Association of active coping to unfair treatment with perceived stress and depressive symptoms in African Americans: mh-grid study.

BACKGROUND: Unfair treatment such as discrimination and racism contribute to depression and perceived stress in African Americans. Although studies have examined how responding to such treatment is associated with ameliorating depressive symptoms and levels of perceived stress, most do not focus on African Americans. The purpose of this study is to assess how talking to others in response to unfair treatment is associated with self-reported depressive symptoms and perceived stress levels in African Americans. METHODS: A sample from the 2010-2013 Minority Health Genomics and Translational Research Bio-Repository Database was used and consisted of 376 African American adults aged 30-55 years old residing in the southern region of the United States. Linear regression models were used to assess the association between talking to others following unfair treatment, compared to keeping it to oneself, on self-reported depressive symptoms and perceived stress. The predictor variable was based on the question "If you have been treated unfairly, do you usually talk to people about it or keep it to yourself?". RESULTS: Talking to someone after being treated unfairly was inversely associated with perceived stress ([Formula: see text]: -3.62, SE: 1.14, p ≤ 0.05) and depressive symptoms ([Formula: see text]: -3.62, SE: 1.14, p ≤ 0.05). CONCLUSIONS: African Americans who talked to others in response to unfair treatment had lower depressive symptoms and perceived stress than those who kept it to themselves. More outreach to African Americans regarding the importance of talk in response to exposure to unfair treatment is needed as a potential coping mechanism.

Modifiable mediators associated with the relationship between adiposity and leukocyte telomere length in US adults: The National Health and Nutrition Examination Survey.

Obesity is associated with age-related health conditions and telomere attrition - a marker of cellular aging. Obesity is attributable to adverse modifiable lifestyle factors. Little is known about the mediation effect of lifestyle factors associated with the relationship between obesity and telomere length. Our objective was to examine this association in the US. Pack years smoked, drinking level per day, physical activity (PA) per week and diet based on Healthy Eating Index (HEI) were assessed as mediators associated with the relationship between adiposity measures and leukocyte telomere length (LTL); adiposity measures included body mass index (BMI), % total body fat (TBF) and waist circumference (WC). Separate adjusted linear regressions and mediation analysis were conducted on a total of 4919 respondents aged 20-84 years using cross-sectional 1999-2002 data from the US National Health and Nutrition Examination Survey. Inadequate PA correlated with 1.28% shorter LTL and was a factor accounting for 35% of the relationship between BMI and LTL (ß = -0.0128, 95% CI = 0.0259, 0.0004, p = .05). Smoking 30-≥59 pack years correlated with 4% shorter LTL and accounted for 21% of the relationship between %TBF and LTL (ß = -0.0386, 95% CI = -0.0742, -0.0030, p = .03). Improvement in diet correlated with 0.11% longer LTL and contributed 25% of the association between %TBF and LTL (ß = 0.0011, 95%CI =0.0004, 0.0018, p = .01). Diet correlated with 0.11% longer LTL and correspond to 28% of the relationship between WC and LTL (ß = 0.0011, 95%CI = 0.0004, 0.0018, p = .03). Interventions to improve modifiable behaviors may ameliorate cellular aging and aging related health conditions due to obesity among US adults.

Circadian CLOCK gene polymorphisms in relation to sleep patterns and obesity in African Americans: findings from the Jackson heart study.

BACKGROUND: Circadian rhythms regulate key biological processes and the dysregulation of the intrinsic clock mechanism affects sleep patterns and obesity onset. The CLOCK (circadian locomotor output cycles protein kaput) gene encodes a core transcription factor of the molecular circadian clock influencing diverse metabolic pathways, including glucose and lipid homeostasis. The primary objective of this study was to evaluate the associations between CLOCK single nucleotide polymorphisms (SNPs) and body mass index (BMI). We also evaluated the association of SNPs with BMI related factors such as sleep duration and quality, adiponectin and leptin, in 2962 participants (1116 men and 1810 women) from the Jackson Heart Study. Genotype data for the selected 23 CLOCK gene SNPS was obtained by imputation with IMPUTE2 software and reference phase data from the 1000 genome project. Genetic analyses were conducted with PLINK RESULTS: We found a significant association between the CLOCK SNP rs2070062 and sleep duration, participants carriers of the T allele showed significantly shorter sleep duration compared to non-carriers after the adjustment for individual proportions of European ancestry (PEA), socio economic status (SES), body mass index (BMI), alcohol consumption and smoking status that reach the significance threshold after multiple testing correction. In addition, we found nominal associations of the CLOCK SNP rs6853192 with longer sleep duration and the rs6820823, rs3792603 and rs11726609 with BMI. However, these associations did not reach the significance threshold after correction for multiple testing. CONCLUSIONS: In this work, CLOCK gene variants were associated with sleep duration and BMI suggesting that the effects of these polymorphisms on circadian rhythmicity may affect sleep duration and body weight regulation in Africans Americans.

Race-specific associations between health-related quality of life and cellular aging among adults in the United States: evidence from the National Health and Nutrition Examination Survey.

PURPOSE: Poor health-related quality of life (HRQOL) could lead to higher morbidity and mortality through telomere attrition or accelerated cellular aging. We conducted a cross-sectional analysis to examine the relationship between four dimensions of HRQOL and leukocyte telomere length (LTL) among a nationally representative sample of 3547 US adults (≥20 years) using the data from the 2001-2002 National Health and Nutrition Examination Survey. METHOD: We used HRQOL survey information collected on individuals' self-rated general health, recent physical health, recent mental health, and recent activity limitation. Telomere length was assessed using quantitative polymerase chain reaction. Multiple linear regressions were used to estimate the relationship between each dimension of HRQOL and log-transformed values of LTL with adjustment for sample weights and design effects. RESULTS: HRQOL-race interactions were significant, and the results were stratified by race. After controlling for demographic factors, disease conditions, and lifestyle variables, worse general health was significantly associated with shorter LTL for Blacks (coefficient, ß: -0.022, 95% Confidence Interval, 95% CI: -0.03 to -0.01), but not for Whites or Mexican Americans. Unwell physical health was associated with shorter telomere length for Whites (ß: -0.005, 95% CI: -0.01 to -0.001) only. Unwell mental health showed no significant association with LTL in any race. CONCLUSIONS: Although longitudinal studies are needed to prove causality, our findings suggest that HRQOL could be associated with LTL shortening. We also found a possible racial difference in this association and recommend additional multiethnic studies to confirm this and to understand the reasons and consequences of this difference.

Obstructive sleep apnea risk and leukocyte telomere length in African Americans from the MH-GRID study.

PURPOSE: Shorter telomere length and obstructive sleep apnea are associated with increased oxidative stress and chronic inflammation, which are both considered leading causes of age-related diseases. Different forms of sleep disordered breathing have been linked to telomere length although their relationship remains uncertain. The purpose of this study was to explore the associations between the risk of obstructive sleep apnea and telomere length in African Americans. METHODS: The analysis included 184 women and 122 men aged 30-55 years from the Morehouse School of Medicine Study. Relative TL (T/S ratio) was measured from peripheral blood leukocytes using quantitative real-time polymerase chain reaction. The Berlin questionnaire was used for OSA risk assessments. Multivariable linear regression models were used to examine the associations between OSA risk and LTL. RESULTS: We observed that LTL varied by OSA risk in women (0.532 ± 0.006 vs. 0.569 ± 0.008) (p = 0.04). Multiple linear regression analysis confirmed that women at higher risk for OSA presented shorter LTL compared to those at lower risk, independent of age, income, education, obesity, smoking, alcohol consumption, and hypertension. These differences were not observed in men. CONCLUSIONS: Our findings suggest that OSA risk may contribute to the acceleration of cellular aging processes through telomere shortening.

Vitamin D Receptor Gene Polymorphisms Are Associated with Abdominal Visceral Adipose Tissue Volume and Serum Adipokine Concentrations but Not with Body Mass Index or Waist Circumference in African Americans: The Jackson Heart Study.

BACKGROUND: The biological actions of vitamin D are mediated through the vitamin D receptor (VDR). Single-nucleotide polymorphisms (SNPs) in the VDR gene have been previously associated with adiposity traits. However, to our knowledge, few studies have included direct measures of adiposity and adipokine concentrations. OBJECTIVE: We examined the association of tagging SNPs in the VDR gene with multiple adiposity measures, including waist circumference (WC), body mass index (BMI), body fat percentage, subcutaneous and visceral adipose tissue (VAT) volume, and serum adipokine (adiponectin and leptin) concentrations in adult African Americans (AAs). METHODS: Data from 3020 participants (61.9% women; mean age, 54.6 y) from the Jackson Heart Study were used for this analysis. Forty-five tag SNPs were chosen with the use of genotype data from the International HapMap project. We used linear regression to test the associations of imputed VDR SNPs with each of the traits, adjusted for age, sex, educational status, physical activity, smoking, alcohol intake, serum vitamin D concentration, European ancestry, and multiple testing. RESULTS: The G allele of the SNP rs4328262 remained associated with increased VAT volume after multiple testing correction (ß = 45.7; P < 0.001). The A allele of another SNP (rs11574070) was nominally associated with body fat percentage (ß = 0.96; P = 0.002). None of the VDR SNPs analyzed showed any link with WC or BMI. The A allele of rs2228570 (ß = 0.08; P = 0.001) for men and the T allele of rs2853563 (ß = 0.04; P < 0.001) for women remained positively associated with serum adiponectin concentrations after multiple testing correction. CONCLUSION: Although we did not find any association for anthropometric measures, we did observe associations of VDR variants with serum adipokines and with the more metabolically active fat, VAT. Therefore, our findings demonstrate a possible role of VDR variants in regulating adipose tissue activity and adiposity among AAs.

Associations between Vitamin D and Cardiovascular Disease Risk Factors in African Americans Are Partly Explained by Circulating Adipokines and C-Reactive Protein: The Jackson Heart Study.

BACKGROUND: Although it is recognized that vitamin D deficiency is associated with cardiovascular disease (CVD) risk factors, and is more common in African Americans (AAs), the pathologic mechanisms by which vitamin D may influence these risk factors are poorly understood. OBJECTIVES: We explored the association between vitamin D status, as reflected by serum 25-hydroxyvitamin D [25(OH)D] concentrations, and CVD risk factors including mean arterial pressure (MAP), fasting plasma glucose (FPG), plasma HDL cholesterol, and waist circumference (WC) in adult AAs. We also tested whether plasma C-reactive protein (CRP), adipokines (adiponectin and leptin), and aldosterone mediated the associations between 25(OH)D and these risk factors. METHODS: Data on 4010 (63.8% women; mean age: 54.0 y) individuals from the Jackson Heart Study were analyzed. Multivariable linear regression models were used to examine the associations of 25(OH)D with CVD risk factors. We used path analysis and bootstrapping methods to quantify and test the share of these associations that was statistically explained by each of the mediators by decomposing the associations into direct and indirect effects. RESULTS: Serum 25(OH)D concentrations were inversely associated with WC, FPG, and MAP and were positively associated with HDL cholesterol in multivariable analysis. A nearly 20% effect of 25(OH)D on MAP was masked by aldosterone (total indirect effect: ß = 0.01, P < 0.05). Approximately 23% of the effect of 25(OH)D on WC (ß = -0.03, P < 0.05) and ∼9% of the effect of 25(OH)D on FPG (ß = -0.02, P < 0.05) were mediated through CRP, adiponectin, and leptin together. A 23% share of the association between 25(OH)D and HDL cholesterol was mediated by adiponectin alone (ß = 0.03, P < 0.05). CONCLUSIONS: Our findings suggest that the associations between vitamin D status and CVD risk factors in AAs are partially mediated through circulating adipokines and CRP. More evidence, however, is required from longitudinal and randomized controlled studies to validate our findings.

Genetic ancestry is associated with measures of subclinical atherosclerosis in African Americans: the Jackson Heart Study.

OBJECTIVE: To determine whether genetic ancestry was associated with subclinical atherosclerosis measures after adjustment for traditional cardiovascular disease risk factors, inflammatory marker, socioeconomic status, and psychosocial factors in a large admixed African American population. APPROACH AND RESULTS: Participants were drawn from the Jackson Heart Study. Participant's percent of European ancestry (PEA) was estimated based on 1747 genetic markers using HAPMIX. Association of PEA with peripheral arterial disease and common carotid intima-media thickness were investigated among 2168 participants and with coronary artery calcification >0 and abdominal aortic calcification >0 among 1139 participants. The associations were evaluated using multivariable regression models. Our results showed that a 1 SD increase in PEA was associated with a lower peripheral arterial disease prevalence after adjusting for age and sex (prevalence ratio=0.90 [95% CI, 0.82-0.99]; P=0.036). Adjustments for traditional cardiovascular disease risk factors, socioeconomic status, and psychosocial factors attenuated this association (prevalence ratio=0.91 [0.82-1.00]; P=0.046). There was also a nonlinear association between PEA and coronary artery calcification and abdominal aortic calcification. The lowest PEA was associated with a lower coronary artery calcification (prevalence ratio=0.75 [0.58-0.96]; P=0.022) and a lower abdominal aortic calcification [prevalence ratio=0.80 [0.67-0.96]; P=0.016) compared with the reference group (10th-90th percentile) after adjusting for traditional cardiovascular disease risk factors, inflammatory marker, socioeconomic status, and psychosocial factors. However, we found no significant association between PEA and common carotid intima-media thickness. CONCLUSIONS: Overall, our findings indicate that genetic ancestry was associated with subclinical atherosclerosis, suggesting unmeasured risk factors and interactions with genetic factors might contribute to the distribution of subclinical atherosclerosis among African Americans.

Association of adiponectin and socioeconomic status in African American men and women: the Jackson heart study.

BACKGROUND: Recent emphasis has been placed on elucidating the biologic mechanism linking socioeconomic status (SES) to cardiovascular disease (CVD). Positive associations of inflammatory biomarkers provide evidence suggestive of a biologic pathway by which SES may predispose to CVD. African Americans have disproportionately lower SES and have a higher prevalence of CVD risk factors compared to most ethnic/racial groups. Adiponectin (an anti-inflammatory marker) is also lower. The objective of this study was to assess the association of adiponectin with SES among African American men and women using the Jackson Heart Study. METHODS: Study sample included 4340 participants. Linear regression was performed separately by SES and stratified by sex. Annual household income and level of education was used as proxies for SES. Crude, age, health behavior and health status adjusted models were analyzed. The main outcome was log-transformed adiponectin. RESULTS: Men in the lowest income group had significantly higher adiponectin than those in the highest income group in the fully adjusted model (ß/standard error [se], p value = .16/.08, p = .0008. Men with < high school level of education had significantly higher adiponectin in the crude and age adjusted models than those with ≥ college degree (.25/.05, p < .0001; .14/.05/ p = .005, respectively). Women with some college or vocational training in the crude and age adjusted models had lower adiponectin compared to women with ≥ college degree (-.09/.03, p = .004; -.06/.03, p = .04, respectively). CONCLUSION: Findings suggest a potential inverse biologic pathway between annual household income and adiponectin among African American men. There was no such finding among women. Findings suggest interventions should be targeted for higher SES African American men to improve adiponectin levels.

Gender-specific associations between ADIPOQ gene polymorphisms and adiponectin levels and obesity in the Jackson Heart Study cohort.

BACKGROUND: Despite the important role of adiponectin in regulating general metabolic homeostasis, analysis of genetic determinants of adiponectin and the related cardio-metabolic traits in African American population has been limited and inconsistent. Considering the high genetic admixture of African Americans and thus the important population stratification that may confound the genetic-trait associations, the objective of this work was to perform a comprehensive analysis of the associations between ADIPOQ variants and adiponectin levels and obesity phenotypes in a large African American population from the Jackson Heart Study (JHS) cohort. METHODS: Genotype data was available for 2968 JHS participants (1131men; 1837women). Single Nucleotide Polymorphisms (SNPs) were selected by a Tag-SNP Approach and literature review. The genotype imputation was performed using IMPUTE2 software and reference phased data from the 1000G project. PLINK software was used for the genetic analysis. Plasma specimens were analyzed by ELISA for adiponectin levels. All analyses were controlled for population stratification assessed by Individual Proportions of European Ancestry (PEA) estimates calculated in HAPMIX using ancestry informative markers (AIMs). RESULTS: We found a gender-dependent association of some ADIPOQ variants and adiponectin levels. In women four of the studied polymorphisms (rs6444174, rs16861205, rs1403697, rs7641507) were associated with adiponectin levels after Bonferroni correction and controlling for the percentage of PEA, age, annual household income and smoking. These results were consistent with the haplotype analysis. The association between the rs12495941 variant and obesity is modulated by the PEA, so that the relationship between the G allele and a higher incidence of obesity was present in those individuals within the lower PEA group. In addition we found an effect modification of obesity on the association between the ADIPOQ rs6444174 SNP and BMI so that the presence of the T allele was negatively and significantly associated with BMI only in participants with a normal weight. CONCLUSIONS: In this large African American cohort, ADIPOQ variants were associated with adiponectin levels in a gender-dependent manner and the relationship of some of these variants with obesity and BMI was modulated by the PEA and obesity status respectively. This suggests that the effects of these polymorphisms on adiponectin and obesity phenotypes are subject to a strong interaction with genetic and environmental factors in African American population.

Association of ADIPOQ gene with type 2 diabetes and related phenotypes in African American men and women: the Jackson Heart Study.

BACKGROUND: African Americans experience disproportionately higher prevalence of type 2 diabetes and related risk factors. Little research has been done on the association of ADIPOQ gene on type 2 diabetes, plasma adiponectin, blood glucose, HOMA-IR and body mass index (BMI) in African Americans. The objective of our research was to assess such associations with selected SNPs. The study included a sample of 3,020 men and women from the Jackson Heart Study who had ADIPOQ genotyping information. Unadjusted and adjusted regression models with covariates were used with type 2 diabetes and related phenotypes as the outcome stratified by sex. RESULTS: There was no association between selected ADIPOQ SNPs with type 2 diabetes, blood glucose, or BMI in men or women. There was a significant association between variant rs16861205 and lower adiponectin in women with minor allele A in the fully adjusted model (ß(SE) p = -.13(0.05), 0.003). There was also a significant association with variant rs7627128 and lower HOMA-IR among men with minor allele A in the fully adjusted model (ß(SE) p = -0.74(0.20), 0.0002). CONCLUSIONS: These findings represent new insights regarding the association of ADIPOQ gene and type 2 diabetes and related phenotypes in African American men and women.

Association of adiponectin with type 2 diabetes and hypertension in African American men and women: the Jackson Heart Study.

BACKGROUND: Adiponectin is a biomarker that is associated with type 2 diabetes and hypertension. Lower circulating level is a risk factor. Higher levels are protective. African Americans have a higher prevalence of type 2 diabetes and hypertension and lower levels of adiponectin when compared to other racial/ethnic groups. Little is known about the association of adiponectin on these health outcomes among African Americans. The purpose of the study was to assess the association of adiponectin on type 2 diabetes and hypertension likelihood among African American men and women in the Jackson Heart Study. METHODS: Separate multivariate logistic regressions were conducted stratified by sex based on cross-sectional data with type 2 diabetes and hypertension as the outcomes. Adiponectin was divided into four quartiles with the highest quartile as the reference. Data was collected from 2000-2004 on 3,663 participants. Data analysis was conducted in calendar year 2014. Two- tailed P < .05 was established as level of significance. RESULTS: In the adjusted multivariate models, adiponectin level was inversely associated with type 2 diabetes among women (odds ratio [OR], 95% confidence interval [CI] = 1.47, [1.02, 2.11], P = .04). There was no association among men. Women with the lowest level of adiponectin were less likely to be hypertensive (OR, 95% CI = 0.66, [0.46, 0.95], p = .02). There was no association among men. CONCLUSION: Findings reveal differential associations between levels of adiponectin with type 2 diabetes and hypertension likelihood among African American women. More research is needed to elucidate this differential association.

A cross-sectional study of the prevalence and risk factors for hypertension in rural Nepali women.

BACKGROUND: The prevalence of hypertension is increasing in much of the South Asian region, including Nepal. This paper reports the prevalence and risk factors of hypertension and pre-hypertension among adult women in a rural community of Nepal. METHODS: Cross-sectional data on socioeconomic status (SES), lifestyle factors and blood pressure (BP) were collected from a cohort of 15,934 women in rural Nepal in 2006-08. Among a subsample (n = 1679), anthropometry and biomarkers of cardiovascular risk were measured. RESULTS: The mean age of women was 34.2 years (range 16.4-71.2 years). More than three percent (3.3%) had hypertension and 14.4% had pre-hypertension. In an adjusted analysis, lower SES, especially lower household farm assets and storage of food for long term consumption, was associated with increased odds of hypertension (OR = 1.14 for mid-level SES and OR = 1.40 for low SES; p for trend < 0.01). Smoking, alcohol use and not working outside the home were also associated with higher risk. In a subsample, both systolic BP (SBP) and diastolic BP (DBP) were positively associated with high triglycerides (SBP ß = 4.1 mm Hg; DBP ß =3.6 mm Hg), high HbA1c (SBP ß = 14.0; DBP ß = 9.2), raised fasting glucose (SBP ß = 10.0; DBP ß = 6.9), high BMI (SBP ß = 6.7; DBP ß = 5.1) and high waist circumference (SBP ß = 6.2; DBP ß = 5.3) after adjusting for potential confounders (p for all <0.01). CONCLUSIONS: Although the prevalence of hypertension was low in this cohort, it was more prevalent among the poorer women and was strongly associated with other cardiovascular risks. These associations at a relatively young age may confer greater risk for cardiovascular disease among women in later life, indicating the need for interventions to reduce the progression from pre-hypertension to hypertension.

Association of Childhood Socioeconomic Status with Leukocyte Telomere Length Among African Americans and the Mediating Role of Behavioral and Psychosocial Factors: Results from the GENE-FORECAST Study.

PURPOSE: We examined if childhood socioeconomic status (SES) was related to adult leucocyte telomere length (TL) using the data of 361 African American (AA) participants from the GENE-FORECAST Study. We also assessed the mediating role of behavioral and psychosocial factors in the association between childhood SES and adult TL. METHODS: Childhood SES was assessed individually by using participant's mother's education and occupation, father's education and occupation, parental home ownership, and family structure. TL was assessed using the quantitative polymerase chain reaction method. Information on potential confounders and mediators were collected. The associations of childhood SES with TL were assessed using multivariable linear regression models. We used path analysis to quantify and test the share of these associations that was statistically explained by each of the mediators (participant's educational attainment, smoking status, physical activity, dietary habit, perceived stress, and depressive symptoms). RESULTS: Mother's education was associated with longer average TL (ß: 0.021; 95% CI: 0.001, 0.04, p=0.038) in confounder adjusted models. Once mediators were introduced in the model, the estimates were reduced and remained marginally significant (ß: 0.017; 95% CI: -0.003, 0.038, p=0.061). According to path model, approximately 19% of the effect of mother's education on TL (ß: 0.004; 95% CI: -0.001, 0.01, p < 0.10) was mediated through participant's own education level. No significant mediation effect was observed for any other mediators. CONCLUSIONS: These data provide evidence that participant's mother's education was positively linked to adult TL in AA population. Participant's own educational level partially explained this association.

Adiposity and Leukocyte Telomere Length in US Adults by Sex-Specific Race/Ethnicity: National Health and Nutrition Examination Survey.

Objective: Little is known about the relationship between adiposity and telomere length in the United States population. The objective of our research was to examine this relationship in a representative, socioeconomically and sex-specific, diverse racial/ethnic population in the United States. Methods: Body mass index (BMI), % total body fat (TBF) and waist circumference (WC) with leukocyte telomere length (LTL) were examined according to sex-specific race/ethnicity using separate adjusted multivariate linear regressions on a sample of 4,919 respondents aged 20-84 years from the National Health and Nutrition Examination Survey's 1999-2002 data. Results: LTL was shortened .41%, .44%, and .16% in African American (AA) women and was associated with increasing BMI, %TBF, and WC, (ß:-.0041, 95%CI: -.0070, -.0012; P=.007; ß:-.0044, 95% CI: -.0081, -.0007; P=.02; ß:-.0016, 95%CI: -.0031, -.0001; P=.04, respectively). LTL was shortened .29% in White women and was associated with increasing %TBF (ß:-.0029, 95%CI: -.0048, -.0009; P=.006). There were no associations among AA men, White men or Mexican American men and women. Conclusions: LTL is associated with an obesity phenotype in AA women. Tailored intervention is needed to ameliorate the burden of excess adiposity and subsequent cellular aging.

Associations of smoking indicators and cotinine levels with telomere length: National Health and Nutrition Examination Survey.

The influence of smoking exposure on telomere length with a focus on the impact of race has rarely been discussed. We performed a cross sectional analysis into the associations of smoking indicators with leukocyte telomere length (LTL) by race among 5864 nationally representative sample of US adults (≥20 years). Data from 1999 to 2002 National Health and Nutrition Examination Survey was used for the analysis. Smoking indicators were assessed by interviews and serum cotinine levels. LTL was quantified by polymerase chain reaction. Multiple linear regressions were used to assess the association with adjustment for covariates, sample weights and design effects separately for Whites, Blacks and Mexican Americans. The intensity of smoking, measured by the average number of cigarettes consumed per day, was negatively associated with LTL among Whites (ß: -3.87, 95% CI: -5.98 to -1.21) and among Blacks (ß: -15.46, 95% CI: -29.79 to -2.12) participants. Compared with cotinine level < 0.05 ng/ml, cotinine level ≥3 ng/ml was associated with shorter LTL (ß: -77.92, 95% CI = -143.05 to -11.70) among Whites, but not among Blacks. We found increased number of cigarette consumption to be associated with shorter LTL in both Blacks and Whites, indicating that the impact of smoking on life-shortening diseases could partly be explained by telomere biology. Increased cotinine concentration however, was associated with shorter LTL only among Whites, not among Blacks. This differential relationship that we observed may have implications in interpreting cotinine as an objective biomarker of smoking exposure across races and warrant additional prospective investigation.

Less Than Ideal Cardiovascular Health Is Associated With Shorter Leukocyte Telomere Length: The National Health and Nutrition Examination Surveys, 1999-2002.

BACKGROUND: The associations between individual cardiovascular disease risk factors and leukocyte telomere length (LTL) have been inconclusive. We investigated the association between LTL and overall cardiovascular health (CVH) as defined by the American Heart Association and whether the association is modified by sex and race/ethnicity. METHODS AND RESULTS: We included 5194 adults (aged ≥20) from the National Health and Nutrition Examination Survey 1999-2002. CVH was defined as a composite score of the 7 metrics (smoking, physical activity, diet, body mass index, blood pressure, total cholesterol, and fasting blood glucose) and categorized as "poor," "intermediate," and "ideal." LTL was assayed from whole blood using the quantitative polymerase chain reaction method relative to standard reference DNA. Multivariable linear regression models were used to estimate the association between CVH and log-transformed LTL. We found strong graded association between CVH and LTL in the overall sample, with evidence of dose-response relationship (P for trend=0.013). Individuals with poor and intermediate CVH had significantly shorter LTL than individuals with ideal CVH (-3.4% [95% CI=-6.0%, -0.8%] and -2.4% [-4.4%, -0.3%], respectively), after adjustment for demographic variables, socioeconomic status, and C-reactive protein. The association was stronger in women (-6.6% [-10.2%, -2.9%] for poor vs ideal CVH) and non-Hispanic whites (-4.3% [-7.1%, -1.4%] for poor vs ideal CVH). CONCLUSIONS: The findings suggest that less-than-ideal CVH is associated with shorter LTL, but this association varies by sex and race/ethnicity. Future longitudinal research is needed to elucidate the mechanisms that underlie the association between CVH and LTL.

Perceived neighborhood problems are associated with shorter telomere length in African American women.

OBJECTIVES: African Americans (AA) experience higher levels of stress related to living in racially segregated and poor neighborhoods. However, little is known about the associations between perceived neighborhood environments and cellular aging among adult AA. This study examined whether perceived neighborhood environments were associated with telomere length (TL) in AA after adjustment for individual-level risk factors. METHODS: The analysis included 158 women and 75 men AA aged 30-55 years from the Morehouse School of Medicine Study. Relative TL (T/S ratio) was measured from peripheral blood leukocytes using quantitative real-time polymerase chain reaction. Multivariable linear regression models were used to examine the associations of perceived neighborhood social cohesion, problems, and overall unfavorable perceptions with log-TL. RESULTS: Women had significantly longer TL than men (0.59 vs. 0.54, p=0.012). After controlling for sociodemographic, and biomedical and psychosocial factors, a 1-SD increase in perceived neighborhood problems was associated with 7.3% shorter TL in women (Mean Difference [MD]=-0.073 (Standard Error=0.03), p=0.012). Overall unfavorable perception of neighborhood was also associated with 5.9% shorter TL among women (MD=-0.059(0.03), p=0.023). Better perceived social cohesion were associated with 2.4% longer TL, but did not reach statistical significance (MD=0.024(0.02), p=0.218). No association was observed between perceived neighborhood environments and TL in men. CONCLUSIONS: Our findings suggest that perceived neighborhood environments may be predictive of cellular aging in AA women even after accounting for individual-level risk factors. Additional research with a larger sample is needed to determine whether perceived neighborhood environments are causally related to TL.

Cost of management of severe pneumonia in young children: systematic analysis.

BACKGROUND: Childhood pneumonia is a major cause of childhood illness and the second leading cause of child death globally. Understanding the costs associated with the management of childhood pneumonia is essential for resource allocation and priority setting for child health. METHODS: We conducted a systematic review to identify studies reporting data on the cost of management of pneumonia in children younger than 5 years old. We collected unpublished cost data on non-severe, severe and very severe pneumonia through collaboration with an international working group. We extracted data on cost per episode, duration of hospital stay and unit cost of interventions for the management of pneumonia. The mean (95% confidence interval, CI) and median (interquartile range, IQR) treatment costs were estimated and reported where appropriate. RESULTS: We identified 24 published studies eligible for inclusion and supplemented these with data from 10 unpublished studies. The 34 studies included in the cost analysis contained data on more than 95 000 children with pneumonia from both low- and-middle income countries (LMIC) and high-income countries (HIC) covering all 6 WHO regions. The total cost (per episode) for management of severe pneumonia was US$ 4.3 (95% CI 1.5-8.7), US$ 51.7 (95% CI 17.4-91.0) and US$ 242.7 (95% CI 153.6-341.4)-559.4 (95% CI 268.9-886.3) in community, out-patient facilities and different levels of hospital in-patient settings in LMIC. Direct medical cost for severe pneumonia in hospital inpatient settings was estimated to be 26.6%-115.8% of patients' monthly household income in LMIC. The mean direct non-medical cost and indirect cost for severe pneumonia management accounted for 0.5-31% of weekly household income. The mean length of stay (LOS) in hospital for children with severe pneumonia was 5.8 (IQR 5.3-6.4) and 7.7 (IQR 5.5-9.9) days in LMIC and HIC respectively for these children. CONCLUSION: This is the most comprehensive review to date of cost data from studies on the management of childhood pneumonia and these data should be helpful for health services planning and priority setting by national programmes and international agencies.

Relationship between obesity and coronary heart disease among urban Bangladeshi men and women.

The aim of the study was to examine the association of different measures of obesity (body mass index or BMI, waist circumference or WC, waist to hip ratio or WHR and waist height ratio or WHtR) with coronary heart disease (CHD) in a Bangladeshi population. The study included 189 hospitalized CHD cases (133 men and 52 women) and 201 controls (137 men and 68 women). Logistic regression was done to assess the associations between obesity and CHD. The mean age was 53.1 ± 8.3 for men and 51.9 ± 8.4 for women. After adjustment for confounders the odds ratio (OR) of CHD for men was 1.69 (95% CI, 1.24-2.32), 1.94 (95% CI 1.40-2.70), and 1.32 (95% CI, 1.01-2.16) per 1 standard deviation (SD) increase in BMI, WC, and WHtR respectively. The OR for women was 2.64 (CI, 1.61-4.34), 1.82 (95% CI 1.12-2.95), 2.32 (95% CI, 1.36-3.96), and 1.94 (95% CI, 1.23-3.07) per 1 SD increase in BMI, WC, WHtR and WHR respectively. Since both total obesity and abdominal adiposity were associated with development of CHD and since measurement of WC and BMI are inexpensive, both should be included in the clinical setting for CHD risk assessment for this group of population.