Latinos are a heterogeneous population in terms of demographics, culture, and genetic admixture from three racial groups (white, African, and Native American). This study examines the role of genetic ancestry and environmental risk factors in the risk of hypertensive disorder of pregnancy among Latinas in Los Angeles County.
Gestational hypertension, preeclampsia, eclampsia, or hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome cases (n = 125), plus unaffected controls (n = 161), were recruited from Los Angeles County + University of Southern California Women’s and Children’s Hospital from 1999 through 2008. Diagnoses were confirmed with extensive chart review. Personal information, demographics, and biospecimens were collected from all participants. Ancestry informative markers were used to estimate genetic ancestry proportions.
After adjusting for European ancestry and key risk factors, African ancestry was positively associated with hypertensive disorders of pregnancy risk for the highest vs. the lowest quartiles of African ancestry (odds ratio = 2.6 [95% confidence interval = 1.1–6.1]). This association was stronger among women born in Mexico with parents born in Mexico (4.3 [1.4–13]). The results from generalized additive models showed a positive association between joint European/African ancestry and hypertensive disorders of pregnancy risk and an inverse association between Native American ancestry and risk. These associations were stronger among women of Mexican origin.
Our findings suggest that higher Native American ancestry among Latinas may protect against hypertensive disorders of pregnancy. Further studies are needed to determine whether this protective effect is driven by specific alleles present in this population or by other risk factors that correlate with Native American ancestry.
From the aDepartment of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA; and bDepartment of Obstetrics and Gynecology, Keck School of Medicine, University of Southern California, Los Angeles, CA.
Submitted 26 July 2011; accepted 4 December 2012; posted 21 January 2013.
Supported by the NICHD, R21 HD046624-02 (to S.A.I.) and the National Institute of Environmental Health Sciences (grant 5P30 ES07048 to M.C.S.).
A.S. and M.L.W. contributed equally to this work.
M.C.S. and S.A.L. jointly directed this work.
Correspondence: Mariana C. Stern, University of Southern California, Keck School of Medicine, Norris Comprehensive Cancer Center, 1441 Eastlake Avenue, Room 5421A, Los Angeles, CA 90089. E-mail: email@example.com.