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The goal of this American Heart Association Guide for Improving Cardiovascular Health at the Community Level (AHA Community Guide) is to provide a comprehensive inventory of evidence-based goals, strategies, and recommendations for cardiovascular disease (CVD) and stroke prevention that can be implemented on a community level. This guide advances the 2003 AHA Community Guide1 and the 2005 AHA statement on guidance for implementation2 by incorporating new evidence for community interventions gained over the past decade, expanding the target audience to include a broader range of community advocates, aligning with the concepts and terminology of the AHA 2020 Impact Goals, and recognizing the contributions of new public and private sector programs involving community interventions. In recent years, expanding arrays of programs and policies have been implemented in increasingly diverse communities to provide tools, strategies, and other best practices to potentially reduce the incidence of initial and recurrent cardiovascular events. The AHA Community Guide complements the AHA statement entitled “Population Approaches to Improve Diet, Physical Activity, and Smoking Habits”3 and supports the AHA 2020 goal4 to “improve the cardiovascular health of all Americans by 20%, while reducing deaths from CVDs and stroke by 20%.” The present AHA Community Guide supports the AHA 2020 goal by identifying exemplary regional or national programs that encourage cardiovascular health behaviors and health factors (formerly addressing risk behaviors and risk factors) from which communities might acquire proven strategies, expertise, and technical assistance for improving cardiovascular health. The AHA Community Guide seeks to prevent the onset of disease (primary prevention) and to maintain optimal cardiovascular health (primordial prevention) among broader segments of the population. Prior research indicates that using public health strategies such as sodium reduction in processed foods to lower blood pressure,5–8 tobacco laws to promote smoking cessation,9–11 and modification of …

BACKGROUND: Despite established relationships between physical activity (PA) or physical fitness (fitness) and metabolic risk, the prospective association is not well understood. The purpose of this study was to determine whether metabolic risk in young adults is associated with 20-year PA or fitness trajectories. METHODS: Young adults were from the Coronary Artery Risk Development in Young Adults (CARDIA) study, baseline ages 18–30 years (n=4161). PA was determined from a self-reported questionnaire administered at baseline and at follow-up exams at years 2, 5, 7, 10, 15, and 20. Fitness (seconds) was estimated from a graded exercise treadmill test at baseline and years 7 and 20. Baseline metabolic risk was calculated using age-adjusted principal components analysis (elevated=top 10% of first factor), for each sex–race group, from mean arterial pressure, glucose, waist circumference, triglycerides, and high-density lipoprotein cholesterol. Repeated measures general linear modeling estimated PA and fitness trajectories over 20 years, separately in sex–race groups, adjusting for age and smoking status. RESULTS: PA was significantly lower among those with elevated metabolic risk compared with normal risk at baseline and each subsequent time point (black and white men, white women; all P

Serum B-type natriuretic peptide (BNP) levels reflect myocardial strain and are known to be elevated in patients with heart failure. To determine if BNP levels are elevated in patients with aortic regurgitation, we measured BNP levels in patients with chronic asymptomatic aortic regurgitation and normal left ventricular systolic function.

Although alcohol consumption and cigarette smoking are common behaviors in reproductive-age women, little is known about the impact of consumption patterns on ovarian reserve. Even less is known about the effects of smoking and alcohol use in reproductive-age African-American women.The objective of the study was to examine the impact of the patterns of alcohol intake and cigarette smoking on anti-Müllerian hormone levels as a marker of ovarian reserve in African-American women.This was a cross-sectional analysis from the baseline clinical visit and data collection of the Study of Environment, Lifestyle, and Fibroids performed by the National Institute of Environmental Health Sciences. A total of 1654 volunteers, aged 23-34 years, recruited from the Detroit, Michigan community completed questionnaires on alcohol intake and cigarette smoking and provided serum for anti-Müllerian hormone measurement. Multivariable linear and logistic regressions were used as appropriate to estimate the effect of a range of exposure patterns on anti-Müllerian hormone levels while adjusting for potential confounders including age, body mass index, and hormonal contraception.Most participants were alcohol drinkers (74%). Of those, the majority (74%) engaged in binge drinking at least once in the last year. Women who reported binge drinking twice weekly or more had 26% lower anti-Müllerian hormone levels compared with current drinkers who never binged (95% confidence interval, -44, -2, P.04). Other alcohol consumption patterns (both past and current) were unrelated to anti-Müllerian hormone. The minority of participants currently (19%) or formerly (7%) smoked, and only 4% of current smokers used a pack a day or more. Neither smoking status nor second-hand smoke exposure in utero, childhood, or adulthood was associated with anti-Müllerian hormone levels.Results suggest that current, frequent binge drinking may have an adverse impact on ovarian reserve. Other drinking and smoking exposures were not associated with anti-Müllerian hormone in this cohort of healthy, young, African-American women. A longitudinal study of how these common lifestyle behaviors have an impact on the variability in age-adjusted anti-Müllerian hormone levels is merited.

Objective To characterize normative antimullerian hormone (AMH) levels and ascertain which factors are associated with AMH in a large cohort of reproductive-age women. Design Cross-sectional study. Setting Not applicable. Patient(s) A total of 1,654 African-American women (AAW) ages 23–34 at recruitment. Intervention(s) Not applicable. Main Outcome Measure(s) Serum AMH measured using an ultrasensitive ELISA. Result(s) The median AMH was 3.18 ng/mL, and there was a significant, but nonlinear, relationship between age and AMH, with levels peaking at age 25. As AMH was not normally distributed, log transformation was performed and used for all analyses. In a multivariable age-adjusted model, body mass index, current use of hormonal contraception, and history of a thyroid condition were inversely associated with AMH, while history of abnormal menstrual bleeding and menstrual cycles longer than 35 days were positively associated with AMH. Conclusion(s) While age is correlated with AMH, it accounts for only a portion of the variation seen. This study adds valuable information to the existing literature on normative AMH levels in young reproductive-age women. While our findings fill a critical data gap for ovarian reserve in AAW, the insights gained will be of benefit for all women.

Objective It is well known that A1c varies by race. However, racial differences in other biomarkers of hyperglycemia are less well characterized. The objective of this study was to determine whether average levels of glycemic markers differ by race in adults with and without diagnosed diabetes, before and after accounting for postchallenge glucose. Research design and methods This cross-sectional study included 2692 middle-aged men and women (5.5% with diagnosed diabetes; 44% African-American; and 56% white) from the Coronary Artery Risk Development in Young Adults Study (2005–2006) who had fasting glucose, 2-hour postchallenge glucose, A1c, glycated albumin, fructosamine, and 1,5-anhydroglucitol (1,5-AG) measured. Multiple linear regression was used to evaluate racial differences in mean levels of each glycemic marker stratified by the diabetes status and adjusted for sociodemographics, cardiovascular factors, and postchallenge glucose. Results Among those with diagnosed diabetes, racial differences were not observed for any of the glycemic markers. In contrast, among those without diagnosed diabetes, African-Americans had higher mean levels than whites of A1c (β=0.19% points; 95% CI 0.14 to 0.24), glycated albumin (β=0.82% points; 95% CI 0.68 to 0.97), fructosamine (β=8.68 μmol/L; 95% CI 6.68 to 10.68), and 2-hour glucose (β=3.50 mg/dL; 95% CI 0.10 to 6.90) after multivariable adjustment, whereas there were no statistically significant racial difference in 1,5-AG. The racial differences observed for A1c, glycated albumin, and fructosamine persisted after further adjustment for fasting and 2-hour glucose and were of similar magnitude (SD units). Conclusions Racial differences in glycemic marker levels were evident among middle-aged adults without diagnosed diabetes even after adjustment for postchallenge glucose. Whether these racial differences in biomarkers of hyperglycemia affect the risk of complications warrants additional study.

Background We tested the hypothesis that selected exercise heart rate responses, specifically those providing indices of autonomic dysfunction, may be associated with incident type 2 diabetes in 2231 apparently healthy men with normal baseline fasting glucose levels. Methods Heart rate reserve was calculated as the difference between the maximal attained heart rate and the supine resting heart rate, whereas heart rate recovery was defined as the maximal heart rate minus the heart rate measured at 2 minutes of recovery after peak or symptom-limited cardiopulmonary exercise testing. Type 2 diabetes was defined as glycated hemoglobin >6.5% or fasting plasma glucose >126 mg/dL at the follow-up examination. Results During a median follow-up interval of 5 years, 90 of the 2231 men (4.0%) developed type 2 diabetes. The relative risks of incident type 2 diabetes in men within the lowest quartiles of heart rate reserve and heart rate recovery versus men comprising the highest quartiles of heart rate reserve and heart rate recovery were 2.71 (95% confidence interval, 1.20-6.11) and 2.81 (95% confidence interval, 1.36-5.78) after adjusting for potential confounding variables. Each unit increment (1 beat/min) in heart rate reserve and heart rate recovery was associated with a 2% to 3% decreased incidence of type 2 diabetes. Conclusions Exercise heart rate reserve and recovery predicted incidence of type 2 diabetes in healthy men, suggesting that autonomic dysfunction may be associated with an increased likelihood for the development of this cardiometabolic risk factor.

Type 2 diabetes in normal-weight adults (body mass index [BMI]25) is a representation of the metabolically obese normal-weight phenotype with unknown mortality consequences.To test the association of weight status with mortality in adults with new-onset diabetes in order to minimize the influence of diabetes duration and voluntary weight loss on mortality.Pooled analysis of 5 longitudinal cohort studies: Atherosclerosis Risk in Communities study, 1990-2006; Cardiovascular Health Study, 1992-2008; Coronary Artery Risk Development in Young Adults, 1987-2011; Framingham Offspring Study, 1979-2007; and Multi-Ethnic Study of Atherosclerosis, 2002-2011. A total of 2625 participants with incident diabetes contributed 27,125 person-years of follow-up. Included were men and women (age40 years) who developed incident diabetes based on fasting glucose 126 mg/dL or greater or newly initiated diabetes medication and who had concurrent measurements of BMI. Participants were classified as normal weight if their BMI was 18.5 to 24.99 or overweight/obese if BMI was 25 or greater.Total, cardiovascular, and noncardiovascular mortality.The proportion of adults who were normal weight at the time of incident diabetes ranged from 9% to 21% (overall 12%). During follow-up, 449 participants died: 178 from cardiovascular causes and 253 from noncardiovascular causes (18 were not classified). The rates of total, cardiovascular, and noncardiovascular mortality were higher in normal-weight participants (284.8, 99.8, and 198.1 per 10,000 person-years, respectively) than in overweight/obese participants (152.1, 67.8, and 87.9 per 10,000 person-years, respectively). After adjustment for demographic characteristics and blood pressure, lipid levels, waist circumference, and smoking status, hazard ratios comparing normal-weight participants with overweight/obese participants for total, cardiovascular, and noncardiovascular mortality were 2.08 (95% CI, 1.52-2.85), 1.52 (95% CI, 0.89-2.58), and 2.32 (95% CI, 1.55-3.48), respectively.Adults who were normal weight at the time of incident diabetes had higher mortality than adults who are overweight or obese.

Background— Because depression is a multidimensional construct and few studies have compared the relative importance of its facets in predicting cardiovascular risk, we evaluated the utility of depressive symptom clusters in predicting the 5-year incidence of coronary artery calcification (CAC). Methods and Results— Participants were 2171 middle-aged adults (58% female; 43% black) from the Coronary Artery Risk Development in Young Adults (CARDIA) study who were free of cardiovascular disease. Depressive symptom clusters ( z scores) were measured by questionnaires in 2000 to 2001, and CAC was measured by electron beam computed tomography in 2000 to 2001 and 2005 to 2006. There were 243 cases (11%) of incident CAC, defined as the absence of CAC at baseline and the presence of CAC at follow-up. Total depressive symptoms (odds ratio, 1.16; 95% confidence interval, 1.02–1.33; P =0.03) and the depressed affect cluster (odds ratio, 1.17; 95% confidence interval, 1.03–1.33; P =0.02) predicted incident CAC; however, the somatic, interpersonal distress, low positive affect, and pessimism clusters did not. The depressed affect–incident CAC relationship was independent of age, sex, race, education, and antidepressant use; was similar across sex and racial groups; and was partially accounted for by tobacco use and mean arterial pressure. Conclusions— In contrast to recent results indicating that the somatic cluster is the most predictive of cardiovascular outcomes, we found that the prospective association between depressive symptoms and incident CAC was driven by the depressed affect cluster. Our findings raise the possibility that there may not be 1 facet of depression that is the most cardiotoxic across all contexts.

Background— No studies have compared first cardiovascular disease (CVD) events and non-CVD death between races in a competing risks framework, which examines risks for numerous events simultaneously. Methods and Results— We used competing Cox models to estimate hazards for first CVD events and non-CVD death within and between races in 3 multicenter, National Heart, Lung, and Blood Institute–sponsored cohorts. Of 14 569 Atherosclerosis Risk in Communities (ARIC) study participants aged 45 to 64 years with mean follow-up of 10.5 years, 11.6% had CVD and 5.0% had non-CVD death as first events; among 4237 Cardiovascular Health Study (CHS) study participants aged 65 to 84 years and followed for 8.5 years, these figures were 43.2% and 15.7%, respectively. Middle-aged blacks were significantly more likely than whites to experience any CVD as a first event; this disparity disappeared by older adulthood and after adjustment for CVD risk factors. The pattern of results was similar for Multi-Ethnic Study of Atherosclerosis (MESA) participants. Traditional Cox and competing risks models yielded different results for coronary heart disease risk. Black men appeared somewhat more likely than white men to experience coronary heart disease with use of a standard Cox model (hazard ratio 1.06; 95% CI 0.90, 1.26), whereas they appeared less likely than white men to have a first coronary heart disease event with use of a competing risks model (hazard ratio, 0.77; 95% CI, 0.60, 1.00). Conclusions— CVD affects blacks at an earlier age than whites; this may be attributable in part to elevated CVD risk factor levels among blacks. Racial disparities in first CVD incidence disappear by older adulthood. Competing risks analyses may yield somewhat different results than traditional Cox models and provide a complementary approach to examining risks for first CVD events.

Genotype does not change over the life course and may thus facilitate earlier identification of individuals at high risk for type 2 diabetes. We hypothesised that a genotype score predicts incident type 2 diabetes from young adulthood and improves diabetes prediction models based on clinical risk factors alone.The Coronary Artery Risk Development in Young Adults (CARDIA) study followed young adults (aged 18-30 years, mean age 25) serially into middle adulthood. We used Cox regression to build nested prediction models for incident type 2 diabetes based on clinical risk factors assessed in young adulthood (age, sex, race, parental history of diabetes, BMI, mean arterial pressure, fasting glucose, HDL-cholesterol and triacylglyercol), without and with a 38-variant genotype score. Models were compared with C statistics and continuous net reclassification improvement indices (NRI).Of 2,439 participants, 830 (34%) were black and 249 (10%) had a BMI ≥ 30 kg/m(2) at baseline. Over a mean 23.9 years of follow-up, 215 (8.8%) participants developed type 2 diabetes. The genotype score significantly predicted incident diabetes in all models, with an HR of 1.08 per risk allele (95% CI 1.04, 1.13) in the full model. The addition of the score to the full model modestly improved reclassification (continuous NRI 0.285; 95% CI 0.126, 0.433) but not discrimination (C statistics 0.824 and 0.829 in full models with and without score). Race-stratified analyses were similar.Knowledge of genotype predicts type 2 diabetes over 25 years in white and black young adults but may not improve prediction over routine clinical measurements.

Low-cardiorespiratory fitness (CRF) has been associated with incident hypertension, but whether temporal changes in CRF are associated with incident hypertension in initially normotensive subjects are not known. We investigated the relationship of baseline CRF and longitudinal changes in CRF with incident hypertension in initially normotensive subjects.Subjects were 3,831 men who participated in two health examinations during 1998-2009. All subjects were free of cardiovascular diseases and hypertension at baseline. CRF was directly measured by peak oxygen uptake using expired gas analysis during a standard treadmill test.During an average of 5 years of follow-up, 373 (9.7%) subjects developed hypertension. The incidence of hypertension was inversely associated with baseline CRF quartiles [Q1 (lowest) 11.8%, Q2 10.4%, Q3 9.1%, and Q4 (highest) 7.5%; P0.05 for trend]. The relative risk (RR) of incident hypertension in the lowest CRF quartile versus the highest CRF quartile was 1.69 (95% CI: 1.22-2.34) after adjustment for risk factors. Each metabolic equivalent increment higher peak oxygen uptake at baseline examination was associated with 10% (RR 0.90, 95% CI: 0.83-0.98) lower incidence of hypertension in multivariate adjusted model. Subjects whose CRF decreased (-1.18 ml/kg/min per year) over time had a 72% increased risk in developing hypertension (RR 1.72, 95% CI: 1.20-2.49) compared to subjects with increased CRF (0.13 ml/kg/min per year) after adjustment for risk factors.These results demonstrate that both baseline CRF levels and changes in CRF over time were associated with the incidence of hypertension independent of risk factors.

Background: Chronic stress associated with living in poverty may lead to higher levels of adiposity due to the adoption of obesity-promoting stress coping behaviors. Social support may provide an alternative means of coping with stress, but very few studies have investigated whether high levels of social support can mitigate the adverse impact of poverty on adiposity. Hypothesis: We hypothesized that social support modified the association between poverty and BMI whereby the association of poverty with BMI was weaker among adults who reported higher social support. Methods: National Health and Nutrition Examination Survey (2005–2008) participants ages 40+ (n=5,768) responded to questions about availability and adequacy of emotional social support (adequate, inadequate, and none) and about availability of financial support (yes/no). Poverty was defined as a poverty:income ratio ≤ 1.3. BMI (kg/m 2 ) was calculated from measured height and weight. Sex-stratified multivariable linear regression with interaction terms for poverty and each measure of social support were used to test for effect measure modification in the relationships between poverty and BMI. Associations of each measure of social support with BMI were modeled separately. Results: Approximately 74.7% of women and 78.3% of men reported adequate emotional support. Available financial support was reported by 80.3% of women and 73.6% of men. Among women, higher poverty was related to higher mean BMI (beta=0.96; SE=0.32). Women who reported adequate emotional support had lower BMI than those who reported inadequate support (beta= −0.83; SE=0.35). Those who reported no available emotional support also had marginally lower mean BMI than women who reported inadequate support (beta= −1.27; SE=0.65; P =0.06). Women who reported having available financial support had lower BMI than those who reported no financial support (beta= −0.97; SE=0.40). There were no significant social support*poverty interactions. The relationship between poverty and BMI was similar in magnitude across levels of emotional support. Poverty was related to higher mean BMI for women who reported available financial support (beta=1.14; SE=0.45) but there was no difference in BMI among those who reported none (beta=0.02; SE=0.54). Neither measure of support was associated with BMI among men. Conclusions: Inadequate emotional support was associated with higher mean BMI in women than those who reported adequate support and those who reported no support. Lack of financial support was also associated with higher mean BMI in women. High social support did not offset the impact of poverty on BMI among women, suggesting social support may not be a sufficient strategy for coping with the stress of poverty.

Lean Locomotor Muscle Mass Associated With Elevated Depressive Symptoms: The Multi-Ethnic Study of Atherosclerosis Rosemay A Remigio-Baker, MPH, PhDc, Matthew A Allison, MD, MPH, PhD, MPH, Pamela J Schreiner, PhD, MS, MS, Mercedes R Carnethon, PhD, Jennifer A Nettleton, PhD, Mahasin J Mujahid, PhD, Moyses Szklo, MD, DrPH, Rosa M Crum, MD, MPH, Manuel Franco, MD, PhD, Nicole Jensky, PhD, Sherita Hill Golden, MD, MHS BACKGROUND: Physical activity reduces depressive symptoms but it is unclear whether one physiologic response to activity, higher lean muscle mass, is associated with depression. METHODS: Using data from 976 men and women (45-84 years) from the Multi-Ethnic Study of Atherosclerosis (MESA) Body Composition, Inflammation and Cardiovascular Disease and the MESA Neighborhood Ancillary Studies, we examined the cross-sectional association between elevated depressive symptoms (EDS, defined as a Center for Epidemiologic Studies for Depression Scale (CES-D) score > 16) and CT-measured lean muscle mass in the abdomen using multilevel mixed-effects linear regression models. Muscles were categorized by functionality (locomotion vs. stabilization/posture) and combined (see Table). Covariates included demographics, antidepressant use, inflammatory markers, health behaviors, social support, comorbidities, body mass index (BMI) and neighborhood factors: physical and social environment (see Table). Gender, physical environment and social environment were also assessed as potential modifiers. RESULTS: Lean mass of muscle for locomotion was 4.25% lower among participants with EDS compared to those without after adjustment for demographics and antidepressant use (95% CI=-8.20, -0.30; see Table). This association remained significant after additional adjustment for inflammatory markers, health behaviors, social support, comorbidities, neighborhood factors and BMI (see Table). Results were significant in the fully-adjusted model (see Table). No association was observed between EDS and muscle for stabilization/posture. There were no interactions by gender or neighborhood factors. CONCLUSION: Elevated depressive symptoms is associated with less lean muscle for locomotion independent of obesity and physical activity; however, further investigation is necessary in larger samples to confirm and determine the clinical relevance of this association. TABLE Percent Difference a in Lean Muscle Mass b , in cm 2 , (95% Confidence Interval) Between Individuals With Versus Without Elevated Depressive Symptoms By Muscle Category c MODEL All Muscle Locomotion d Stabilization/ Posture e MODEL 1: Univariate −5.75 (-11.0, -0.49)+ −9.25 (-15.3, -3.25)+ −5.04 (-10.4, 0.28) MODEL 2: Demographics f −1.96 (-4.94, 1.01) −4.35 (-8.30, -0.45)+ −1.48 (-4.58, 1.62) MODEL 3: Model 1 + Antidepressant Use −1.88 (-4.88, 1.11) −4.25 (-8.20, -0.30)+ −1.40 (-4.52, 1.72) MODEL 4: Model 3 + Inflammatory Markers g −1.84 (-4.83, 1.15) −4.20 (-8.15, -0.25)+ −1.38 (-4.49, 1.75) MODEL 5: Model 3+ Health Behaviors h −2.28 (-5.26, 0.68) −4.35 (-8.25, -0.45)+ −1.85 (-4.95, 1.25) MODEL 6: Model 3+ Social Support −1.75 (-4.83, 1.33) −4.35 (-8.45, -0.30)+ −1.22 (-4.43, 1.98) MODEL 7: Model 3 + Comorbidity i −1.89 (-4.88, 1.10) −4.05 (-8.00, -0.10)+ −1.45 (-4.56, 1.66) MODEL 8: Model 3 + Neighborhood Factors j −1.49 (-4.47, 1.48) −4.20 (-8.15, -0.25)+ −0.99 (-4.09, 2.11) MODEL 9: Model 3 + Body Mass Index −2.46 (-5.36, 0.45) −4.60 (-8.55, -0.70)+ −1.98 (-5.03, 1.05) MODEL 10: Fully-Adjusted Model −2.11 (-5.07, 0.85) −4.55 (-8.55, -0.60)+ −1.66 (-4.76, 1.44) a Percent difference is calculated by diving the estimate by the mean of the muscle category (x100). b Mean (range): for all muscle mass [117.3 cm 2 (42.9-228.7 cm 2 )]; for locomotion muscle mass [20.0 cm 2 (4.7-40.7 cm 2 )]; for stabilization/posture muscle mass [97.3 cm 2 (36.9 - 198.3 cm 2 )] c There were no significant interaction by gender, physical environment or social environment d Muscle for locomotion: psoas e Muscle for stabilization and posture: rectus abdominus, obliques, paraspinal f Demographics: age, race, gender, marital status, study site, highest level of education attained, income level g Inflammatory Markers: Interleukin-6, C-reactive protein h Health Behaviors: Pack-years of smoking, alcohol intake/week, total intentional exercise, daily caloric intake, dietary patterns (1. High-fat and processed food; 2. Vegetables and fish; 3. Beans, tomatoes and refined grains; 4. Whole grain and fruits) i Comorbidity: Having at least one of the following: Cancer, Type II Diabetes and Hypertension j Neighborhood Factors: Median Income, % with High School education, Physical Environment (walking environment, availability of healthy foods), Social Environment (aesthetic quality, safety and social cohesion) + Significant p-value < 0.05

Introduction: Recent studies report an association between early age at menarche and risk of type 2 diabetes (T2D). However, information in young women is limited to self-reported diabetes in primarily white populations. We explored the association of age at menarche and clinically-defined T2D among young black and white women (mean age 25 at baseline) in the Coronary Artery Risk Development in Young Adults (CARDIA) cohort. Hypothesis: We assessed the hypothesis that the rate for T2D will decrease with each 1 year increase in age at menarche. Methods: Our analysis included 1,258 white and 1,341 black women (total=2,599) who participated in CARDIA during 1985-2006. We used Cox proportional hazards models to estimate hazard ratios (HR) for T2D (yes/no as determined at clinic visits) by continuous age at menarche. We excluded women with diabetes at baseline, missing age at menarche, or menarche 18 years. T2D was defined cumulatively from baseline among non-pregnant women as fasting blood glucose ≥ 126 mg/dl, A1C ≥ 6.5%, 2-hour oral glucose tolerance ≥ 200 mg/dl, or use of diabetes medication. Adjusted models included race (except race stratified models) and parental history of diabetes, as well as baseline age, education, and BMI as covariates. Results: Mean age at menarche was 12.6 years (SD=1.5; black=12.5, white=12.7). We identified 176 cases of T2D over 20 years of follow-up (cumulative incidence=6.8%). Among all women, the rate for T2D decreased by 16% for each 1 year increase in menarche age ( Table 1 ); we found no evidence of nonlinearity. HRs remained protective, but no longer statistically significant after adjustment for BMI. HRs were lower for white women compared to black women, although a test for race by menarche age interaction was not significant (p=0.26). Conclusions: We found evidence to support the hypothesis that early menarche increases the rate for T2D among young women. Higher baseline BMI among women with earlier menarche appears to attenuate the association of age at menarche and future glucose metabolism. Table 1. Hazard Ratio (HR) of Type 2 Diabetes for Each One Year Increase in Age at Menarche in the CARDIA Study, 1985-2006 Crude Model 1 Model 2 # T2D HR 95% CI HR 95% CI HR 95% CI All Women 176 0.84 0.76, 0.93 0.88 0.79, 0.98 0.94 0.85, 1.04 White 46 0.78 0.64, 0.96 0.83 0.68, 1.02 0.93 0.76, 1.16 Black 130 0.90 0.80, 1.01 0.90 0.80, 1.02 0.96 0.85, 1.08 Model 1: adjusted for race (except for race-stratified models), family history of diabetes, baseline age, and participant level of education at baseline (HS) Model 2: adjusted for variables in Model 1 plus baseline BMI

Introduction: Autonomic nervous system (ANS) dysfunction may contribute to the elevated incidence of hypertension, diabetes and coronary heart disease (CHD) among persons with shortened sleep duration. However, prior studies were conducted in adults who had obstructive sleep apnea (OSA), a correlate of short sleep, or using experimental designs that restricted sleep. To explore whether sleep duration is associated with ANS function in adults free from OSA, we tested whether sleep duration was associated with heart rate variability (HRV) indices that represent autonomic modulation of heart rate. Methods: The Chicago Area Sleep Study (CASS) identified men and women ages 35-64 via commercially available telephone listings. Data from 406 participants who had an apnea/hypopnea indexTM ) were studied. Participants wore wrist actigraphs for 7 days (Actiwatch TM ) to determine average sleep duration, sleep percentage (% of time during overnight sleep interval spent sleeping) and minutes of wake after sleep onset (WASO). A validated questionnaire, the Epworth Sleepiness Scale (ESS), was used to determine daytime sleepiness. Electrocardiograms were continuously recorded from participants for 10 minutes s from supine participants; time and frequency domain HRV indices were calculated from the RR interval to estimate overall autonomic modulation of heart rate (standard deviation of normal RR intervals [SDNN]) and parasympathetic modulation heart rate (high frequency power [HF], square root of the mean squared difference of successive R-R intervals [rMSSD]). Height and weight were measured and hypertension and diabetes were determined according to JNC-VII and American Diabetes Association 2010 criteria, respectively. Results: Participants’ mean age was 47.5 years, and 56% were female. Average sleep duration was 7.03 hours (SD=1.15), sleep percentage was 83% (SD=20.1), WASO was 41.4 min (SD=21) and the ESS score was 6.75 (SD=4.1). Following adjustment for age, race, sex, BMI, hypertension, diabetes, physical activity and smoking, sleep duration (per 1 hr) was significantly (p Conclusions: In contrast to prior studies, shorter sleep duration was associated with more favorable parasympathetic modulation of HR. These unexpected findings may suggest that ANS dysfunction associated with OSA may be attributed to hypoxemia rather than the direct effects of shortened sleep duration.

Background: Excess visceral adiposity tissue (VAT) is associated with elevated free fatty acids that contribute to dyslipidemia, beta cell dysfunction, and insulin resistance. Greater physical activity (PA) is associated with lower VAT cross-sectionally, but whether PA during young adulthood is associated with VAT at middle age independent of general obesity is unclear. Objective: To quantify by sex and race the associations between PA levels in young adulthood with visceral adiposity measured 25 years later. Methods: The Coronary Artery Risk Development in Young Adults (CARDIA) study is a population-based, prospective, observational study of black and white men and women. Habitual PA was determined as the average of baseline and year 7 levels (18–37 yrs) of the CARDIA Physical Activity Score. VAT (cm3) was assessed by computed tomography at the year 25 exam (43–55 yrs, n=1822). Results: Early adulthood PA levels were 15.2% lower in blacks compared to whites (p Conclusions: White men and women engaging in higher PA levels at earlier ages may demonstrate lower visceral adiposity later in life, yet these findings suggest that PA may not be a solely effective approach at reducing/preventing cardiometabolic risk from excess visceral adiposity in black adults. Racial variations in the influence of young adulthood PA on visceral adiposity at middle age may reflect differential influences of PA, PA intensity, or other unmeasured risk factors (e.g., psychosocial stress) on adiposity distribution.

Purpose: To determine whether baseline metabolic risk in young adults is associated with physical activity (PA) trajectories over 20 years. Methods: The sample included young adults from the Coronary Artery Risk Development in Young Adults (CARDIA) study, baseline ages 18–30 years (n= 4161). PA was determined from self-reported questionnaire at baseline and at years 2,5,7,10,15 and 20 of follow-up. Baseline metabolic risk was calculated using age-adjusted principal components analysis (elevated=top 10% of first factor), within sex-by-race groups, from mean arterial pressure (1/3(SBP-DBP)+DBP), glucose, waist circumference, triglycerides, and high-density lipoprotein cholesterol. Repeated measures general linear modeling was used to generate PA trajectories over 20 years, separately in black men, white men, black women and white women, adjusting for age and smoking status. Time by metabolic risk interaction terms did not contribute significantly to any model for any sex-by-race group and were therefore not included in final models. Results: In black men, white men, and white women, PA (in exercise units) at baseline was significantly lower among those with elevated metabolic risk (elevated risk vs. normal risk: black men 473.0 ± 27.0 vs. 572.0 ± 22.7; white men: 498.0 ±20.6 vs. 568.7 ± 17.3; white women: 402.4 ± 17.0 vs. 481.1 ± 14.3), and these differences persisted over 20 years (black men: −98.9 ± 16.4, white men: −70.8 ± 12.5 , white women: −78.7 ± 10.2; all p Conclusion: Elevated metabolic risk is associated with lower levels of PA in early adulthood, and these differences persist over 20 years. Despite these lower levels at baseline, the PA trajectory declines at similar rates for those with and without elevated metabolic risk. Young adults with elevated metabolic risk are important to identify early, in order to prevent PA level gap which remains over 20 years between those with and without elevated metabolic risk.

Neuroendocrine abnormalities, such as activation of the hypothalamic-pituitary-adrenal (HPA) axis, are associated with obesity; however, few large-scale population-based studies have examined HPA axis and markers of obesity. We examined the cross-sectional association of the cortisol awakening response (CAR) and diurnal salivary cortisol curve with obesity. The Multi-Ethnic Study of Atherosclerosis (MESA) Stress Study includes 1,002 White, Hispanic, and Black men and women (mean age 65±9.8 years) who collected up to 18 salivary cortisol samples over 3 days. Cortisol profiles were modeled using regression spline models that incorporated random parameters for subject-specific effects. Cortisol curve measures included awakening cortisol, CAR (awakening to 30 minutes post-awakening), early decline (30 minutes to 2 hours post-awakening), late decline (2 hours post-awakening to bedtime), and the corresponding areas under the curve (AUC). Body-mass-index (BMI) and waist circumference (WC) were used to estimate adiposity. For the entire cohort, both BMI and WC were negatively correlated with awakening cortisol (p

Background: Over 65 million Americans live in Primary Care Health Professional Shortage Areas (HPSAs) which are associated with less preventive care, poorer general health and an increased risk for hospitalizations. However, little is known about how living in a HPSA impacts primary prevention for CVD. Methods: We used data from CARDIA, a multi-center cohort study of black and white men and women. Participants who had risk factor data and geocoded addresses available at year 20 (2005) were included in this analysis (n=3479). Primary care HPSAs were defined using data from US HRSA. Diabetes, hypertension and hyperlipidemia prevalence and control were defined according to ADA Guidelines 2000, JNC VI, and ATP III, respectively. Individuals who reported being diagnosed or reported use of medications were considered aware of the risk factor. The prevalence of smoking and obesity was also examined. Neighborhood (census block) characteristics were derived from Census 2000 and ACCRA. Multivariable Poisson models were used to examine the independent association of HPSA residence with each outcome. Results: Over 11% of CARDIA participants live in a HPSA. Residents of HPSAs were more likely to be female (64% vs 56%), African American (81% vs 43%), have low education, and low income. HPSA residents had more difficulty paying for food/basics and medical care, had poorer access to medical care and lived in areas with a higher cost of healthcare and low neighborhood SES. HPSA residents had a higher prevalence of hypertension (PR 1.39, 95% CI 1.18-1.65), obesity (1.30, 1.16-1.45) and smoking (1.72, 1.46-2.03) and were less likely to have their hypertension (0.79, 0.66-0.95) or hyperlipidemia (0.66, 0.44-0.99) controlled as compared to non-residents. The association between HPSA and risk factors prevalence was explained by race and neighborhood SES. The cost of medical care and having a usual source of care were the largest mediators of the association between HPSA residence and risk factor control. Conclusion: The increased prevalence and poorer control of CVD risk factors in HPSAs, can be explained by the demographic and neighborhood characteristics of their residents. Future interventions should be targeted to these high-risk populations found within HPSAs.

Background and Purpose— Few studies have assessed post-glucose load measures of insulin resistance and ischemic stroke risk, and data are sparse for older adults. We investigated whether fasting and post-glucose load measures of insulin resistance were related to incident ischemic stroke in nondiabetic, older adults. Methods— Participants were men and women in the Cardiovascular Health Study, age 65+ years and without prevalent diabetes or stroke at baseline, followed for 17 years for incident ischemic stroke. The Gutt insulin sensitivity index was calculated from baseline body weight and from fasting and 2-hour postload insulin and glucose; a lower Gutt index indicates higher insulin resistance. Results— Analyses included 3442 participants (42% men) with a mean age of 73 years. Incidence of ischemic stroke was 9.8 strokes per 1000 person-years. The relative risk (RR) for lowest quartile versus highest quartile of Gutt index was 1.64 (95% CI, 1.24–2.16), adjusted for demographics and prevalent cardiovascular and kidney disease. Similarly, the adjusted RR for highest quartile versus lowest quartile of 2-hour glucose was 1.84 (95% CI, 1.39–2.42). In contrast, the adjusted RR for highest quartile versus lowest quartile of fasting insulin was 1.10 (95% CI, 0.84–1.46). Conclusions— In nondiabetic, older adults, insulin resistance measured by Gutt index or 2-hour glucose, but not by fasting insulin, was associated with risk of incident ischemic stroke.

Background: The assessment of fat mass and fat-free mass in relation to the symptom-limited maximal exercise duration (Maxdur) of a treadmill test allows for insight into the association of body composition with treadmill performance potential. Objective: We investigated the complex associations between fat mass and fat-free mass and Maxdur in a population setting. Design: The Maxdur of a graded exercise treadmill test and body composition by dual-energy X-ray absorptiometry were estimated in 2413 black and white men and women aged 38–50 y from the Coronary Artery Risk Development in Young Adults (CARDIA) cohort. Results: The mean Maxdur was ’7.5 s shorter per kilogram of fat mass in both men and women and independent of the fat-free mass, height, race, television watching, physical activity, systolic blood pressure, lung function, and education. Fat mass modified the association of the fat-free mass with the Maxdur (2-way interaction P , 0.001), and the interaction was stronger in women than in men. In men in the lowest fat-mass quartile, the Maxdur was 1.3 s longer per kilogram of fat-free mass and was 0.5 s shorter per kilogram of fat-free mass in the highest fat-mass quartile. In contrast, in women with the least fat mass, the Maxdur was 2.7 s longer per kilogram of fat-free mass and was 2.8 s shorter per kilogram of fat-free mass in the highest fat-mass quartile. Conclusions: The Maxdur was negatively related to fat mass. Fatfree mass in obese people contributed little to the treadmill performance potential as assessed by the Maxdur, although the contribution of fat-free mass was positive in thinner people. Am J Clin Nutr doi: 10.3945/ajcn.110.008995.

Lower extremity fat mass (LEFM) has been shown to be favorably associated with glucose metabolism. However, it is not clear whether this relationship is similar across varying levels of obesity. We hypothesized that lower amounts of LEFM is associated with higher insulin resistance (IR) and this association may vary according to weight status. Participants with available measures were examined from the Coronary Artery Risk Development in Young Adults study (CARDIA), a multi-center longitudinal study of the etiology of atherosclerosis in black and white men and women aged 38-50 years old in 2005-2006 (n = 1,579). The homeostasis model assessment of IR (HOMA(IR)) was calculated to estimate IR, regional adiposity was measured using dual energy X-ray absorptiometry (DXA), and weight status was defined according to BMI categories. Obese and overweight participants exhibited higher IR, total fat mass (FM), trunk FM (TFM), and LEFM compared to normal weight participants. After controlling for age, height, race, study center, education, smoking, and cardiorespiratory fitness (CRF), greater LEFM was significantly associated with higher IR only in normal weight men and women. Further adjustment for TFM revealed that lower LEFM was significantly associated with higher IR in overweight and obese men and women and the positive association in normal weight individuals was attenuated. These results suggest that excess adiposity in the lower extremities may attenuate the metabolic risk observed at a given level of abdominal adiposity in overweight and obese individuals. Weight status presents additional complexity since the metabolic influence of adipose tissue may not be homogenous across anatomic regions or level of obesity.

Background There is increasing evidence to suggest that racial disparities exist in outcomes for trauma. Minorities and the uninsured have been found to have higher mortality rates for blunt and penetrating trauma. However, mechanisms for these disparities are incompletely understood. Limiting the inquiry to a homogenous group, those with lower extremity vascular injuries (LEVIs), may clarify these disparities. Methods The National Trauma Data Bank (NTDB; version 7.0, American College of Surgeons) was used for this study. LEVIs were identified using codes from the International Classification of Diseases, 9th revision. Univariate and multivariate analyses were performed using Stata software (version 11; StataCorp, LP, College Station, TX). Results Records were reviewed for 4,928 LEVI patients. The mechanism of injury was blunt in 2,452 (49.8%), penetrating in 2,452 (49.8%), and unknown in 24 cases (0.5%). Mortality was similar by mechanism (7.6% overall). Regression analysis using mechanism as a covariate revealed a significantly worse mortality for people of color (POC; odds ratio [OR], 1.45; 95% confidence interval [CI], 1.03–2.02; P = .03) and the uninsured (UN; OR, 1.62; 95% CI, 1.15–2.23; P = .006). However, when separate analyses were performed stratifying by mechanism, no significant mortality disparities were found for blunt trauma (POC OR, 1.28; 95% CI, 0.85–1.96; P = .23; UN OR, 1.33; 95% CI, 0.78–2.22; P = .29), but disparities remained for penetrating trauma (POC OR, 1.81; 95% CI, 0.93–3.57; P = .08; UN OR, 1.85; 95% CI, 1.18–2.94; P = .009). Conclusion For patients with LEVI, mortality disparities based on race or insurance status were only observed for penetrating trauma. It is possible that injury heterogeneity or patient cohort differences may partly explain mortality disparities that have been observed between racial and socioeconomic groups.

Despite the persistence of the obesity epidemic and its contribution to development of metabolic and cardiovascular diseases, a growing number of studies have described a paradoxically longer survival (the obesity paradox) among overweight and obese adults with and without chronic diseases.1 Whereas the obesity paradox has previously been observed among adults with chronic kidney disease, heart failure, and cancer, a growing number of studies have investigated this question in the setting of diabetes mellitus. Whether the obesity paradox is present in diabetes mellitus is of particular interest given the importance of obesity in the pathogenesis of diabetes mellitus and the development of complications. In this issue of Circulation , Zhao et al2 report a U-shaped association between weight status and mortality among adults with diabetes mellitus, whereby the lowest mortality rates are observed among adults who are overweight or obese. These findings are consistent with some3,4 but not all5 previous findings. Article see p 2143 The present study was carried out using administrative data from the Louisiana State University Health Care Services Division, a healthcare plan that includes 7 public hospitals and affiliated clinics, which cover approximately 35% of the Louisiana population. Patients were studied as part of the Louisiana State University Hospital–Based Longitudinal Study (LSUHLS). Nearly 35 000 black and white adults with a new diagnosis of type 2 diabetes mellitus between 1999 and 2009 were followed for an average of 9 years for mortality. There are several unique features of the present study, including the use of administrative data, which included multiple measures of body mass index (BMI) captured over time, large samples of both blacks and whites, and adults with …

Each year, the American Heart Association (AHA), in conjunction with the Centers for Disease Control and Prevention, the National Institutes of Health, and other government agencies, brings together the most up-to-date statistics on heart disease, stroke, other vascular diseases, and their risk factors and presents them in its Heart Disease and Stroke Statistical Update. The Statistical Update is a valuable resource for researchers, clinicians, healthcare policy makers, media professionals, the lay public, and many others who seek the best national data available on disease morbidity and mortality and the risks, quality of care, medical procedures and operations, and costs associated with the management of these diseases in a single document. Indeed, since 1999, the Statistical Update has been cited more than 8700 times in the literature (including citations of all annual versions). In 2009 alone, the various Statistical Updates were cited ≈1600 times (data from ISI Web of Science). In recent years, the Statistical Update has undergone some major changes with the addition of new chapters and major updates across multiple areas. For this year’s edition, the Statistics Committee, which produces the document for the AHA, updated all of the current chapters with the most recent nationally representative data and inclusion of relevant articles from the literature over the past year and added a new chapter detailing how family history and genetics play a role in cardiovascular disease (CVD) risk. Also, the 2011 Statistical Update is a major source for monitoring both cardiovascular health and disease in the population, with a focus on progress toward achievement of the AHA’s 2020 Impact Goals. Below are a few highlights from this year’s Update.

To estimate the association of age with maximal HR (MHR).Data were obtained from the Coronary Artery Risk Development in Young Adults (CARDIA) study. Participants were black and white men and women aged 18-30 yr in 1985-1986 (year 0). A symptom-limited maximal graded exercise test was completed at years 0, 7, and 20 by 4969, 2583, and 2870 participants, respectively. After exclusion, 9622 eligible tests remained.In all 9622 tests, estimated MHR (eMHR, bpm) had a quadratic relation to age in the age range of 18-50 yr, eMHR = 179 + 0.29 x age - 0.011 x age(2). The age-MHR association was approximately linear in the restricted age ranges of consecutive tests. In 2215 people who completed tests of both years 0 and 7 (age range = 18-37 yr), eMHR = 189 - 0.35 x age; and in 1574 people who completed tests of both years 7 and 20 (age range = 25-50 yr), eMHR = 199 - 0.63 x age. In the lowest baseline body mass index (BMI) quartile, the rate of decline was 0.24 bpm*yr(-1) between years 0 and 7 and 0.51 bpm*yr(-1) between years 7 and 20, whereas in the highest baseline BMI quartile, there was a linear rate of decline of approximately 0.7 bpm.yr for the full age range of 18-50 yr.Clinicians making exercise prescriptions should be aware that the loss of symptom-limited MHR is much slower in young adulthood and more pronounced in later adulthood. In particular, MHR loss is very slow in those with the lowest BMI younger than 40 yr.

Although adiposity is a well-known risk factor for type 2 diabetes among young and middle-aged adults, the relationship between diabetes and measures of body composition in older adults is unclear. Several measures of body composition change with aging. These changes include increased body mass index (BMI) and fat mass, loss of muscle mass, redistribution of adipose tissue, and height shrinkage. Because there is a high prevalence of obesity and diabetes in older aging adults, it is important to clarify the relationship between adiposity, changes in parameters of body composition, and diabetes risk in this population. This prospective population-based study investigated the relationship between measures of overall body fat and fat distribution, changes in these measures, and the risk of incident type 2 diabetes in a population of 4193 men and women aged ≥65 years. This investigation is part of the Cardiovascular Health Study, a large population-based study of older ambulatory, noninstitutionalized adults. Anthropometric data on body composition measures and bioelectrical impedance data on fat mass were collected at baseline and anthropometric measurements repeated 3 years later. The presence of diabetes was defined by use of insulin or oral hypoglycemic agents, or a fasting glucose level ≥126 mg/dL. The participants were followed for a median of 12.4 years (range, 0.9-17.8 years). Of the 4193 participants, 2457 were women and 1736 were men. Over the 12.4-year follow-up, there were 339 new cases of diabetes (7.1/1000 person-years). Comparison of the hazard ratios for women in the highest quintile of baseline measures of adiposity with those in the lowest showed that the following were strongly related to the risk of type 2 diabetes: BMI at baseline (adjusted hazard ratio [aHR], 3.7; 95% confidence interval [CI], 2.3-6.2), BMI at 50 years of age (aHR; 3.2; 95% CI, 1.9-5.5), weight (aHR, 3.5; 95% CI, 2.1-5.7), fat mass (aHR, 3.3; 95% CI, 2.0-5.6), waist circumference (aHR, 3.6; 95% CI, 2.2-6.0), waist-hip ratio (aHR, 1.9; 95% CI, 1.1-3.2), and waist-height ratio (aHR, 3.6; 95% CI, 2.2-5.9). There was no significant statistical interaction with stratification of the data by gender or race. Stratification by age, however, showed that the HRs in participants aged ≥75 years were about half as large as those in patients aged 65 to 74 years. Compared to participants whose weight remained stable (±2 kg) throughout the study period, those with the greatest weight gain (9 kg or more) from 50 years of age to baseline had a nearly 3-fold greater risk of developing type 2 diabetes during follow-up (aHR, 2.8; 95% CI, 1.9-4.3). Between baseline and the third annual visit, participants with a greater than 10-cm increase in waist size had an increased risk of developing type 2 diabetes (HR, 1.7; 95% CI, 1.1-2.8) compared to those with a gain or loss of 2 cm or less. These findings show that measures of overall and central adiposity and weight gain are strongly associated with the risk of incident type 2 diabetes in both men and women during middle age and after the age of 65 years.

Fitness and physical activity are each inversely associated with the development of hypertension. We tested whether fitness and physical activity were independently associated with the 20-year incidence of hypertension in 4618 men and women. Hypertension was determined in participants who had systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mm Hg or who reported antihypertensive medication use. Fitness was estimated based on the duration of a symptom-limited graded exercise treadmill test, and physical activity was self-reported. The incidence rate of hypertension was 13.8 per 1000 person-years (n=1022). Both baseline fitness (hazard ratio: 0.63 [95% CI: 0.56 to 0.70 per SD]; 2.9 minutes) and physical activity (hazard ratio: 0.86 [95% CI: 0.79 to 0.84 per SD]; 297 exercise units) were inversely associated with incident hypertension when included jointly in a model that also adjusted for age, sex, race, baseline smoking status, systolic blood pressure, alcohol intake, high-density lipoprotein cholesterol, dietary fiber, dietary sodium, fasting glucose, and body mass index. The magnitude of association between physical activity and hypertension was strongest among participants in the high fitness (hazard ratio: 0.80 [95% CI: 0.68 to 0.94]) category, whereas the magnitude of association between fitness and hypertension was similar across tertiles of physical activity. The estimated proportion of hypertension cases that could be prevented if participants moved to a higher fitness category (ie, preventive fraction) was 34% and varied by race and sex group. Fitness and physical activity are each associated with incident hypertension, and low fitness may account for a substantial proportion of hypertension incidence.

OBJECTIVE To examine the relationship of parity with diabetes and markers of glucose homeostasis in older women. RESEARCH DESIGN AND METHODS We used data from the female participants in the Cardiovascular Health Study, a longitudinal cohort of adults aged ≥65 years. These data included an assessment of parity (baseline) and fasting serum levels of glucose, insulin, and medication use (baseline and follow-up). We estimated both the cross-sectional relationship of parity with baseline diabetes and the relationship of parity with incident diabetes. RESULTS In unadjusted analyses, women with grand multiparity (≥5 live births) had a higher prevalence of diabetes at baseline compared with those with fewer births and with nulliparous women (25 vs. 12 vs. 15%; P < 0.001). In regression models controlling for age and race, grand multiparity was associated with increased prevalence of diabetes (prevalence ratio 1.57 [95% CI 1.20–2.06]); with addition of demographic and clinical factors to the model, the association was attenuated (1.33 [1.00–1.77]). In final models that included body anthropometrics, the association was no longer significant (1.21 [0.86–1.49]). In those without diabetes at baseline, parity was not associated with incident diabetes or with fasting glucose; however, there was a modest association of parity with fasting insulin and homeostasis assessment model of insulin resistance. CONCLUSIONS Grand multiparity is associated with diabetes in elderly women in cross-sectional analyses. This relationship seems to be confounded and/or mediated by variation in body weight and sociodemographic factors by parity status. In older nondiabetic women, higher parity does not pose an ongoing risk of developing diabetes.

The authors used data from the Multi-Ethnic Study of Atherosclerosis and latent trajectory class modeling to determine patterns of neighborhood poverty over 20 years (1980-2000 residential history questionnaires were geocoded and linked to US Census data). Using these patterns, the authors examined 1) whether trajectories of neighborhood poverty were associated with differences in the amount of subclinical atherosclerosis (common carotid intimal-media thickness) and 2) associated risk factors (body mass index, hypertension, diabetes, current smoking) at baseline (January 2000-August 2002). The authors found evidence of 5 stable trajectory groups with differing levels of neighborhood poverty ( approximately 6%, 12%, 20%, 30%, and 45%) and 1 group with 29% poverty in 1980 and approximately 11% in 2000. Mostly for women, higher cumulative neighborhood poverty was generally significantly associated with worse cardiovascular outcomes. Trends generally persisted after adjustment for adulthood socioeconomic position and race/ethnicity, although they were no longer statistically significant. Among women who had moved during the 20 years, the long-term measure had stronger associations with outcomes (except smoking) than a single, contemporaneous measure. Results indicate that cumulative 20-year exposure to neighborhood poverty is associated with greater cardiovascular risk for women. In residentially mobile populations, single-point-in-time measures underestimate long-term effects.

Physical inactivity is an established risk factor for cardiovascular diseases. However, although physical activity is recommended as a component of healthy lifestyle, the amount (intensity, duration, and frequency) of physical activity required to protect against coronary heart disease (CHD) and cerebrovascular disease (ie, stroke) is unclear. In general, there is a graded inverse association of physical activity with CHD and total cardiovascular disease (the combination of CHD and stroke). The patterns of association between physical activity dose and stroke are less clear; individual studies suggest a threshold effect for benefits, whereas meta-analytic studies report a graded inverse association. Despite known differences in physical activity behaviors between men and women, the patterns of association between dose of activity and cardiovascular diseases are similar by gender. Observational studies of walking behaviors and one recent clinical trial suggest that lower “doses” of physical activity are associated with a lower risk of cardiovascular disease. Thus, with very few specific cautions, there is enough evidence to recommend to healthy adults that any activity is beneficial and that more activity is even better.

OBJECTIVE Many studies have documented associations between inflammation and type 2 diabetes incidence. We assessed potential variability in this association in the major U.S. racial/ethnic groups. RESEARCH DESIGN AND METHODS Incident type 2 diabetes was assessed among men and women aged 45–84 years without prior clinical cardiovascular disease or diabetes in the prospective Multi-Ethnic Study of Atherosclerosis. Interleukin (IL)-6, fibrinogen, and C-reactive protein (CRP) were measured at baseline (2000–2002); fasting glucose and diabetes medication use was assessed at baseline and three subsequent in-person exams through 2007. Type 2 diabetes was defined as use of diabetes drugs or glucose ≥126 mg/dl. Covariates included baseline demographics, clinic, smoking, alcohol, exercise, hypertension medication, systolic blood pressure, insulin resistance, and BMI. Cox proportional hazards regression was used to calculate hazard ratios (HRs) by quartiles of CRP, IL-6, and fibrinogen. RESULTS Among 5,571 participants (mean age 61.6 years, 53% female, 42.1% white, 11.5% Chinese, 25.7% black, and 20.7% Hispanic), 410 developed incident diabetes during a median follow-up time of 4.7 years (incidence 16.8 per 1,000 person-years). CRP, IL-6, and fibrinogen levels were associated with incident diabetes in the entire sample. After adjustment, the associations were attenuated; however, quartile 4 (versus quartile 1) of IL-6 (HR 1.5 [95% CI 1.1–2.2]) and CRP (1.7 [1.3–2.4]) remained associated with incident diabetes. In stratified analyses, similar associations were observed among white, black, and Hispanic participants. CONCLUSIONS Higher levels of inflammation predict short-term incidence of type 2 diabetes in a multiethnic American sample.

Several models for estimating risk of incident diabetes in US adults are available. The authors aimed to determine the discriminative ability and calibration of published diabetes risk prediction models in a contemporary multiethnic cohort. Participants in the Multi-Ethnic Study of Atherosclerosis without diabetes at baseline (2000–2002; n = 5,329) were followed for a median of 4.75 years. The predicted risk of diabetes was calculated using published models from the Framingham Offspring Study, the Atherosclerosis Risk in Communities (ARIC) Study, and the San Antonio Heart Study. The mean age of participants was 61.6 years (standard deviation, 10.2); 29.3% were obese, 53.1% had hypertension, 34.9% had a family history of diabetes, 27.5% had high triglyceride levels, 33.8% had low high density lipoprotein cholesterol levels, and 15.3% had impaired fasting glucose. There were 446 incident cases of diabetes (fasting glucose level ≥126 mg/dL or initiation of antidiabetes medication use) diagnosed during follow-up. C statistics were 0.78, 0.84, and 0.83 for the Framingham, ARIC, and San Antonio risk prediction models, respectively. There were significant differences between observed and predicted diabetes risks (Hosmer-Lemeshow goodness-of-fit chi-squared test for each model: P < 0.001). The recalibrated and best-fit models achieved sufficient goodness of fit (each P > 0.10). The Framingham, ARIC, and San Antonio models maintained high discriminative ability but required recalibration in a modern, multiethnic US cohort.

The combined impact of lifestyle factors on incidence of diabetes mellitus later in life is not well established. The objective of this study was to determine how lifestyle factors, assessed in combination, relate to new-onset diabetes in a broad and relatively unselected population of older adults.We prospectively examined associations of lifestyle factors, measured using repeated assessments later in life, with incident diabetes mellitus during a 10-year period (1989-1998) among 4883 men and women 65 years or older (mean [SD] age at baseline, 73 [6] years) enrolled in the Cardiovascular Health Study. Low-risk lifestyle groups were defined by physical activity level (leisure-time activity and walking pace) above the median; dietary score (higher fiber intake and polyunsaturated to saturated fat ratio, lower trans-fat intake and lower mean glycemic index) in the top 2 quintiles; never smoked or former smoker more than 20 years ago or for fewer than 5 pack-years; alcohol use (predominantly light or moderate); body mass index less than 25 (calculated as weight in kilograms divided by height in meters squared); and waist circumference of 88 cm for women or 92 cm for men. The main outcome measure was incident diabetes defined annually by new use of insulin or oral hypoglycemic medications. We also evaluated fasting and 2-hour postchallenge glucose levels.During 34,539 person-years, 337 new cases of drug-treated diabetes mellitus occurred (9.8 per 1000 person-years). After adjustment for age, sex, race, educational level, and annual income, each lifestyle factor was independently associated with incident diabetes. Overall, the rate of incident diabetes was 35% lower (relative risk, 0.65; 95% confidence interval, 0.59-0.71) for each 1 additional lifestyle factor in the low-risk group. Participants whose physical activity level and dietary, smoking, and alcohol habits were all in the low-risk group had an 82% lower incidence of diabetes (relative risk, 0.18; 95% confidence interval, 0.06-0.56) compared with all other participants. When absence of adiposity (either body mass index25 or waist circumferenceor =88/92 cm for women/men) was added to the other 4 low-risk lifestyle factors, incidence of diabetes was 89% lower (relative risk, 0.11; 95% confidence interval, 0.01-0.76). Overall, 9 of 10 new cases of diabetes appeared to be attributable to these 5 lifestyle factors. Associations were slightly attenuated, but still highly significant, for incident diabetes defined by medication use or glucose level.Even later in life, combined lifestyle factors are associated with a markedly lower incidence of new-onset diabetes mellitus.

We tested that slow heart rate recovery (HRR) after exercise testing, indicative of decreased parasympathetic nervous system activity, is associated with the development of type 2 diabetes in 1,813 healthy men.Heart rate recovery was calculated as the difference between maximum heart rate during the exercise test and heart rate 1 min after cessation of the exercise test.During an average of 6.4 years of follow-up, 64 (3.5%) subjects developed type 2 diabetes. The unadjusted relative risk (RR) of developing incident diabetes in the slowest versus the fastest HRR quartile was 3.13 (95% CI, 1.28-7.65). However, the association was no longer significant after adjustment for diabetes risk factors and baseline glucose (RR = 2.28, 95% CI, 0.87-5.95).Slow HRR is associated with the development of type 2 diabetes, but these relationships were largely explained by baseline fasting glucose in healthy men.

Depressive symptoms are associated with development of type 2 diabetes, but it is unclear whether type 2 diabetes is a risk factor for elevated depressive symptoms.To examine the bidirectional association between depressive symptoms and type 2 diabetes.Multi-Ethnic Study of Atherosclerosis, a longitudinal, ethnically diverse cohort study of US men and women aged 45 to 84 years enrolled in 2000-2002 and followed up until 2004-2005.Elevated depressive symptoms defined by Center for Epidemiologic Studies Depression Scale (CES-D) score of 16 or higher, use of antidepressant medications, or both. The CES-D score was also modeled continuously. Participants were categorized as normal fasting glucose (100 mg/dL), impaired fasting glucose (100-125 mg/dL), or type 2 diabetes (or = 126 mg/dL or receiving treatment). Analysis 1 included 5201 participants without type 2 diabetes at baseline and estimated the relative hazard of incident type 2 diabetes over 3.2 years for those with and without depressive symptoms. Analysis 2 included 4847 participants without depressive symptoms at baseline and calculated the relative odds of developing depressive symptoms over 3.1 years for those with and without type 2 diabetes.In analysis 1, the incidence rate of type 2 diabetes was 22.0 and 16.6 per 1000 person-years for those with and without elevated depressive symptoms, respectively. The risk of incident type 2 diabetes was 1.10 times higher for each 5-unit increment in CES-D score (95% confidence interval [CI], 1.02-1.19) after adjustment for demographic factors and body mass index. This association persisted following adjustment for metabolic, inflammatory, socioeconomic, or lifestyle factors, although it was no longer statistically significant following adjustment for the latter (relative hazard, 1.08; 95% CI, 0.99-1.19). In analysis 2, the incidence rates of elevated depressive symptoms per 1000-person years were 36.8 for participants with normal fasting glucose; 27.9 for impaired fasting glucose; 31.2 for untreated type 2 diabetes, and 61.9 for treated type 2 diabetes. Compared with normal fasting glucose, the demographic-adjusted odds ratios of developing elevated depressive symptoms were 0.79 (95% CI, 0.63-0.99) for impaired fasting glucose, 0.75 (95% CI, 0.44-1.27) for untreated type 2 diabetes, and 1.54 (95% CI, 1.13-2.09) for treated type 2 diabetes. None of these associations with incident depressive symptoms were materially altered with adjustment for body mass index, socioeconomic and lifestyle factors, and comorbidities. Findings in both analyses were comparable across ethnic groups.A modest association of baseline depressive symptoms with incident type 2 diabetes existed that was partially explained by lifestyle factors. Impaired fasting glucose and untreated type 2 diabetes were inversely associated with incident depressive symptoms, whereas treated type 2 diabetes showed a positive association with depressive symptoms. These associations were not substantively affected by adjustment for potential confounding or mediating factors.

Background To assess the importance of the obesity epidemic on cardiovascular disease (CVD) risk, we determined the prevalence of obesity and the relationship of obesity to CVD risk factors and subclinical vascular disease. Methods The Multi-Ethnic Study of Atherosclerosis is an observational cohort study involving 6814 persons aged 45 to 84 years who were free of clinical CVD at baseline (2000-2002). The study assessed the association between body size and CVD risk factors, medication use, and subclinical vascular disease (coronary artery calcium, carotid artery intimal medial thickness, and left ventricular mass). Results A large proportion of white, African American, and Hispanic participants were overweight (60% to 85%) and obese (30% to 50%), while fewer Chinese American participants were overweight (33%) or obese (5%). Hypertension and diabetes were more prevalent in obese participants despite a much higher use of antihypertensive and/or antidiabetic medications. Obesity was associated with a greater risk of coronary artery calcium (17%), internal carotid artery intimal medial thickness greater than 80th percentile (32%), common carotid artery intimal medial thickness greater than 80th percentile (45%), and left ventricular mass greater than 80th percentile (2.7-fold greater) compared with normal body size. These associations persisted after adjustment for traditional CVD risk factors. Conclusions These data confirm the epidemic of obesity in most but not all racial and ethnic groups. The observed low prevalence of obesity in Chinese American participants indicates that high rates of obesity should not be considered inevitable. These findings may be viewed as indicators of potential future increases in vascular disease burden and health care costs associated with the obesity epidemic.

To examine the association of psychosocial factors with heart rate (HR) and its variability across multiple ethnic groups and by gender. Increased HR and reduced HR variability are markers of increased cardiovascular risk.Between 2000 and 2002, 6814 men and women (2624 Whites, 1895 African-Americans, 1492 Hispanics, and 803 Chinese) aged 45 to 84 years took part in the first examination of the Multi-Ethnic Study of Atherosclerosis. Associations of psychosocial variables with mean values of HR and its short-term variability were tested, using multivariate regression models.In age, gender, race/ethnicity, and risk factor-adjusted analyses, a depressive symptom score was positively associated with HR and inversely associated with HR variability (standard deviation of normal-to-normal (N-N) interbeat intervals (SDNN) and the root mean square of successive differences in N-N intervals (RMSSD)). The adjusted mean differences per 1-SD (8 points) increment of depression score for HR, RMSSD, and SDNN were 0.5 (95% confidence interval (CI), 0.2-0.7), -0.8 (95% CI, -1.5 to -0.2), and -0.7 (95% CI, -1.1 to -0.2). The social support score was inversely associated with HR, but nonsignificantly associated with RMSSD and SDNN. There was no association of trait anger or trait anxiety with HR, RMSSD, or SDNN. Associations were generally consistent in men and women.These findings generally support the hypothesis that depression may be associated with increased HR and reduced HR variability, which increase the risk of cardiovascular diseases.

The inverse association between physical activity and diabetes is attributable to a number of biologically plausible mechanisms. We hypothesize that physical activity-induced improvements in autonomic function are one mechanism by which higher levels of activity are inversely associated with diabetes development. Evidence in support of our hypothesis is derived from a combination of observational studies and clinical trials.

OBJECTIVE—Based on prior research showing inverse associations between heart rate and life expectancy, we tested the hypothesis that adults with higher resting heart rate in middle age were more likely to have diagnosed diabetes or to experience diabetes mortality in older age (>65 years). RESEARCH DESIGN AND METHODS—Resting heart rate was measured at baseline (1967–1973) in the Chicago Heart Association Detection Project in Industry. We used Medicare billing records to identify diabetes-related hospital claims and non–hospital-based diabetes expenses from 1992 to 2002 in 14,992 participants aged 35–64 years who were free from diabetes at baseline. Diabetes-related mortality was determined from 1984 to 2002 using National Death Index codes 250.XX (ICD-8 and -9) and E10–E14 (ICD-10). RESULTS—After age 65, 1,877 participants had diabetes-related hospital claims and 410 participants had any mention of diabetes on their death certificate. The adjusted (demographic characteristics, cigarette smoking, and years of Medicare eligibility) odds of having a diabetes-related claim was ∼10% higher (odds ratio [OR] 1.10 [95% CI 1.05–1.16]) per 12 bpm higher baseline heart rate. Following adjustment for BMI and postload glucose at baseline, the association attenuated to nonsignificance. Higher heart rate was associated with diabetes mortality in adults aged 35–49 years at baseline following adjustment for postload glucose and BMI (1.21 [1.03–1.41]). CONCLUSIONS—Higher resting heart rate is associated with diabetes claims and mortality in older age and is only due in part to BMI and concurrently measured glucose.

A major limitation of past work on the social patterning of atherosclerosis has been the reliance on measures of neighborhood or individual-level socioeconomic position (SEP) assessed at a single point in time in adulthood. Risk of chronic disease is thought to accumulate throughout the life-course, so the use of a measure for a single point in time may result in inaccurate estimates of the social patterning of subclinical disease. Using data from the US Multi-Ethnic Study of Atherosclerosis (MESA), we examined the relation between childhood SEP [CSEP] (father or caretaker's education), adulthood SEP [ASEP] (a summary score of income, education, and wealth), and 20-year average exposure to neighborhood poverty [NSEP] (residential addresses geocoded and linked to census data) and the prevalence of subclinical atherosclerosis, as assessed by common carotid intimal-medial thickness (IMT) in mid to late adulthood. Participants were 45-84 years of age at baseline and were sampled from six study sites in the United States. After adjustment for age, CSEP and ASEP were both inversely and independently associated with IMT in men. All three indicators CSEP, ASEP, and NSEP were inversely and independently associated with IMT in women. Associations were somewhat reduced after adjustment for cardiovascular risk factors, suggesting that these factors may play a mediating role. There was evidence of heterogeneity in effects of NSEP by gender, and in the effects of ASEP and NSEP by race/ethnicity. Our results contribute to the growing body of work that shows that SEP at multiple points in the life-course, and at the individual and neighborhood level, contributes to the development of atherosclerosis.

Previous studies have evaluated the strength of the association between traditional risk factors and cardiovascular disease (CVD) across varying lengths of follow-up in men. However, to our knowledge, little is known regarding the behavior of these risk factors across time in women. Thus, we sought to determine the association between traditional risk factors in men and women across follow-up periods of 0 to 10, 10 to 20, and >20 years. We studied 9,033 men and 7,575 women (ages 40 to 59 years) from 1967 to 1973 from the Chicago Heart Association Detection Project in Industry. Multivariable-adjusted Cox proportional hazard models were constructed to compare the hazard ratios (HRs) and 95% confidence intervals (CI) for CVD risk factors measured at baseline across different periods of follow-up (0 to 10, 10 to 20, and >20 years). In women, the HRs for smoking and diabetes mellitus were strongest at 0 to 10 years (HR 5.38, 95% CI 2.99 to 9.67 and 3.84, 95% CI 1.82 to 8.13, respectively) but decreased at >20 years (HR 1.71, 95% CI 1.48 to 1.97 and 1.60, 95% CI 1.10 to 2.32, respectively). In men, the HR (per 4 kg/m 2 ) for body mass index appeared to increase (0 to 10 years, 1.01, 95% CI 0.90 to 1.14; >20 years, 1.20, 95% CI 1.13 to 1.28). In women, the association was similar across all follow-up periods. For both men and women, the HR for total serum cholesterol remained unchanged across the follow-up. In conclusion, we found gender differences in the patterns of association between risk factors measured at baseline and CVD death across different periods of follow-up. In women, the increased risk associated with both diabetes mellitus and smoking was most prominent in the early follow-up periods.

THE IMPACT OF ALCOHOL CONSUMPTION ON OVARIAN RESERVE IN REPRODUCTIVE-AGE AFRICAN AMERICAN WOMEN. L. Hawkins Bressler, L. A. Bernardi, P. D. De Chavez, D. Baird, M. Carnethon, E. E. Marsh. Department of Obstetrics and Gynecology, Northwestern University, Chicago, IL; Northwestern University, Chicago, IL; Epidemiology, National Institute of Environmental Health Sciences, Research Triangle Park, NC; Department of Epidemiology, Northwestern University, Chicago, IL; Feinberg SOM Northwestern University, Chicago, IL.

To examine the association of menarche timing with cardiometabolic risk factors into early to mid-adulthood, comparing African American and White women.Analyses included 2583 women (African American = 1333; White = 1250) from the Coronary Artery Risk Development in Young Adults cohort study over 25 years of follow-up (1985-2011). Outcomes included type 2 diabetes, metabolic syndrome, adiposity, glucose, insulin, blood pressure, and blood lipids. Cox models or repeated measures linear regression models estimated the association between age at menarche and the outcomes.Each 1-year earlier age at menarche was associated with higher mean body mass index among African American (0.88 ± 0.12 kg/m(2), P.0001) and White (0.89 ± 0.10 kg/m(2), P.0001) women. After body mass index adjustment, each 1-year earlier age at menarche was associated with higher triglycerides (2.26 ± 0.68 mg/dL, P = .001) and glucose (0.34 ± 0.11 mg/dL, P = .002), and greater risk for incident impaired fasting glucose (hazard ratio = 1.13, 95% CI 1.04-1.20) and metabolic syndrome (hazard ratio 1.19, 95% CI 1.11-1.26) among White women only.Excess adiposity associated with earlier menarche is sustained through mid-adulthood, and primarily drives higher cardiometabolic risk factor levels. However, White women with earlier menarche had increased risk of a number of insulin-resistance related conditions independent of adiposity. The cardiometabolic impact of earlier menarche was weaker in African American women despite higher average adiposity. Weight maintenance would likely reduce but may not completely eliminate the elevated cardiometabolic risk of earlier menarche.