletion on chromosome 5 (chr5:141988181). No polymorphisms reached GWS in the EA. One GWS region (chromosome 1: rs1890881) emerged from a trans‐ancestral meta‐analysis (EA + AA) of ANYDEP, and was attributable to alcohol dependence in both samples. Four genes (AA: CRKL, DZIP3, SBK3; EA: P2RX6) and four sets of genes were significantly enriched within biological pathways for hemostasis and signal transduction. GWS signals did not replicate in two independent samples but there was weak evidence for association between rs1890881 and alcohol intake in the UK Biobank. Among 118 AA and 481 EA individuals from the Duke Neurogenetics Study, rs75168521 and rs1890881 genotypes were associated with variability in reward‐related ventral striatum activation. This study identified novel loci for substance dependence and provides preliminary evidence that these variants are also associated with individual differences in neural reward reactivity. Gene discovery efforts in non‐European samples with distinct patterns of substance use may lead to the identification of novel ancestry‐specific genetic markers of risk.     

Lower Serum Adiponectin Levels in African‐American Boys

Objective: To examine adiponectin, an adipocyte‐secreted hormone with anti‐inflammatory and insulin‐sensitizing effects, in relation to race or gender in younger subjects. Research Methods and Procedures: The relationship of adiponectin, quantitated by radioimmunoassay, to anthropometric and metabolic factors (fasting insulin, glucose, and leptin) and reproductive hormones was examined in 46 healthy African Americans (25 girls/21 boys) and 40 whites (20 girls/20 boys) ranging in age from 12 to 21 years. Results: There was no statistical difference in BMI or in BMI percentile among the four groups. Sums of skinfolds, but not skinfold percentile, were significantly lower in boys than girls (p = 0.001 and p = 0.896, respectively), whereas there was no difference between racial groups. Leptin was significantly greater in girls (p = 0.0002). There was no difference in fasting serum glucose, insulin, or homeostasis model assessment score among any of the groups. There was a significant negative univariate relationship between serum adiponectin and both BMI and BMI percentile for the entire group (p = 0.006 and p = 0.005). In a multivariate model, BMI percentile (p = 0.005) and the interaction between race and gender (p = 0.026) were significant predictors of serum adiponectin. In this model, African‐American boys had the lowest serum adiponectin level, 37% less than white boys, who had the highest adiponectin levels. Discussion: Serum adiponectin levels are reduced in young obese subjects (African Americans and whites) and are lower in African‐American boys than white boys. A lower adiponectin level in African‐American boys may predispose this group to a greater risk of diabetes and cardiovascular disease.     

Energy Expenditure and Adiposity in Nigerian and African‐American Women

Objective: Obesity is a prevalent condition in industrialized societies and is increasing around the world. We sought to assess the relative importance of resting energy expenditure (REE) and activity EE (AEE) in two populations with different rates of obesity. Methods and Procedures: Women of African descent between 18 and 59 years of age were recruited from rural Nigeria and from metropolitan Chicago. Total EE (TEE) was measured using the doubly labeled water (DLW) technique and REE by indirect calorimetry; AEE was calculated as the difference between TEE and the sum of REE plus a factor for the thermic effect of food. In the analyses all EE parameters were adjusted for body size using a regression method. Comparisons were made between the groups and associations between EE and adiposity examined. Results: A total of 149 Nigerian and 172 African‐American women completed the protocol. All body size measurements were lower in the Nigerian women. Adjusted TEE and REE were higher in the Nigerian cohort but adjusted AEE did not differ significantly. Adjustment for parity, seasonality, and recent illness did not modify mean AEE or adiposity. In neither cohort was there a meaningful association between measures of AEE and adiposity. Discussion: In these cohorts of women from very different environments, AEE did not differ significantly nor was it associated cross‐sectionally with adiposity. If generalizable, these findings suggest that reduction in AEE may have less of a role in the development of obesity than anticipated. The possibility remains that variation in type and duration of activity plays a role not captured by total AEE.     

Apolipoprotein A‐II Polymorphism and Visceral Adiposity in African‐American and White Women

To determine the association between the ?265 T to C substitution in the apolipoprotein A‐II (APOA‐II) gene and levels of visceral adipose tissue (VAT) in a group of premenopausal African‐American and white women, we genotyped 237 women (115 African‐American and 122 white) for this polymorphism. Body composition was assessed by DXA, and VAT was determined from a single computed tomography scan. In addition to VAT, we examined the association between the polymorphism and other phenotypes (total body fat, total abdominal adipose tissue, and subcutaneous abdominal adipose tissue). The mutant C allele in the APOA‐II gene was less frequent in African‐American compared with white women, 23% vs. 36%, respectively (p < 0.01). VAT was significantly higher in carriers of the C allele compared with noncarriers after adjustment for total body fat (p < 0.05). When separate analyses by ethnic group were conducted, the association between the polymorphism and VAT was observed in white (p < 0.05) but not African‐American (p = 0.57) women. There was no association between the polymorphism and the other phenotypes. These results indicate a significant association between the T265C APOA‐II polymorphism and levels of VAT in premenopausal women. This association is present in white but not African‐American women.     

Plasma Adiponectin Levels in High Risk African‐Americans with Normal Glucose Tolerance,Impaired Glucose Tolerance,and Type 2 Diabetes**

Objective: We studied plasma adiponectin, insulin sensitivity, and insulin secretion before and after oral glucose challenge in normal glucose tolerant, impaired glucose tolerant, and type 2 diabetic first degree relatives of African‐American patients with type 2 diabetes. Research Methods and Procedures: We studied 19 subjects with normal glucose tolerance (NGT), 8 with impaired glucose tolerance (IGT), and 14 with type 2 diabetes. Serum glucose, insulin, C‐peptide, and plasma adiponectin levels were measured before and 2 hours after oral glucose tolerance test. Homeostasis model assessment‐insulin resistance index (HOMA‐IR) and HOMA‐β cell function were calculated in each subject using HOMA. We empirically defined insulin sensitivity as HOMA‐IR < 2.68 and insulin resistance as HOMA‐IR > 2.68. Results: Subjects with IGT and type 2 diabetes were more insulin resistant (as assessed by HOMA‐IR) when compared with NGT subjects. Mean plasma fasting adiponectin levels were significantly lower in the type 2 diabetes group when compared with NGT and IGT groups. Plasma adiponectin levels were 2‐fold greater (11.09 ± 4.98 vs. 6.42 ± 3.3811 μg/mL) in insulin‐sensitive (HOMA‐IR, 1.74 ± 0.65) than in insulin‐resistant (HOMA‐IR, 5.12 ± 2.14) NGT subjects. Mean plasma adiponectin levels were significantly lower in the glucose tolerant, insulin‐resistant subjects than in the insulin sensitive NGT subjects and were comparable with those of the patients with newly diagnosed type 2 diabetes. We found significant inverse relationships of adiponectin with HOMA‐IR (r = ?0.502, p = 0.046) and with HOMA‐β cell function (r = ?0.498, p = 0.042) but not with the percentage body fat (r = ?0.368, p = 0.063), serum glucose, BMI, age, and glycosylated hemoglobin A1C (%A1C). Discussion: In summary, we found that plasma adiponectin levels were significantly lower in insulin‐resistant, non‐diabetic first degree relatives of African‐American patients with type 2 diabetes and in those with newly diagnosed type 2 diabetes. We conclude that a decreased plasma adiponectin and insulin resistance coexist in a genetically prone subset of first degree African‐American relatives before development of IGT and type 2 diabetes.     

Effects of BMI on the risk and frequency of AIS 3+ injuries in motor‐vehicle crashes

Objective: Determine the effects of BMI on the risk of serious‐to‐fatal injury (Abbreviated Injury Scale ≥ 3 or AIS 3+) to different body regions for adults in frontal, nearside, farside, and rollover crashes. Design and Methods: Multivariate logistic regression analysis was applied to a probability sample of adult occupants involved in crashes generated by combining the National Automotive Sampling System (NASS‐CDS) with a pseudoweighted version of the Crash Injury Research and Engineering Network database. Logistic regression models were applied to weighted data to estimate the change in the number of occupants with AIS 3+ injuries if no occupants were obese. Results: Increasing BMI increased risk of lower‐extremity injury in frontal crashes, decreased risk of lower‐extremity injury in nearside impacts, increased risk of upper‐extremity injury in frontal and nearside crashes, and increased risk of spine injury in frontal crashes. Several of these findings were affected by interactions with gender and vehicle type. If no occupants in frontal crashes were obese, 7% fewer occupants would sustain AIS 3+ upper‐extremity injuries, 8% fewer occupants would sustain AIS 3+ lower‐extremity injuries, and 28% fewer occupants would sustain AIS 3+ spine injuries. Conclusions: Results of this study have implications on the design and evaluation of vehicle safety systems.     

Self‐Efficacy as a Predictor of Weight Change in African‐American Women

Objective: Although self‐efficacy has received increasing attention for its role in weight loss, there is less research examining this relationship in minority samples. The purpose of this study was to determine whether self‐efficacy for weight loss was predictive of weight change in a sample of African‐American women. Research Methods and Procedures: Subjects were 106 overweight or obese, low‐income African‐American women participating in a weight management intervention that involved either personalized monthly sessions with their primary care physician or standard care. Weight and self‐efficacy for weight loss were assessed at baseline and at the end of the 6‐month treatment. Results: For subjects in the personalized intervention, baseline self‐efficacy was predictive of subsequent weight change, such that higher levels of self‐efficacy before treatment were associated with less weight loss. In contrast, improvements in self‐efficacy during treatment were associated with greater weight loss for the personalized intervention group. Discussion: Results suggest high self‐efficacy for weight loss before treatment may be detrimental to success, whereas treatments that improve participants’ self‐efficacy may result in greater weight loss. High pretreatment self‐efficacy may be indicative of overconfidence or lack of experience with the difficulties associated with weight loss efforts. Whereas replication is needed, our results suggest that self‐efficacy is an important variable to consider when implementing weight loss interventions.     

Physical Activity and Reduced Intra‐abdominal Fat in Midlife African‐American and White Women

The purpose of our study was to determine whether self‐reported physical activity (PA), including recreational, household, and exercise activities, is associated with intra‐abdominal fat (IAF) in community‐dwelling white and black midlife women. We performed a cross‐sectional study of 369 women from the Chicago site of the Study of Women's Health Across the Nation (SWAN) ancillary study, the SWAN Fat Patterning Study. PA level was the independent variable, and IAF, assessed by computerized tomography (CT) scan, was the dependent variable. Measures were obtained at SWAN Fat Patterning Baseline visit between August 2002 and December 2005. Linear regression models explored the association between PA and IAF. The first model included IAF as the outcome and total score PA as the main predictor, adjusting for total percent fat mass, age, and ethnicity. The second model included education, parity, sex hormone–binding globulin (SHBG) level, and depressive symptoms, measured by Center for Epidemiological Studies‐Depression (CES‐D) scale. Each 1‐point higher total PA score was associated with a 4.0 cm² lower amount of IAF (P = 0.004), independent of total percent fat mass, age, ethnicity, SHBG level, educational level, CES‐D, and parity. Associations did not differ between white and black women. This study demonstrates a significant negative association between PA and IAF independent of multiple covariates in midlife women. Our findings suggest that motivating white and black women to increase PA during midlife may lessen IAF, which may have a positive impact on subsequent development of diabetes and cardiovascular disease.     

Genetic and Environmental Influences on Body‐Fat Measures among African‐American Twins

Objective: To investigate the genetic and environmental influences on body‐fat measures including waist circumference (WC), waist‐to‐hip ratio (WHR), and body mass index (BMI) among African‐American men and women. Research Methods and Procedures: Measurements were taken as part of the Carolina African American Twin Study of Aging. This sample currently comprises 146 same‐sex African‐American twins with an average age of 50 years (range, 22 to 88 years). This analysis included 26 monozygotic and 29 dizygotic men and 45 monozygotic and 46 dizygotic women. Maximum likelihood quantitative genetic analysis was used. Results: In men, additive genetic effects accounted for 77% of the variance in WC, 59% in WHR, and 89% in BMI. In women, additive genetic effects accounted for 76% of the variance in WC, 56% in WHR, and 73% in BMI. The remaining variance in both men and women was attributed to unique environmental effects (WC, 21%; WHR, 36%; BMI, 11% in men and WC, 22%; WHR, 38%; BMI, 27% in women) and age (WC, 2%; WHR, 5% in men and WC, 2%; WHR, 6% in women). When BMI was controlled in the analysis of WC and WHR, it accounted for a portion of the genetic and environmental variance in WHR and over one‐half of the genetic and environmental variance in WC. Discussion: There are both genetic and environmental influences on WC, WHR, and BMI, and independent of BMI, there are genetic and environmental effects on WC and WHR among both genders. The results from this African‐American twin sample are similar to findings among white twin samples.     

Obesity and Sugar‐sweetened Beverages in African‐American Preschool Children: A Longitudinal Study

A representative sample of 365 low‐income African‐American preschool children aged 3–5 years was studied to determine the association between sugar‐sweetened beverage consumption (soda, fruit drinks, and both combined) and overweight and obesity. Children were examined at a dental clinic in 2002–2003 and again after 2 years. Dietary information was collected using the Block Kids Food Frequency Questionnaire. A BMI score was computed from recorded height and weight. Overweight and obesity were defined by national reference age‐sex specific BMI: those with an age‐sex specific BMI ≥85th, but <95th percentile as overweight and those with BMI ≥95th age‐sex specific percentile as obese. The prevalence of overweight was 12.9% in baseline, and increased to 18.7% after 2 years. The prevalence of obesity increased from 10.3 to 20.4% during the same period. Baseline intake of soda and all sugar‐sweetened beverages were positively associated with baseline BMI z‐scores. After adjusting for covariates, additional intake of fruit drinks and all sugar‐sweetened beverages at baseline showed significantly higher odds of incidence of overweight over 2 years. Among a longitudinal cohort of African‐American preschool children, high consumption of sugar‐sweetened beverages was significantly associated with an increased risk for obesity.     

Association of FTO Gene Variants With Adiposity in African‐American Adolescents

The prevalence of obesity continues to increase significantly, with the largest rise in the African‐American adolescents. Genetic contributions to obesity are being identified with the advent of genome‐wide association studies (GWAS). Specifically, variants of the fat mass and obesity associated (FTO) gene have been associated with obesity in populations of European descent. The studies in African Americans have been inconclusive. To further evaluate the association of the FTO gene and adiposity in African Americans, we genotyped 47 single‐nucleotide polymorphisms (SNPs), including seven SNPs previously reported to be significant in the literature in a cohort consisting of 561 non‐Hispanic white and 497 African‐American individuals. Analysis of our data showed 17 SNPs to be associated with BMI Z‐score (BMI‐Z) in our study population. The strongest association was found in the African Americans. The most significant SNP was rs8057044, which was associated with BMI‐Z in the African Americans (P = 0.00054). SNP rs9939609 was found to be significant in the non‐Hispanic white population (P = 0.028). Our data confirm the association between FTO and adiposity suggesting that FTO is a childhood obesity susceptibility gene. Our data also identify a novel SNP of the FTO gene (rs8057044) that is associated with measures of adiposity in the African‐American population.