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Author Notes:

Correspondence: smjenn@umich.edu; Tel.: +1-734-615-9455

See publication for full list of author contributions.

The authors thank the staff and participants of the ARIC, HRS, JHS and MESA studies for their important contributions.

Genotyping quality control and final preparation of the data were performed by the Genetics Coordinating Center at the University of Washington.

The authors also wish to thank the participants and staff of the JHS.

The authors declare no conflict of interest.

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Research Funding:

Analysis for this project was supported by the Center for Integrative Approaches to Health Disparities at the University of Michigan, National Institute on Minority Health and Health Disparities (NIMHD, P60 MD002249), National Heart, Lung and Blood Institute (NHLBI, R01 HL101161) and the National Institute on Aging (NIA, R03 AG046389).

The Atherosclerosis Risk in Communities Study is carried out as a collaborative study supported by NHLBI contracts (HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C and HHSN268201100012C), R01HL087641, R01HL59367 and R01HL086694; the National Human Genome Research Institute (NHGRI) contract U01HG004402; and the National Institutes of Health (NIH) contract HHSN268200625226C. The authors thank the staff and participants of the ARIC study for their important contributions.

Infrastructure was partly supported by Grant Number UL1RR025005, a component of the NIH and NIH Roadmap for Medical Research.

The Health and Retirement Study (HRS) is supported by the NIA (U01AG009740). HRS genotyping was funded separately by the NIA (RC2 AG036495, RC4 AG039029) and was conducted by the NIH Center for Inherited Disease Research (CIDR) at Johns Hopkins University.

The Jackson Heart Study is supported and conducted in collaboration with Jackson State University (HHSN268201300049C and HHSN268201300050C), Tougaloo College (HHSN268201300048C) and the University of Mississippi Medical Center (HHSN268201300046C and HHSN268201300047C) contracts from the NHLBI and the NIMHD.

MESA and the MESA SHARe project are conducted and supported by the NHLBI in collaboration with MESA investigators.

Support for MESA is provided by contracts HHSN268201500003I, N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, N01-HC-95169, UL1-TR-000040, UL1-TR-001079, UL1-TR-001881 and DK063491.

Funding for MESA SHARe genotyping was provided by NHLBI Contract N02-HL-64278.

MESA genotyping was performed at Affymetrix (Santa Clara, CA, USA) and the Broad Institute of Harvard and MIT (Boston, MA, USA) using the Affymetrix Genome-Wide Human SNP Array 6.0.

Keywords:

  • blood pressure
  • chronic burden
  • depression
  • gene-by-environment interaction
  • genetics
  • hypertension
  • non-burden test
  • psychosocial factors
  • socioeconomic status

Gene-by-psychosocial factor interactions influence diastolic blood pressure in european and african ancestry populations: Meta-analysis of four cohort studies

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Journal Title:

International Journal of Environmental Research and Public Health

Volume:

Volume 14, Number 12

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Type of Work:

Article | Final Publisher PDF

Abstract:

Inter-individual variability in blood pressure (BP) is influenced by both genetic and nongenetic factors including socioeconomic and psychosocial stressors. A deeper understanding of the gene-by-socioeconomic/psychosocial factor interactions on BP may help to identify individuals that are genetically susceptible to high BP in specific social contexts. In this study, we used a genomic region-based method for longitudinal analysis, Longitudinal Gene-Environment-Wide Interaction Studies (LGEWIS), to evaluate the effects of interactions between known socioeconomic/ psychosocial and genetic risk factors on systolic and diastolic BP in four large epidemiologic cohorts of European and/or African ancestry. After correction for multiple testing, two interactions were significantly associated with diastolic BP. In European ancestry participants, outward/trait anger score had a significant interaction with the C10orf107 genomic region (p = 0.0019). In African ancestry participants, depressive symptom score had a significant interaction with the HFE genomic region (p = 0.0048). This study provides a foundation for using genomic region-based longitudinal analysis to identify subgroups of the population that may be at greater risk of elevated BP due to the combined influence of genetic and socioeconomic/psychosocial risk factors.

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© 2017 by the authors. Licensee MDPI, Basel, Switzerland.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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