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DNA methylation near MAD1L1, KDM2B, and SOCS3 mediates the effect of socioeconomic status on elevated body mass index in African American adults

Abstract Obesity and poverty disproportionally affect African American persons. Epigenetic mechanisms could partially explain the association between socioeconomic disadvantage and body mass index (BMI). We examined the extent to which epigenetic mechanisms mediate the effect of socioeconomic status...

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Bibliographic Details
Published in:Human molecular genetics 2024-10, Vol.33 (20), p.1748-1757
Main Authors: Glover, LáShauntá, Lilly, Adam G, Justice, Anne E, Howard, Annie Green, Staley, Brooke S, Wang, Yujie, Kamens, Helen M, Ferrier, Kendra, Bressler, Jan, Loehr, Laura, Raffield, Laura M, Sims, Mario, North, Kari E, Fernández-Rhodes, Lindsay
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Language:English
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Summary:Abstract Obesity and poverty disproportionally affect African American persons. Epigenetic mechanisms could partially explain the association between socioeconomic disadvantage and body mass index (BMI). We examined the extent to which epigenetic mechanisms mediate the effect of socioeconomic status (SES) on BMI. Using data from African American adults from the Atherosclerosis Risk in Communities (ARIC) Study (n = 2664, mean age = 57 years), education, income, and occupation were used to create a composite SES score at visit 1 (1987–1989). We conducted two methylation-wide association analyses to identify associations between SES (visit 1), BMI and cytosine-phosphate-guanine (CpG) sites measured at a subsequent visit (1990–1995). We then utilized structural equation modeling (SEM) to test whether identified sites mediated the association between earlier SES and BMI in sex-stratified models adjusted for demographic and risk factor covariates. Independent replication and meta-analyses were conducted using the Jackson Heart Study (JHS, n = 874, mean age 51 years, 2000–2004). Three CpG sites near MAD1L1, KDM2B, and SOCS3 (cg05095590, cg1370865, and cg18181703) were suggestively associated (P-value 
ISSN:0964-6906
1460-2083
1460-2083
DOI:10.1093/hmg/ddae112