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American Journal of Epidemiology Advance Access originally published online on October 23, 2009
American Journal of Epidemiology 2009 170(11):1382-1385; doi:10.1093/aje/kwp326
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American Journal of Epidemiology © The Author 2009. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

Invited Commentary

Invited Commentary: Maternal Effects in Preterm Birth—Effects of Maternal Genotype, Mitochondrial DNA, Imprinting, or Environment?

Julian Little*

* Correspondence to Dr. Julian Little, Department of Epidemiology and Community Medicine, University of Ottawa, 451 Smyth Road, Ottawa, Ontario K1H 8M5, Canada (e-mail: jlittle{at}uottawa.ca).

Received for publication July 21, 2009. Accepted for publication August 6, 2009.

Preterm birth is an important public health problem. A wide range of risk factors has been investigated, of which the strongest established is a woman's previous history of preterm birth. In this issue of the Journal, Boyd et al. (Am J Epidemiol. 2009;170(11):1358–1364) and Svensson et al. (Am J Epidemiol. 2009;170(11):1365–1372), using data on singleton livebirths from national birth registers linked with multigeneration databases, found evidence that maternal genetic factors impact on the risk for preterm birth, whereas paternal and probably fetal genetic factors do not. Possible caveats include missing information, the range of maternal risk factors included in the analyses, possible misclassification of these risk factors, and possible vertical transmission of microbial flora or behaviors from mother to daughter. Weinberg and Shi (Am J Epidemiol. 2009;170(11):1373–1381) build on the evidence regarding potential mechanisms underlying the heritability of preterm birth from these 2 and other studies, to evaluate the comparative ability of different study designs to distinguish among these potential mechanisms. These studies have different strengths, and a portfolio of studies of different designs and with more detailed phenotyping than previously done will be needed to probe further the etiology of preterm birth and thereby provide tools for its control.

bias (epidemiology); epigenesis, genetic; family health; genetics; premature birth; research design; risk factors

Abbreviations: CI, confidence interval


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A. C. Svensson, S. Sandin, S. Cnattingius, M. Reilly, Y. Pawitan, C. M. Hultman, and P. Lichtenstein
Svensson et al. Respond to "Maternal Genes and Environment in Preterm Birth"
Am. J. Epidemiol., December 1, 2009; 170(11): 1386 - 1387.
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