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We thank Non et al for their comments. First, we observed an increasing trend in preterm delivery (PTD; odds ratio [OR], 1.5 vs 1.7), spontaneous PTD (OR, 1.3 vs 1.7), very PTD (OR, 1.4 vs 2.1), and PTD accompanied by histologic chorioamnionitis (OR, 1.1 vs 1.2), but not in other traits; specifically, medically indicated PTD (OR, 2.1 vs 1.9), near-term PTD (OR, 1.6 vs 1.5), and PTD with maternal hypertensive disorder (OR, 2.4 vs 2.2) were noted. This may be due to at least 2 reasons: (1) PTD has heterogeneous causes. The 7 traits may represent different subphenotypes of PTD, thus, may have different associations with ancestry informative markers; and (2) we may not have adequate statistical power because of a smaller sample size in each subgroup. Because we did not correct for multiple testing, we agree with Non et al that the detected signals may (or may not) be retained after correction for multiple testing.

Second, we agree it would not be ideal to use Yoruban and white subjects from the HapMap project as 2 parental populations. However, they may serve as surrogate ancestral populations because those 2 populations have been used to estimate individual admixture in existing literatures.¹ In addition, as pointed out in the second paragraph in the “Comment” section, “the estimates in the study sample were comparable with those reported in previous studies.” Therefore, we are confident regarding the estimates of individual admixture.

We agree that our study did not account for all the possible sociocultural factors (such as poverty, social support, residential segregation, and discrimination) when we examined the association between PTD and genetic ancestry. However, as indicated by decades of research and the recent Institute of Medicine report that sociodemographic risk factors cannot fully explain the striking and persistent racial disparity in PTD, PTD is likely a complex disease that is influenced by multiple genetic and environmental factors and their interactions.² Given the promise of admixture mapping in other diseases with prominent racial disparity,³ our study represents a novel approach to search for other possible causes of PTD beyond sociocultural factors.

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References 

1. Reiner AP, Carlson CS, Ziv E, Irbarren C, Jaquish CE, Nickerson DA. Genetic ancestry, population sub-structure, and cardiovascular disease-related traits among African-American participants in the CARDIA study. Hum Genet. 2007;121:565–575
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2. Preterm birth: cause, consequences, and prevention. Washington, DC: Institute of Medicine of the National Academies (Committee on Understanding Premature Birth and Assuring Healthy Outcomes Board on Health Sciences Policy); 2006;
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3. Freedman ML, Haiman CA, Patterson N, et al. Admixture mapping identifies 8q24 as a prostate cancer risk locus in African-American men. Proc Natl Acad Sci U S A. 2006;103:14068–14073
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