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  • 1
    Online Resource
    Online Resource
    Whole genome sequence analysis of blood lipid levels in 〉66,000 individuals
    Springer Science and Business Media LLC ; 2022
    In:  Nature Communications Vol. 13, No. 1 ( 2022-10-11)
    Details
    In: Nature Communications, Springer Science and Business Media LLC, Vol. 13, No. 1 ( 2022-10-11)
    Abstract: Blood lipids are heritable modifiable causal factors for coronary artery disease. Despite well-described monogenic and polygenic bases of dyslipidemia, limitations remain in discovery of lipid-associated alleles using whole genome sequencing (WGS), partly due to limited sample sizes, ancestral diversity, and interpretation of clinical significance. Among 66,329 ancestrally diverse (56% non-European) participants, we associate 428M variants from deep-coverage WGS with lipid levels; ~400M variants were not assessed in prior lipids genetic analyses. We find multiple lipid-related genes strongly associated with blood lipids through analysis of common and rare coding variants. We discover several associated rare non-coding variants, largely at Mendelian lipid genes. Notably, we observe rare LDLR intronic variants associated with markedly increased LDL-C, similar to rare LDLR exonic variants. In conclusion, we conducted a systematic whole genome scan for blood lipids expanding the alleles linked to lipids for multiple ancestries and characterize a clinically-relevant rare non-coding variant model for lipids.
    Type of Medium: Online Resource
    ISSN: 2041-1723
    URL: Article
    DOI: 10.1038/s41467-022-33510-7
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
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  • 2
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    Abstract 021: Higher Levels of Ideal Cardiovascular Health Are Associated With Lower Risk of Incident Type 2 Diabetes Mellitus Among Individuals With Normal Fasting Glucose but Not Impaired Fasting Glucose: The Reasons for Geographic and Racial Differences in Stroke Study
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Circulation Vol. 137, No. suppl_1 ( 2018-03-20)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 137, No. suppl_1 ( 2018-03-20)
    Abstract: Aims/hypothesis: Ideal cardiovascular health (ICH) is associated with lower risk of incident diabetes, but whether this association varies by baseline glycemia (normal [ 〈 100 mg/dL] vs. impaired fasting glucose [100-125 mg/dL] ) remains to be clarified. We assessed the incidence of diabetes based on American Heart Association (AHA) ICH components stratified by glycemic status to determine whether ICH is more effective for primordial or primary prevention of diabetes among middle-aged and older adults. Methods: This study included 7,662 non-Hispanic whites and African Americans from the REasons for Geographic and Racial Differences in Stroke (REGARDS) Study without prevalent diabetes at baseline (2003-2006), who completed the follow-up exam (2013-2016). Participants were categorized as having ideal, intermediate or poor cardiovascular health, as defined by the AHA 2020 Impact Goals, based on baseline ICH components (total cholesterol, blood pressure, dietary intake, tobacco use, physical activity and body-mass index (BMI)). We categorized participants based on their total number of components that were ideal (0-1 “poor”, 2-3 “intermediate”, and 4+ “ideal”). Incident rate ratios (IRR) were calculated using modified poisson regression adjusting for age, sex, education, income, race, alcohol use, estimated glomerular filtration rate, urine albumin:creatinine ratio and high-sensitivity C-reactive protein. After confirming significant interactions with multiplicative interaction terms and application of likelihood ratio test, we stratified by glycemic status (normal vs. impaired fasting glucose). Results: Among REGARDS participants (mean age 63.0 [SD 8.4] years, 56% female, 26% African American), there were 560 incident diabetes cases (median follow-up 9.5 years). Overall, those with 2-3 and 4+ ICH components vs. 0-1 components had 31% (IRR 0.69; 95% CI 0.61, 0.79) and 71% lower (IRR 0.29; 95% CI 0.20, 0.42) risk of diabetes, respectively. Among 5,930 participants with normal fasting glucose, these risks were 36% (IRR 0.64; 95% CI 0.52, 0.79) and 80% lower (IRR 0.20; 95% CI 0.10, 0.37), while among 1,732 participants with baseline impaired fasting glucose these risks were 8% (IRR 0.92; 95% CI 0.80,1.07) and 13% lower (IRR 0.87; 95% CI 0.58,1.30) (p for interaction by baseline glucose status 〈 0.0001). Conclusions/interpretation: Meeting an increasing number of ideal levels of dietary intake, physical activity, smoking, blood pressure, cholesterol and BMI was associated with a dose-dependent lower risk of diabetes for individuals with normal fasting glucose but not impaired fasting glucose. This suggests the AHA 2020 guidelines may be more effective for primordial versus primary prevention of diabetes among middle-aged and older adults.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.137.suppl_1.021
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
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  • 3
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    Abstract MP50: Neighborhood Social And Economic Environment And Heart Failure Risk Among Adults With & Without Diabetes: The Reasons For Geographic And Racial Differences In Stroke (regards) Study
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Vol. 143, No. Suppl_1 ( 2021-05-25)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 143, No. Suppl_1 ( 2021-05-25)
    Abstract: Background: Heart failure (HF) mortality rates have been increasing since 2011. Individual-level education and occupation have been inversely associated with HF mortality among those with diabetes mellitus (DM) but not among those without DM. However, less is known about the association between neighborhood social and economic environment (NSEE) and HF risk and whether this association varies by DM status. Methods: This study included 21,244 Black and White adults age 〉 =45 years at baseline (2003-07) from the REGARDS Study. NSEE quartiles were created using z-scores based on 6 census tract variables from year 2000 (% 〈 high school education, % unemployed, % household with 〈 $30,000, % living in poverty, % on public assistance, % without car). Incident HF events (fatal or non-fatal) were adjudicated based on hospitalization with HF signs and symptoms, supportive imaging or biomarkers. Diabetes was defined as fasting glucose 〉 =126 mg/dL or random glucose 〉 =200 mg/dL or use of diabetes medications. Cox proportional hazards regression was used to obtain hazard ratios (95% CI) with HF follow-up through 2016. Results: Mean age was 65 years, 54% were women, 61% were White and 18% had prevalent DM at baseline. During a median 10.1 years, 829 incident HF events occurred. Among adults with DM, neighborhood disadvantage was associated with an increased HF risk , but this association was not statistically significant (Table). Among adults without DM, the risk of HF was higher for participants living in any neighborhood that was not the most advantaged, and the magnitude of association was smiliar across NSEE quartiles. Conclusion: Adults living in disadvantaged neighborhoods had a higher risk of HF, particularly among those without DM. Addressing neighborhood social and economic conditions may be important for HF prevention.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.143.suppl_1.MP50
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
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  • 4
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    Online Resource
    Abstract P128: The Epigenomic Signature of Life's Simple 7
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Circulation Vol. 137, No. suppl_1 ( 2018-03-20)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 137, No. suppl_1 ( 2018-03-20)
    Abstract: Introduction: Life’s Simple 7 (LS7) comprises seven health factors and behaviors promoted by the American Heart Association to reduce cardiovascular morbidity and mortality. Despite compelling evidence of inverse association between LS7 adherence and a variety of adverse health outcomes, the epigenetic sequelae of healthy lifestyle have not been comprehensively characterized and may offer valuable insights into the underlying biological mechanisms. Hypothesis: We hypothesized that LS7 adherence is associated with an epigenetic signature that is consistent with the deceleration of the aging process. Methods: Using data from the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN, n=853), we have estimated cross-sectional associations between epigenome-wide DNA methylation at 487,432 cytosine-phosphate-guanine (CpG) sites in CD4+ T-cells and the number of achieved LS7 goals as measured by study staff (blood pressure, body mass index, total cholesterol, and fasting glucose) or reported by the participant (diet, smoking, physical activity). The associations were tested using linear mixed models adjusted for age, sex, study site, technical artifacts (fixed effects), and family relatedness (random effect). Additionally, we tested associations between LS7 compliance and age acceleration, estimated from DNA methylation data and chronological age using two complementary validated algorithms (1: Horvath and 2: Hannum). These linear mixed models adjusted for chronological age, sex, study site, CD4+ T-cell subtype estimates (fixed effects), and family relatedness (random effect). Epigenome-wide association results were considered statistically significant if they fell under the Bonferroni corrected threshold (alpha=0.05/487,432= 1.03x10 -7 ). Results: Methylation of an intronic CpG site in CPT1A , cg00574958, was positively associated with the number of achieved LS7 goals at the epigenome-wide significance level (beta= 0.008, SE= 0.001, P= 4.7x10 -8 ). CPT1A encodes a key enzyme in the beta-oxidation process and has previously been linked to fasting triglycerides, body mass index, and adiponectin levels. Age acceleration was associated with LS7 adherence under the Hannum algorithm (beta=-0.01, SE= 0.006, P= 0.02) but not the Horvath algorithm (beta=-0.005, SE= 0.004, P= 0.18). Conclusions: Achievement of LS7 goals was significantly associated with methylation variation in CPT1A , a critical lipid metabolism gene, and was associated with age deceleration in the Hannum but not the Horvath models. Following independent replication, future studies should consider interrogating CPT1A methylation in relation to cardiovascular morbidity and mortality in a prospective setting.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.137.suppl_1.p128
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
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  • 5
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    Abstract MP19: An eGFR Polygenic Score Predicts Chronic Kidney Disease in African Americans
    Ovid Technologies (Wolters Kluwer Health) ; 2023
    In:  Circulation Vol. 147, No. Suppl_1 ( 2023-02-28)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 147, No. Suppl_1 ( 2023-02-28)
    Abstract: Chronic kidney disease (CKD) is a risk factor for cardiovascular disease and early death. Genetic factors contribute to CKD, and recently, polygenic scores (PGS) have been developed to quantify risk for complex diseases, such as CKD. However, African ancestry populations are underrepresented in both CKD genetic studies and PGS development overall; moreover, European-ancestry derived PGSs demonstrate diminished predictive performance in African ancestry populations. This study aimed to develop a PGS for CKD using genotype and phenotype data from African American (AA) participants of observational cohort studies. We obtained score weights from a meta-analysis of genome-wide association studies (GWAS) for estimated glomerular filtration rate (eGFR) in the Million Veteran Program (MVP) and Reasons for Geographical and Racial Differences in Stroke (REGARDS) Study (total n~66,000). We then optimized the PGS in a cohort of AAs from the Hypertension Genetic Epidemiology Network (HyperGEN) Study (n~1,900) using the PRS-CS software and evaluated the predictive performance of the PGS at multiple global shrinkage parameters. We further adjusted the PGS for APOL1 risk status. In HyperGEN, the eGFR-based PGS was significantly associated with the odds of prevalent CKD—defined as baseline eGFR 〈 60 mL/min/1.73m 2 — in logistic regression models adjusted for age, sex, and population structure. Further, accounting for APOL1 risk status—a putative variant for CKD unique to those of sub-Saharan African descent—improved the score’s accuracy, with the APOL1 -adjusted PGS explaining 1.9% (1.1% without APOL1 ) of the variance in CKD and an area under the curve (AUC) of 58.9% [95% CI: 53.0%-64.9%] (without APOL1 , 58.2% [95% CI: 52.3%-64.1%]). Sensitivity analyses and validation in external cohorts, as well as comparisons to previously published PGS, are ongoing. In this study, we developed a PGS that was significantly associated with CKD with improved predictive accuracy in AAs over previously published PGS.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.147.suppl_1.MP19
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
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  • 6
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    Online Resource
    Abstract P251: Epigenome-Wide Study of Erythrocyte Fatty Acids in the Genetics of Lipid Lowering Drugs and Diet Network
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Vol. 129, No. suppl_1 ( 2014-03-25)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 129, No. suppl_1 ( 2014-03-25)
    Abstract: Introduction: Dietary fatty acids have a role in many physiological mechanisms that influence cardiovascular health. An emerging body of evidence suggests that dietary fats may interact with genetic variants in regulating tissue levels of fatty acids, thus impacting disease risk. Epigenetic changes such as DNA methylation are a promising mechanism underlying such interactions. However, no studies to date have investigated the relationship between DNA methylation and tissue fatty acids at the genome-wide level. Methods: We have performed the first epigenome-wide association study (EWAS) of erythrocyte concentrations of polyunsaturated, monounsaturated, saturated, and trans fatty acids in 958 participants of the Genetics of Diet and Lipid Lowering Drugs Network (GOLDN). We assayed the methylation status of approximately 450,000 CpG sites in CD4+ T-cells. To investigate the associations between methylation of each CpG site and red blood cell fatty acids, we fit linear mixed models adjusted for age, sex, cell purity, and family structure. Results: The strongest association was observed between the methylation status of a CpG site in PDE4D, previously linked to systemic inflammation and stroke, and red blood cell trans fatty acids (P=4x10-7). In the analysis of polyunsaturated fatty acids, we found inverse associations with the methylation status of two CpG sites in BRSK2 (P=9x10-6 and P=1x10-5 respectively), as well as with a CpG site located in a “gene desert” on chromosome 14 proximally to VRK1 (P=5x10-7). BRSK2 encodes a kinase previously shown to control epigenetic programs that determine T-cell function. The top hits for monounsaturated and saturated fatty acids were located in ATL2 (P=1x10-6) and FGD2 (P=1x10-5), respectively. Conclusions: We present preliminary evidence of cross-sectional association between the methylation status of several biologically relevant genomic regions and erythrocyte concentrations of polyunsaturated, trans, monounsaturated, and saturated fatty acids. Upon successful validation, these findings further current understanding of gene-fatty acid interactions in human health and disease.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.129.suppl_1.p251
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
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  • 7
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    Genetic Characterization of Rebounding Human Immunodeficiency Virus Type 1 in Plasma during Multiple Interruptions of Highly Active Antiretroviral Therapy
    American Society for Microbiology ; 2003
    In:  Journal of Virology Vol. 77, No. 5 ( 2003-03), p. 3229-3237
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 77, No. 5 ( 2003-03), p. 3229-3237
    Abstract: Various strategies of interrupting highly active antiretroviral therapy (HAART) are being investigated for the treatment of human immunodeficiency virus (HIV) infection. Interruptions of greater than 2 weeks frequently result in rebound of plasma HIV RNA. In order to discern changes in the viral population that might occur during cycles of treatment interruption, we evaluated the homology of HIV-1 envelope gene sequences over time in 12 patients who received four to seven cycles of 4 weeks off HAART followed by 8 weeks on HAART by using the heteroduplex tracking assay and novel statistical tools. HIV populations in 9 of 12 patients diverged from those found in the first cycle in at least one subsequent cycle. The substantial genetic changes noted in HIV env did not correlate with increased or decreased log changes in levels of plasma HIV RNA ( P 〉 0.5). Thus, genetic changes in HIV env itself did not contribute in a systematic way to changes in levels of plasma viremia from cycle to cycle of treatment interruption. In addition, the data suggest that there may be multiple compartments contributing to the rebound of plasma viremia and to viral diversity from cycle to cycle of intermittent therapy.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.77.5.3229-3237.2003
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2003
    detail.hit.zdb_id: 1495529-5
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  • 8
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    A 6-CpG validated methylation risk score model for metabolic syndrome: The HyperGEN and GOLDN studies
    Public Library of Science (PLoS) ; 2021
    In:  PLOS ONE Vol. 16, No. 11 ( 2021-11-15), p. e0259836-
    Details
    In: PLOS ONE, Public Library of Science (PLoS), Vol. 16, No. 11 ( 2021-11-15), p. e0259836-
    Abstract: There has been great interest in genetic risk prediction using risk scores in recent years, however, the utility of scores developed in European populations and later applied to non-European populations has not been successful. The goal of this study was to create a methylation risk score (MRS) for metabolic syndrome (MetS), demonstrating the utility of MRS across race groups using cross-sectional data from the Hypertension Genetic Epidemiology Network (HyperGEN, N = 614 African Americans (AA)) and the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN, N = 995 European Americans (EA)). To demonstrate this, we first selected cytosine-guanine dinucleotides (CpG) sites measured on Illumina Methyl450 arrays previously reported to be significantly associated with MetS and/or component conditions in more than one race/ethnic group ( CPT1A cg00574958, PHOSPHO1 cg02650017, ABCG1 cg06500161, SREBF1 cg11024682, SOCS3 cg18181703, TXNIP cg19693031). Second, we calculated the parameter estimates for the 6 CpGs in the HyperGEN data (AA) and used the beta estimates as weights to construct a MRS in HyperGEN (AA), which was validated in GOLDN (EA). We performed association analyses using logistic mixed models to test the association between the MRS and MetS, adjusting for covariates. Results showed the MRS was significantly associated with MetS in both populations. In summary, a MRS for MetS was a strong predictor for the condition across two race groups, suggesting MRS may be useful to examine metabolic disease risk or related complications across race/ethnic groups.
    Type of Medium: Online Resource
    ISSN: 1932-6203
    URL: Article
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    DOI: 10.1371/journal.pone.0259836
    DOI: 10.1371/journal.pone.0259836.g001
    DOI: 10.1371/journal.pone.0259836.t001
    DOI: 10.1371/journal.pone.0259836.t002
    DOI: 10.1371/journal.pone.0259836.t003
    DOI: 10.1371/journal.pone.0259836.t004
    DOI: 10.1371/journal.pone.0259836.s001
    DOI: 10.1371/journal.pone.0259836.r001
    DOI: 10.1371/journal.pone.0259836.r002
    DOI: 10.1371/journal.pone.0259836.r003
    DOI: 10.1371/journal.pone.0259836.r004
    Language: English
    Publisher: Public Library of Science (PLoS)
    Publication Date: 2021
    detail.hit.zdb_id: 2267670-3
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  • 9
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    Deep coverage whole genome sequences and plasma lipoprotein(a) in individuals of European and African ancestries
    Springer Science and Business Media LLC ; 2018
    In:  Nature Communications Vol. 9, No. 1 ( 2018-07-04)
    Details
    In: Nature Communications, Springer Science and Business Media LLC, Vol. 9, No. 1 ( 2018-07-04)
    Abstract: Lipoprotein(a), Lp(a), is a modified low-density lipoprotein particle that contains apolipoprotein(a), encoded by LPA , and is a highly heritable, causal risk factor for cardiovascular diseases that varies in concentrations across ancestries. Here, we use deep-coverage whole genome sequencing in 8392 individuals of European and African ancestry to discover and interpret both single-nucleotide variants and copy number (CN) variation associated with Lp(a). We observe that genetic determinants between Europeans and Africans have several unique determinants. The common variant rs12740374 associated with Lp(a) cholesterol is an eQTL for SORT1 and independent of LDL cholesterol. Observed associations of aggregates of rare non-coding variants are largely explained by LPA structural variation, namely the LPA kringle IV 2 (KIV2)-CN. Finally, we find that LPA risk genotypes confer greater relative risk for incident atherosclerotic cardiovascular diseases compared to directly measured Lp(a), and are significantly associated with measures of subclinical atherosclerosis in African Americans.
    Type of Medium: Online Resource
    ISSN: 2041-1723
    URL: Article
    DOI: 10.1038/s41467-018-04668-w
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2018
    detail.hit.zdb_id: 2553671-0
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  • 10
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    DataSheet2.xlsx
    Frontiers Media SA ; 2021
    In:  Frontiers in Genetics Vol. 12 ( 2021-12-21)
    Details
    In: Frontiers in Genetics, Frontiers Media SA, Vol. 12 ( 2021-12-21)
    Abstract: Background: African Americans (AAs) suffer a higher stroke burden due to hypertension. Identifying genetic contributors to stroke among AAs with hypertension is critical to understanding the genetic basis of the disease, as well as detecting at-risk individuals. Methods: In a population comprising over 10,700 AAs treated for hypertension from the Genetics of Hypertension Associated Treatments (GenHAT) and Reasons for Geographic and Racial Differences in Stroke (REGARDS) studies, we performed an inverse variance-weighted meta-analysis of incident stroke. Additionally, we tested the predictive accuracy of a polygenic risk score (PRS) derived from a European ancestral population in both GenHAT and REGARDS AAs aiming to evaluate cross-ethnic performance. Results: We identified 10 statistically significant ( p & lt; 5.00E-08) and 90 additional suggestive ( p & lt; 1.00E-06) variants associated with incident stroke in the meta-analysis. Six of the top 10 variants were located in an intergenic region on chromosome 18 ( LINC01443-LOC644669 ). Additional variants of interest were located in or near the COL12A1, SNTG1 , PCDH7 , TMTC1 , and NTM genes . Replication was conducted in the Warfarin Pharmacogenomics Cohort (WPC), and while none of the variants were directly validated, seven intronic variants of NTM proximal to our target variants, had a p -value & lt;5.00E-04 in the WPC. The inclusion of the PRS did not improve the prediction accuracy compared to a reference model adjusting for age, sex, and genetic ancestry in either study and had lower predictive accuracy compared to models accounting for established stroke risk factors. These results demonstrate the necessity for PRS derivation in AAs, particularly for diseases that affect AAs disproportionately. Conclusion: This study highlights biologically plausible genetic determinants for incident stroke in hypertensive AAs. Ultimately, a better understanding of genetic risk factors for stroke in AAs may give new insight into stroke burden and potential clinical tools for those among the highest at risk.
    Type of Medium: Online Resource
    ISSN: 1664-8021
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fgene.2021.781451
    DOI: 10.3389/fgene.2021.781451.s001
    DOI: 10.3389/fgene.2021.781451.s002
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2606823-0
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