BACKGROUND AND PURPOSE:Population-wide reductions in cardiovascular disease incidence and mortality have not been shared equally by African Americans. The burden of cardiovascular disease in the ...African American community remains high and is a primary cause of disparities in life expectancy between African Americans and whites. The objectives of the present scientific statement are to describe cardiovascular health in African Americans and to highlight unique considerations for disease prevention and management.
METHOD:The primary sources of information were identified with PubMed/Medline and online sources from the Centers for Disease Control and Prevention.
RESULTS:The higher prevalence of traditional cardiovascular risk factors (eg, hypertension, diabetes mellitus, obesity, and atherosclerotic cardiovascular risk) underlies the relatively earlier age of onset of cardiovascular diseases among African Americans. Hypertension in particular is highly prevalent among African Americans and contributes directly to the notable disparities in stroke, heart failure, and peripheral artery disease among African Americans. Despite the availability of effective pharmacotherapies and indications for some tailored pharmacotherapies for African Americans (eg, heart failure medications), disease management is less effective among African Americans, yielding higher mortality. Explanations for these persistent disparities in cardiovascular disease are multifactorial and span from the individual level to the social environment.
CONCLUSIONS:The strategies needed to promote equity in the cardiovascular health of African Americans require input from a broad set of stakeholders, including clinicians and researchers from across multiple disciplines.
Objective: Obesity is a major driver of cardiometabolic risk. Abdominal visceral adipose tissue (VAT) and sc adipose tissue (SAT) may confer differential metabolic risk profiles. We investigated the ...relations of VAT and SAT with cardiometabolic risk factors in the Jackson Heart Study cohort.
Methods: Participants from the Jackson Heart Study (n = 2477; 64% women; mean age, 58 yr) underwent multidetector computed tomography, and the volumetric amounts of VAT and SAT were assessed between 2007 and 2009. Cardiometabolic risk factors were examined by sex in relation to VAT and SAT.
Results: Men had a higher mean volume of VAT (873 vs. 793 cm3) and a lower mean volume of SAT (1730 vs. 2659 cm3) than women (P = 0.0001). Per 1-sd increment in either VAT or SAT, we observed elevated levels of fasting plasma glucose and triglyceride, lower levels of high-density lipoprotein-cholesterol, and increased odds ratios for hypertension, diabetes, and metabolic syndrome. The effect size of VAT in women was larger than that of SAT fasting plasma glucose, 5.51 ± 1.0 vs. 3.36 ± 0.9; triglyceride, 0.17 ± 0.01 vs. 0.05 ± 0.01; high-density lipoprotein-cholesterol, −5.36 ± 0.4 vs. −2.85 ± 0.4; and odds ratio for hypertension, 1.62 (1.4–1.9) vs. 1.40 (1.2–1.6); diabetes, 1.82 (1.6–2.1) vs. 1.58 (1.4–1.8); and metabolic syndrome, 3.34 (2.8–4.0) vs. 2.06 (1.8–2.4), respectively; P < 0.0001 for difference between VAT and SAT. Similar patterns were also observed in men. Furthermore, VAT remained associated with most risk factors even after accounting for body mass index (P ranging from 0.006–0.0001). The relationship of VAT to most risk factors was significantly different between women and men.
Conclusions: Abdominal VAT and SAT are both associated with adverse cardiometabolic risk factors, but VAT remains more strongly associated with these risk factors. The results from this study suggest that relations with cardiometabolic risk factors are consistent with a pathogenic role of abdominal adiposity in participants of African ancestry.
Both visceral and subcutaneous adipose tissues are associated with adverse cardiometabolic risk factors, but visceral adipose tissue remains more strongly associated with these risk factors.
Persistently low white blood cell count (WBC) and neutrophil count is a well-described phenomenon in persons of African ancestry, whose etiology remains unknown. We recently used admixture mapping to ...identify an approximately 1-megabase region on chromosome 1, where ancestry status (African or European) almost entirely accounted for the difference in WBC between African Americans and European Americans. To identify the specific genetic change responsible for this association, we analyzed genotype and phenotype data from 6,005 African Americans from the Jackson Heart Study (JHS), the Health, Aging and Body Composition (Health ABC) Study, and the Atherosclerosis Risk in Communities (ARIC) Study. We demonstrate that the causal variant must be at least 91% different in frequency between West Africans and European Americans. An excellent candidate is the Duffy Null polymorphism (SNP rs2814778 at chromosome 1q23.2), which is the only polymorphism in the region known to be so differentiated in frequency and is already known to protect against Plasmodium vivax malaria. We confirm that rs2814778 is predictive of WBC and neutrophil count in African Americans above beyond the previously described admixture association (P = 3.8 x 10(-5)), establishing a novel phenotype for this genetic variant.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
John Henryism connotes a strong behavioral predisposition to engage in effortful, active coping with difficult social and economic stressors. This behavioral predisposition is measured by the 12 item ...John Henryism Scale for Active Coping (JHAC). The John Henry hypothesis predicts that the well-known inverse socioeconomic status (SES)-blood pressure association will be stronger among persons who score high rather than low on the JHAC. We tested this hypothesis in a large African American cohort using baseline data from the Jackson Heart Study. Unlike previous studies, we used multiple indicators of SES: income, education, occupation, childhood SES and cumulative SES. Because the hypothesis is most relevant for adults still in the labor force, we excluded retired participants, yielding a sample size of 3978. Gender-specific Poisson regression models for hypertension adjusting for age, John Henryism, SES, and a John Henryism-SES interaction term, were fit to examine associations. Separate models were fit for each SES indicator. We found some evidence that John Henryism modified the association between income and hypertension in men: low income was associated with higher prevalence of hypertension in men who scored high on John Henryism (prevalence ratio (PR) for low vs. high income tertile 1.12), but with lower hypertension prevalence among men who scored low on John Henryism (PR 0.85, one sided P value for multiplicative interaction <0.05). For women, the association of low income with higher hypertension prevalence was stronger at lower than higher levels of John Henryism (PR 1.27 and 1.06 at low and high levels of John Henryism respectively, P value<0.05). There was no evidence that John Henryism modified the associations of hypertension with other SES indicators in men or women. The modest support of the John Henryism Hypothesis in men only, adds to the literature on this subject, but underscores questions regarding the gender, spatial, socioeconomic and historical contexts in which the hypothesis is valid.
•John Henryism connotes a strong behavioral predisposition of effortful active coping.•Inverse SES-BP association hypothesized as stronger with high than low John Henryism.•We tested this hypothesis using the baseline data from the Jackson Heart Study.•Unlike previous studies we used multiple indicators of socioeconomic status.•Modest support found raises questions about context in which hypothesis is applicable.
It has been hypothesized that low access to healthy and nutritious food increases health disparities. Low-accessibility areas, called food deserts, are particularly commonplace in lower-income ...neighborhoods. The metrics for measuring the food environment's health, called food desert indices, are primarily based on decadal census data, limiting their frequency and geographical resolution to that of the census. We aimed to create a food desert index with finer geographic resolution than census data and better responsiveness to environmental changes.
We augmented decadal census data with real-time data from platforms such as Yelp and Google Maps and crowd-sourced answers to questionnaires by the Amazon Mechanical Turks to create a real-time, context-aware, and geographically refined food desert index. Finally, we used this refined index in a concept application that suggests alternative routes with similar ETAs between a source and destination in the Atlanta metropolitan area as an intervention to expose a traveler to better food environments.
We made 139,000 pull requests to Yelp, analyzing 15,000 unique food retailers in the metro Atlanta area. In addition, we performed 248,000 walking and driving route analyses on these retailers using Google Maps' API. As a result, we discovered that the metro Atlanta food environment creates a strong bias towards eating out rather than preparing a meal at home when access to vehicles is limited. Contrary to the food desert index that we started with, which changed values only at neighborhood boundaries, the food desert index that we built on top of it captured the changing exposure of a subject as they walked or drove through the city. This model was also sensitive to the changes in the environment that occurred after the census data was collected.
Research on the environmental components of health disparities is flourishing. New machine learning models have the potential to augment various information sources and create fine-tuned models of the environment. This opens the way to better understanding the environment and its effects on health and suggesting better interventions.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
The burden of pain is unequal across demographic groups, with broad and persisting race differences in pain-related outcomes in the United States. Members of racial and ethnic minorities frequently ...report more pervasive and severe pain compared with those in the majority, with at least some disparity attributable to differences in socioeconomic status. Whether race disparities in pain-related health outcomes exist among former professional football players is unknown. We examined the association of race with pain outcomes among 3995 former professional American-style football players who self-identified as either Black or White. Black players reported more intense pain and higher levels of pain interference relative to White players, even after controlling for age, football history, comorbidities, and psychosocial factors. Race moderated associations between several biopsychosocial factors and pain; higher body mass index was associated with more pain among White but not among Black players. Fatigue and psychosocial factors were more strongly related to pain among Black players relative to White players. Collectively, the substantial social and economic advantages of working as a professional athlete did not seem to erase race-related disparities in pain. We highlight an increased burden of pain among elite Black professional football players and identify race-specific patterns of association between pain and biopsychosocial pain risk factors. These findings illuminate potential future targets of interventions that may serve to reduce persistent disparities in the experience and impact of pain.
RATIONALE:Two distinct alleles in the gene encoding apolipoprotein L1 (APOL1), a major component of high-density lipoprotein, confer protection against Trypanosoma brucei rhodesiense infection and ...also increase risk for chronic kidney disease. Approximately 14% of Americans with African ancestry carry 2 APOL1 risk alleles, accounting for the high chronic kidney disease burden in this population.
OBJECTIVE:We tested whether APOL1 risk alleles significantly increase risk for atherosclerotic cardiovascular disease (CVD) in African Americans.
METHODS AND RESULTS:We sequenced APOL1 in 1959 randomly selected African American participants in the Jackson Heart Study (JHS) and evaluated associations between APOL1 genotypes and renal and cardiovascular phenotypes. Previously identified association between APOL1 genotypes and chronic kidney disease was confirmed (P=2.4×10). Among JHS participants with 2 APOL1 risk alleles, we observed increased risk for CVD (50/763 events among participants without versus 37/280 events among participants with 2 risk alleles; odds ratio, 2.17; P=9.4×10). We replicated this novel association of APOL1 genotype with CVD in Women’s Health Initiative (WHI) participants (66/292 events among participants without versus 37/101 events among participants with 2 risk alleles; odds ratio, 1.98; P=8.37×10; JHS and WHI combined, P=8.5×10; odds ratio, 2.12). The increased risk for CVD conferred by APOL1 alleles was robust to correction for both traditional CVD risk factors and chronic kidney disease.
CONCLUSIONS:APOL1 variants contribute to atherosclerotic CVD risk, indicating a genetic component to cardiovascular health disparities in individuals of African ancestry. The considerable population of African Americans with 2 APOL1 risk alleles may benefit from intensive interventions to reduce CVD.
Plasma metabolomics profiling is an emerging methodology to identify metabolic pathways underlying cardiovascular health (CVH). The objective of this study was to define metabolomic profiles ...underlying CVH in a cohort of Black adults, a population that is understudied but suffers from disparate levels of CVD risk factors. The Morehouse-Emory Cardiovascular (MECA) Center for Health Equity study cohort consisted of 375 Black adults (age 53 ± 10, 39% male) without known CVD. CVH was determined by the AHA Life's Simple 7 (LS7) score, calculated from measured blood pressure, body mass index (BMI), fasting blood glucose and total cholesterol, and self-reported physical activity, diet, and smoking. Plasma metabolites were assessed using untargeted high-resolution metabolomics profiling. A metabolome wide association study (MWAS) identified metabolites associated with LS7 score after adjusting for age and sex. Using Mummichog software, metabolic pathways that were significantly enriched in metabolites associated with LS7 score were identified. Metabolites representative of these pathways were compared across clinical domains of LS7 score and then developed into a metabolomics risk score for prediction of CVH. We identified novel metabolomic signatures and pathways associated with CVH in a cohort of Black adults without known CVD. Representative and highly prevalent metabolites from these pathways included glutamine, glutamate, urate, tyrosine and alanine, the concentrations of which varied with BMI, fasting glucose, and blood pressure levels. When assessed in conjunction, these metabolites were independent predictors of CVH. One SD increase in the novel metabolomics risk score was associated with a 0.88 higher LS7 score, which translates to a 10.4% lower incident CVD risk. We identified novel metabolomic signatures of ideal CVH in a cohort of Black Americans, showing that a core group of metabolites central to nitrogen balance, bioenergetics, gluconeogenesis, and nucleotide synthesis were associated with CVH in this population.
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