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Social determinants of health (SDoH), or the socioeconomic, environmental, and psychosocial conditions in which individuals spend their daily lives, substantially influence obesity as a cardiovascular disease (CVD) risk factor. The coronavirus disease 2019 (COVID-19) pandemic highlighted the converging epidemics of obesity, CVD, and social inequities globally. Obesity and CVD serve as independent risk factors for COVID-19 severity and lower-resourced populations most impacted by adverse SDoH have the highest COVID-19 mortality rates. Better understanding the interplay between social and biologic factors that contribute to obesity-related CVD disparities are important to equitably address obesity across populations. Despite efforts to investigate SDoH and their biologic effects as drivers of health disparities, the connections between SDoH and obesity remain incompletely understood. This review aims to highlight the relationships between socioeconomic, environmental, and psychosocial factors and obesity. We also present potential biologic factors that may play a role in the biology of adversity, or link SDoH to adiposity and poor adipo-cardiology outcomes. Finally, we provide evidence for multi-level obesity interventions targeting multiple aspects of SDoH. Throughout, we emphasize areas for future research to tailor health equity-promoting interventions across populations to reduce obesity and obesity-related CVD disparities. [ABSTRACT FROM AUTHOR]

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Background: Cardiovascular disease is a leading economic and medical burden in the United States (US). As an important risk factor for cardiovascular disease, hypertension represents a critical point of intervention. Less is known about longitudinal effects of neighborhood deprivation on blood pressure outcomes, especially in light of new hypertension guidelines.Methods: Longitudinal data from the Dallas Heart Study facilitated multilevel regression analysis of the relationship between neighborhood deprivation, blood pressure change, and incident hypertension over a 9-year period. Factor analysis explored neighborhood perception, which was controlled for in all analyses. Neighborhood deprivation was derived from US Census data and divided into tertiles for analysis. Hypertension status was compared using pre-2017 and 2017 hypertension guidelines.Results: After adjusting for covariates, including moving status and residential self-selection, we observed significant associations between residing in the more deprived neighborhoods and 1) increasing blood pressure over time and 2) incident hypertension. In the fully adjusted model of continuous blood pressure change, significant relationships were seen for both medium (SBP: β = 4.81, SE = 1.39, P = .0005; DBP: β = 2.61, SE = 0.71, P = .0003) and high deprivation (SBP: β = 7.64, SE = 1.55, P < .0001; DBP: β = 4.64, SE = 0.78, P < .0001). In the fully adjusted model of incident hypertension, participants in areas of high deprivation had 1.69 higher odds of developing HTN (OR 1.69; 95% CI 1.02, 2.82), as defined by 2017 hypertension guidelines. Results varied based on definition of hypertension used (pre-2017 vs. 2017 guidelines).Conclusion: These findings highlight the potential impact of adverse neighborhood conditions on cardiometabolic outcomes, such as hypertension. [ABSTRACT FROM AUTHOR]

Purpose Decreased cardiorespiratory fitness (CRF) is associated with an increased risk of cardiovascular disease. However, little is known how the interaction of diet, physical activity (PA), and sedentary time (ST) affects CRF among adolescents. By using a nationally representative sample of U.S. adolescents, we used cluster analysis to investigate the interactions of these behaviors with CRF. We hypothesized that distinct clustering patterns exist and that less healthy clusters are associated with lower CRF. Methods We used 2003–2004 National Health and Nutrition Examination Survey data for persons aged 12–19 years (N = 1,225). PA and ST were measured objectively by an accelerometer, and the American Heart Association Healthy Diet Score quantified diet quality. Maximal oxygen consumption ( V ˙ O 2 ​ max ) was measured by submaximal treadmill exercise test. We performed cluster analysis to identify sex-specific clustering of diet, PA, and ST. Adjusting for accelerometer wear time, age, body mass index, race/ethnicity, and the poverty-to-income ratio, we performed sex-stratified linear regression analysis to evaluate the association of cluster with V ˙ O 2 ​ max . Results Three clusters were identified for girls and boys. For girls, there was no difference across clusters for age ( p  = .1), weight ( p  = .3), and BMI ( p  = .5), and no relationship between clusters and V ˙ O 2 ​ max . For boys, the youngest cluster ( p  < .01) had three healthy behaviors, weighed less, and was associated with a higher V ˙ O 2 ​ max compared with the two older clusters. Conclusions We observed clustering of diet, PA, and ST in U.S. adolescents. Specific patterns were associated with lower V ˙ O 2 ​ max for boys, suggesting that our clusters may help identify adolescent boys most in need of interventions. [ABSTRACT FROM AUTHOR]

Objectives The authors sought to examine the relationship between visceral adipose tissue (VAT) and vascular inflammation (VI) by 18 F-Fluorodeoxyglucose ( 18 F-FDG) positron-emission tomography (PET)/computed tomography (CT) in psoriasis (PSO). Furthermore, we evaluated whether treatment of PSO modulated VAT and VI. Background PSO, a chronic inflammatory skin disease, is associated with VI by 18 F-FDG PET/CT and increased cardiometabolic risk including adipose tissue dysregulation. Recently, VI was associated with future cardiovascular events; however, the relationship of visceral and subcutaneous adiposity with VI in PSO has yet to be evaluated. Methods Consecutive PSO patients (N = 77) underwent 18 F-FDG PET/CT scans to measure VI and abdominal adiposity. A subset of PSO patients with severe skin disease was scanned at 1 year following PSO treatment (N = 13). Results The cohort was middle aged (51.8 ± 12.6 years), predominantly male (n = 44, 57%), had low cardiovascular risk by Framingham 10-year risk (median 4 years [interquartile range (IQR): 2 to 7 years]), and mild-to-moderate skin disease (5.2 [IQR: 3.0 to 8.5]). PSO disease severity associated with VAT (β = 0.33; p = 0.004) beyond SAT (β = 0.30; p = 0.005). VAT (β = 0.55; p < 0.001), but not SAT (β = 0.15; p = 0.11), associated with VI beyond cardiovascular risk factors. We followed a subset of severe PSO patients treated aggressively for PSO and observed improvement in PSO severity and VAT, which was associated with an improvement in VI at 1 year beyond cardiovascular risk factors (β = 0.53; p = 0.049). Conclusions Volume-based CT measurement of VAT may capture metabolic risk associated with VI compared to subcutaneous adipose tissue in PSO. PSO treatment associated with a decrease in VAT as well as decrease in VI suggesting VAT as a relevant biomarker related to VI in PSO. [ABSTRACT FROM AUTHOR]

Introduction Despite a proposed connection between neighborhood environment and obesity, few longitudinal studies have examined the relationship between change in neighborhood socioeconomic deprivation, as defined by moving between neighborhoods, and change in body weight. The purpose of this study is to examine the longitudinal relationship between moving to more socioeconomically deprived neighborhoods and weight gain as a cardiovascular risk factor. Methods Weight (kilograms) was measured in the Dallas Heart Study (DHS), a multiethnic cohort aged 18–65 years, at baseline (2000–2002) and 7-year follow-up (2007–2009, N=1,835). Data were analyzed in 2013–2014. Geocoded addresses were linked to Dallas County, TX, census block groups. A block group-level neighborhood deprivation index (NDI) was created. Multilevel difference-in-difference models with random effects and a Heckman correction factor (HCF) determined weight change relative to NDI change. Results Forty-nine percent of the DHS population moved (263 to higher NDI, 586 to lower NDI, 47 within same NDI), with blacks more likely to move than whites or Hispanics ( p <0.01), but similar baseline BMI and waist circumference were observed in movers versus non-movers ( p >0.05). Adjusting for HCF, sex, race, and time-varying covariates, those who moved to areas of higher NDI gained more weight compared to those remaining in the same or moving to a lower NDI (0.64 kg per 1-unit NDI increase, 95% CI=0.09, 1.19). Impact of NDI change on weight gain increased with time ( p =0.03). Conclusions Moving to more–socioeconomically deprived neighborhoods was associated with weight gain among DHS participants. [ABSTRACT FROM AUTHOR]

Background: Physical activity (PA) participation differs by ethnicity, but contributing factors and cardiovascular (CV) outcomes related to these disparities are not well understood. We determined whether health beliefs regarding the benefit of PA contribute to ethnic differences in participation and assessed how these differences impact CV mortality. Methods: The Dallas Heart Study is a longitudinal study of CV health. We assessed PA participation and health perceptions by questionnaire among 3,018 African American, Hispanic, and white men and women at baseline visit (2000-2002). Participant mortality was obtained through 2008 using the National Death Index. Results: African Americans (odds ratio 0.65, 95% CI 0.53-0.80) and Hispanics (odds ratio 0.34, 95% CI 0.26-0.45) were less likely to be physically active compared with whites even after accounting for income, educational status, age, sex, body mass index, diabetes, hypertension, and hyperlipidemia. Beliefs regarding the benefits of PA did not contribute to this disparity, as >94% of individuals felt PA was effective in preventing a heart attack across ethnicity. Physical activity participation was associated with a lower risk of all-cause mortality (hazard ratio [HR] 0.66, 95% CI 0.46-0.93) and CV disease death (HR 0.56, 95% CI 0.32-0.97) in multivariable adjusted models. Similar results were seen when restricting to African Americans (CV disease death, HR 0.57, 95% CI 0.31-1.05). Conclusions: Ethnic minorities reported less PA participation, and lack of PA was associated with higher CV mortality overall and among African Americans. Health perception regarding the benefits of PA did not contribute to this difference, indicating there are other ethnic-specific factors contributing to physical inactivity that require future study. [Copyright &y& Elsevier]

Neighborhood socioeconomic deprivation is associated with increased cardiovascular risk factors, including inflammation. Inflammation plays an important role in modifying the cardioprotective function of high-density lipoprotein (HDL). Moreover, recent studies suggest that very high HDL is associated with adverse cardiovascular disease (CVD) outcomes. Thus, we sought to explore the relationships between neighborhood socioeconomic deprivation as a marker of chronic stress, inflammation, proprotein convertase subtilisin/kexin type 9 (PCSK9) (a core component of the HDL proteome), HDL characterisitcs, and biological aging as a predictor of CVD and all-cause mortality. Sixty African American subjects were recruited to the NIH Clinical Center as part of a community-based participatory research-designed observational study. Neighborhood deprivation index (NDI), a marker of neighborhood socioeconomic deprivation, was measured using US Census data. HDL characteristics (cholesterol, particle number, size, subspecies) were determined from NMR lipoprotein profiling, and plasma cytokines (IL-1β, IL-6, IL-8, TNFα, IFNγ) were measured using an ELISA-based multiplex technique. Epigenetic clock biomarkers of aging were measured using DNA methylation data obtained from participants' buffy coat samples. We used linear regression modeling adjusted for atherosclerotic cardiovascular disease (ASCVD) risk score, body mass index (BMI), and lipid-lowering medication use to investigate relationships of interest. NDI directly associated with large HDL particle count (H7P) and IFNγ and trended toward significance with HDL-C and PCSK9. IFNγ and PCSK9 then directly associated with H7P. H7P also directly associated with higher DNA methylation phenotypic age (PhenoAge). We highlight associations between neighborhood socioeconomic deprivation, IFNγ, PCSK9, HDL subspecies, and epigenetic biomarkers of aging. Taken together, our findings suggest indirect pathways linking neighborhood deprivation-related stress and inflammation to HDL and immune epigenetic changes. Moreover, these results add to recent work showing the pathogenicity of high HDL levels and underscore the need to understand how chronic stress-related inflammation and lipoprotein subspecies relate to CVD risk across diverse populations. [Display omitted] • Neighborhood socioeconomic deprivation associates with IFNγ, PCSK9, and H7P. • IFNγ and PCSK9 associate with H7P. • H7P associates with DNAm PhenoAge. • Chronic stress-related inflammation may modify the cardioprotective capacity of HDL. [ABSTRACT FROM AUTHOR]

Persistent skin inflammation and impaired resolution are the main contributors to psoriasis and associated cardiometabolic complications. Omega-3 polyunsaturated fatty acids (PUFAs), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), are known to exert beneficial effects on inflammatory response and lipid function. However, a specific role of omega-3 PUFAs in psoriasis and accompanied pathologies are still a matter of debate. Here, we carried out a direct comparison between EPA and DHA 12 weeks diet intervention treatment of psoriasis-like skin inflammation in the K14-Rac1V12 mouse model. By utilizing sensitive techniques, we targeted EPA- and DHA-derived specialized pro-resolving lipid mediators and identified tightly connected signaling pathways by RNA sequencing. Treatment with experimental diets significantly decreased circulating pro-inflammatory cytokines and bioactive lipid mediators, altered psoriasis macrophage phenotypes and genes of lipid oxidation. The superficial role of these changes was related to DHA treatment and included increased levels of resolvin D5, protectin DX and maresin 2 in the skin. EPA treated mice had less pronounced effects but demonstrated a decreased skin accumulation of prostaglandin E 2 and thromboxane B 2. These results indicate that modulating psoriasis skin inflammation with the omega-3 PUFAs may have clinical significance and DHA treatment might be considered over EPA in this specific disease. [Display omitted] [ABSTRACT FROM AUTHOR]

Lifetime risk estimation for cardiovascular disease (CVD) has been proposed as a useful strategy to improve risk communication in the primary prevention setting. However, the perception of lifetime risk for CVD is unknown. We included 2,998 subjects from the Dallas Heart Study. Lifetime risk for developing CVD was classified as high (≥39%) versus low (<39%) according to risk factor burden as described in our previously published algorithm. Perception of lifetime risk for myocardial infarction was assessed by way of a 5-point scale. Baseline characteristics were compared across levels of perceived lifetime risk. Multivariable logistic regression analyses were performed to determine the association of participant characteristics with level of perceived lifetime risk for CVD and with correctness of perceptions. Of the 2,998 participants, 64.8% (n = 1,942) were classified as having high predicted lifetime risk for CVD. There was significant discordance between perceived and predicted lifetime risk. After multivariable adjustment, family history of premature myocardial infarction, high self-reported stress, and low perceived health were all strongly associated with high perceived lifetime risk (odds ratio [OR] 2.37, 95% confidence interval [CI] 1.72 to 3.27; OR 2.17, 95% CI 1.66 to 2.83; and OR 2.71, 95% CI 2.09 to 3.53; respectively). However, the association between traditional CVD risk factors and high perceived lifetime risk was more modest. In conclusion, misperception of lifetime risk for CVD is common and frequently reflects the influence of factors other than traditional risk factor levels. These findings highlight the importance of effectively communicating the significance of traditional risk factors in determining the lifetime risk for CVD. [ABSTRACT FROM AUTHOR]

Objectives: The aim of this study was to assess the impact of extreme (class III) obesity (body mass index [BMI] ≥40 kg/m(2)) on care and outcomes in patients with ST-segment elevation myocardial infarction (STEMI).Background: Although its prevalence is increasing rapidly, little is known about the impact of extreme obesity on STEMI presentation, treatments, complication rates, and outcomes.Methods: The relationship between BMI and baseline characteristics, treatment patterns, and risk-adjusted in-hospital outcomes was quantified for 50,149 patients with STEMI from the National Cardiovascular Data Registry (NCDR) ACTION Registry-GWTG.Results: The proportions of patients with STEMI by BMI category were as follows: underweight (BMI <18.5 kg/m(2)) 1.6%, normal weight (18.5 kg/m(2) ≤BMI <25 kg/m(2)) 23.5%, overweight (25 kg/m(2) ≤BMI <30 kg/m(2)) 38.7%, class I obese (30 kg/m(2) ≤BMI <35 kg/m(2)) 22.4%, class II obese (35 kg/m(2) ≤BMI <40 kg/m(2)) 8.7%, and class III obese 5.1%. Extreme obesity was associated with younger age at STEMI presentation (median age 55 years for class III obese vs. 66 years for normal weight); a higher prevalence of diabetes, hypertension, and dyslipidemia; a lower prevalence of smoking; and less extensive coronary artery disease and higher left ventricular ejection fraction. Process-of-care measures were similar across BMI categories, including the extremely obese. Using class I obesity as the referent, risk-adjusted in-hospital mortality rates were significantly higher only for class III obese patients (adjusted odds ratio: 1.64; 95% confidence interval: 1.32 to 2.03).Conclusions: Patients with extreme obesity present with STEMI at younger ages and have less extensive coronary artery disease, better left ventricular systolic function, and similar processes and quality of care. Despite these advantages, extreme obesity remains independently associated with higher in-hospital mortality. [ABSTRACT FROM AUTHOR]