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BMI, physical activity, and breast cancer subtype in white, black, and Sea Island breast cancer survivors.
Ford, ME, Bauza, CE, Findlay, VJ, Turner, DP, Abraham, LM, Moore, LA, Magwood, G, Alberg, AJ, Gaymon, K, Knight, KD, et al
Advances in cancer research. 2020;:83-102
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Abstract
Higher BMI, lower rates of physical activity (PA), and hormone receptor-negative breast cancer (BC) subtype are associated with poorer BC treatment outcomes. We evaluated the prevalence of high BMI, low PA level, and BC subtype among survivors with white/European American (EA) and African American (AA) ancestry, as well as a distinct subset of AAs with Sea Island/Gullah ancestry (SI). We used the South Carolina Central Cancer Registry to identify 137 (42 EAs, 66 AAs, and 29 SIs) women diagnosed with BC and who were within 6-21 months of diagnosis. We employed linear and logistic regression to investigate associations between BMI, PA, and age at diagnosis by racial/ethnic group. Most participants (82%) were overweight/obese (P=0.46). BMI was highest in younger AAs (P=0.02). CDC PA guidelines (≥150min/week) were met by only 28% of participants. The frequency of estrogen receptor (ER)-negative BC subtype was lower in EAs and SIs than in AAs (P<0.05). This is the first study to identify differences in obesity and PA rates, and BC subtype in EAs, AAs, and SIs. BMI was higher, PA rates were lower, and frequency of ER-negative BC was higher in AAs as compared to EAs and SIs. This study highlights the need to promote lifestyle interventions among BC survivors, with the goal of reducing the likelihood of a BC recurrence. Integrating dietary and PA interventions into ongoing survivorship care is essential. Future research could evaluate potential differential immune responses linked to the frequency of triple negative BC in AAs.
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Association between "solute carrier family 30 member 8" (SLC30A8) gene polymorphism and susceptibility to type 2 diabetes mellitus in Chinese Han and minority populations: an updated meta-analysis.
Wang, Y, Duan, L, Yu, S, Liu, X, Han, H, Wang, J, Li, W
Asia Pacific journal of clinical nutrition. 2018;(6):1374-1390
Abstract
BACKGROUND AND OBJECTIVES In China, some studies have been reported that solute carrier family 30 member 8 (SLC30A8) gene polymorphism might increase the risk of T2DM, but some are not. The aim of this meta-analysis was to systematically investigate the association between the rs13266634 polymorphism of the SLC30A8 gene and T2DM in Chinese Han and ethnic minority populations. METHODS AND STUDY DESIGN All published electronic articles were retrieved from Pubmed, Web of Knowledge, Chinese National Knowledge Infrastructure (CNKI), Wanfang database, VIP database and Google scholar. Pooled OR and 95% CI were calculated using random- or fixed-effects models. RESULTS Twenty-five articles involving 62,285 subjects were included in this metaanalysis. Considering the total population, significant associations between the rs13266634 polymorphism and T2DM were observed under the allele model (C vs T: OR=1.23, 95% CI=1.18-1.29), the additive models ( CC vs TT: OR=1.44, 95% CI=1.32-1.56; CC vs CT: OR=1.08, 95% CI=1.02-1.15; CT vs TT: OR=1.25, 95% CI=1.15- 1.37), the dominant model (CC vs CT+TT: OR=1.24, 95% CI=1.17-1.32) and the recessive model (CC+CT vs TT: OR=1.26, 95% CI=1.16-1.35). Based on subgroup analysis, besides the CC vs CT model, these associations were stronger in the ethnic minority groups than in the Han population. Moreover, no association was observed under the CC vs CT model (OR=1.26, 95% CI=0.95-1.66, p=0.105) in ethnic minority groups. CONCLUSIONS Chinese C allele carriers could have an increased risk of T2DM. Well-designed future studies should be conducted with a larger sample size to better understand this association in ethnic minority groups.
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The role of race and ethnicity in sleep, circadian rhythms and cardiovascular health.
Egan, KJ, Knutson, KL, Pereira, AC, von Schantz, M
Sleep medicine reviews. 2017;:70-78
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Abstract
In recent years, strong evidence has emerged suggesting that insufficient duration, quality, and/or timing of sleep are associated with cardiovascular disease (CVD), and various mechanisms for this association have been proposed. Such associations may be related to endophenotypic features of the sleep homeostat and the circadian oscillator, or may be state-like effects of the environment. Here, we review recent literature on sleep, circadian rhythms and CVD with a specific emphasis on differences between racial/ethnic groups. We discuss the reported differences, mainly between individuals of European and African descent, in parameters related to sleep (architecture, duration, quality) and circadian rhythms (period length and phase shifting). We further review racial/ethnic differences in cardiovascular disease and its risk factors, and develop the hypothesis that racial/ethnic health disparities may, to a greater or smaller degree, relate to differences in parameters related to sleep and circadian rhythms. When humans left Africa some 100,000 years ago, some genetic differences between different races/ethnicities were acquired. These genetic differences have been proposed as a possible predictor of CVD disparities, but concomitant differences in culture and lifestyle between different groups may equally explain CVD disparities. We discuss the evidence for genetic and environmental causes of these differences in sleep and circadian rhythms, and their usefulness as health intervention targets.
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A systematic review of lifestyle counseling for diverse patients in primary care.
Melvin, CL, Jefferson, MS, Rice, LJ, Nemeth, LS, Wessell, AM, Nietert, PJ, Hughes-Halbert, C
Preventive medicine. 2017;:67-75
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Abstract
Prior research and systematic reviews have examined strategies related to weight management, less is known about lifestyle and behavioral counseling interventions optimally suited for implementation in primary care practices generally, and among racial and ethnic patient populations. Primary care practitioners may find it difficult to access and use available research findings on effective behavioral and lifestyle counseling strategies and to assess their effects on health behaviors among their patients. This systematic review compiled existing evidence from randomized trials to inform primary care providers about which lifestyle and behavioral change interventions are shown to be effective for changing patients' diet, physical activity and weight outcomes. Searches identified 444 abstracts from all sources (01/01/2004-05/15/2014). Duplicate abstracts were removed, selection criteria applied and dual abstractions conducted for 106 full text articles. As of June 12, 2015, 29 articles were retained for inclusion in the body of evidence. Randomized trials tested heterogeneous multi-component behavioral interventions for an equally wide array of outcomes in three population groups: diverse patient populations (23 studies), African American patients only (4 studies), and Hispanic/Mexican American/Latino patients only (2 studies). Significant and consistent findings among diverse populations showed that weight and physical activity related outcomes were more amenable to change via lifestyle and behavioral counseling interventions than those associated with diet modification. Evidence to support specific interventions for racial and ethnic minorities was promising, but insufficient based on the small number of studies.
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The Role of Advanced Glycation End-Products in Cancer Disparity.
Turner, DP
Advances in cancer research. 2017;:1-22
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While the socioeconomic and environmental factors associated with cancer disparity have been well documented, the contribution of biological factors is an emerging field of research. Established disparity factors such as low income, poor diet, drinking alcohol, smoking, and a sedentary lifestyle may have molecular effects on the inherent biological makeup of the tumor itself, possibly altering cell signaling events and gene expression profiles to profoundly alter tumor development and progression. Our understanding of the molecular and biological consequences of poor lifestyle is lacking, but such information may significantly change how we approach goals to reduce cancer incidence and mortality rates within minority populations. In this review, we will summarize the biological, socioeconomic, and environmental associations between a group of reactive metabolites known as advanced glycation end-products (AGEs) and cancer health disparity. Due to their links with lifestyle and the activation of disease-associated pathways, AGEs may represent both a biological consequence and a bio-behavioral indicator of poor lifestyle which may be targeted within specific populations to reduce disparities in cancer incidence and mortality.
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Influence of APOE Gene Polymorphism on Interindividual and Interethnic Warfarin Dosage Requirement: A Systematic Review and Meta-Analysis.
Yu, WY, Sun, X, Wadelius, M, Huang, L, Peng, C, Ma, WL, Yang, GP
Cardiovascular therapeutics. 2016;(5):297-307
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BACKGROUND Warfarin is the most extensively used coumarin anticoagulant. It has been shown that the anticoagulant effect of warfarin is associated with genetic variation. Apolipoprotein E (ApoE) is a possible candidate to influence the maintenance dose of warfarin. ApoE affects the vitamin K cycle by mediating the uptake of vitamin K into the liver. The vitamin K cycle is the drug target of warfarin. However, the association between genetic variants of the APOE gene and warfarin dose requirement is still controversial. METHODS Revman 5.3 software was used to analyze the relationship between APOE genotypes and warfarin dose requirements. RESULTS In our meta-analysis, the E2/E2 genotype was significantly associated with warfarin dose. E2/E2 patients required 12% (P = 0.0002) lower mean daily warfarin dose than E3/E3 carriers. In addition, subgroup analysis showed that Asians with the E4/E4 genotype tended to need lower warfarin maintenance doses, while the African American E4/E4 carriers needed slightly higher doses than E3/E3 carriers; however, these subgroups were very small. CONCLUSION This is the first meta-analysis of the association between APOE genotypes and warfarin dose. APOE E2/E2 might be one of the factors affecting warfarin dose requirements. The effect of APOE may vary between ethnicities.
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Self-reported race/ethnicity in the age of genomic research: its potential impact on understanding health disparities.
Mersha, TB, Abebe, T
Human genomics. 2015;(1):1
Abstract
This review explores the limitations of self-reported race, ethnicity, and genetic ancestry in biomedical research. Various terminologies are used to classify human differences in genomic research including race, ethnicity, and ancestry. Although race and ethnicity are related, race refers to a person's physical appearance, such as skin color and eye color. Ethnicity, on the other hand, refers to communality in cultural heritage, language, social practice, traditions, and geopolitical factors. Genetic ancestry inferred using ancestry informative markers (AIMs) is based on genetic/genomic data. Phenotype-based race/ethnicity information and data computed using AIMs often disagree. For example, self-reporting African Americans can have drastically different levels of African or European ancestry. Genetic analysis of individual ancestry shows that some self-identified African Americans have up to 99% of European ancestry, whereas some self-identified European Americans have substantial admixture from African ancestry. Similarly, African ancestry in the Latino population varies between 3% in Mexican Americans to 16% in Puerto Ricans. The implication of this is that, in African American or Latino populations, self-reported ancestry may not be as accurate as direct assessment of individual genomic information in predicting treatment outcomes. To better understand human genetic variation in the context of health disparities, we suggest using "ancestry" (or biogeographical ancestry) to describe actual genetic variation, "race" to describe health disparity in societies characterized by racial categories, and "ethnicity" to describe traditions, lifestyle, diet, and values. We also suggest using ancestry informative markers for precise characterization of individuals' biological ancestry. Understanding the sources of human genetic variation and the causes of health disparities could lead to interventions that would improve the health of all individuals.
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Association of leptin gene -2548 G/A polymorphism with obesity: a meta-analysis.
Zhang, L, Yuan, LH, Xiao, Y, Lu, MY, Zhang, LJ, Wang, Y
Annals of nutrition & metabolism. 2014;(2):127-36
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BACKGROUND A common single-nucleotide polymorphism identified in the 5'-untranslated region of the leptin gene (LEP -2548 G/A polymorphism) may be associated with obesity, but the existing research findings are inconsistent, so we conducted this meta-analysis. METHODS Medline, Embase and ISI Web of Science databases were searched to identify relevant studies. Meta-analysis of the total and subgroup populations was conducted using allelic, additive, dominant and recessive models, and odds ratios and their 95% confidence intervals were calculated in a fixed-effect model if no heterogeneity (evaluated as I(2) statistic) existed. Otherwise, a random-effects model was adopted. Subgroup analysis was performed by ethnicity. Meta-regression and the HETRED analysis were used to explore the potential sources of between-study heterogeneity. Egger's test and influence analysis were conducted to evaluate the publication bias and study power, respectively. RESULTS The final selection enrolled 9 studies, including 2,988 subjects (1,372 obese subjects and 1,616 controls). No significant association was identified between the LEP -2548 G/A polymorphism and obesity for all genetic models in the overall population and Caucasians. We found a significant association with allelic, additive and dominant models for subjects of mixed race from South America. Notwithstanding, this significance should be treated cautiously for it is based on a rather small sample (788 involved subjects). CONCLUSIONS In total, the combined analysis of data from current and published studies suggested that the LEP -2548 G/A polymorphism does not contribute to the development of obesity, despite the fact that a significant association exists in a small subgroup from South America. Further studies are needed to elucidate the relationship. .
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Genetic predictors for cardiovascular disease in hispanics.
Qi, L, Campos, H
Trends in cardiovascular medicine. 2011;(1):15-20
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A less favorable cardiovascular risk factor profile but paradoxically lower cardiovascular morbidity and mortality have been observed in Hispanics--a pattern often referred to as the Hispanic paradox. It has been proposed that the specific genetic susceptibility of this admixed population and gene-environment interactions may partly explain the paradox. During the past few years, there have been major advances in the identification of genetic risk factors using genome-wide association studies (GWAS) for cardiovascular disease, especially in Caucasians. However, no GWAS of cardiovascular disease have been reported in Hispanics. In the Costa Rican Heart Study, we reported both the consistency and disparity of genetic effects on risk of coronary heart disease (CHD) between Hispanics and other ethnic groups. We demonstrated that the improvement in the identified genetic markers on discrimination of CHD in Hispanics was modest. Future genetic research on Hispanics should consider the diversity in genetic structure, lifestyle, and socioeconomics among various subpopulations and comprehensively evaluate potential gene-environment interactions in relation to cardiovascular risk.
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Conceptualizing child health disparities: a role for developmental neurogenomics.
Francis, DD
Pediatrics. 2009;(Suppl 3):S196-202
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Biological, psychological, and social processes interact over a lifetime to influence health and vulnerability to disease. Those interested in studying and understanding how and why racial/ethnic and social disparities emerge need to focus on the intersection of these processes. Recent work exploring molecular epigenetic mechanisms of gene expression (in humans as well and other mammalian systems) has provided evidence demonstrating that the genome is subject to regulation by surrounding contexts (eg, cytoplasmic, cellular, organismic, social). The developing stress axis is exquisitely sensitive to regulation by social forces represented at the level of the epigenome. Old assumptions about an inert genome are simply incorrect. Epigenetic processes may provide the missing link that will allow us to understand how social and political conditions, along with individual subjective experiences, can directly alter gene expression and thereby contribute to observed social inequalities in health. Developmental neurogenomics may provide the direct link between the biological and social/psychological worlds. These biological mechanisms of plasticity (at the level of gene expression and regulation) may play a profound role in how we conceptualize health inequalities by informing our concepts regarding the somatization or embodiment of social inequalities.