Race, Genes and Preterm Delivery
African Americans have 60% higher risk for preterm (<37 weeks gestation) delivery (PTD) birth and three times the risk for extreme (<28 weeks gestation) PTD (1.8%) as whites (0.5%)J Eighty percent of the racial disparity in neonatal mortality is attributable to PTD of infants less than 1,000 g. Traditional socioeconomic and behavioral risk factors do not fully explain racial disparity in PTD. Even second-generation, high-socioeconomic-status African-American women experience high rates of PTD. Urogenital infections, short birth intervals, among other factors, likely contribute to this disparity but do not seem to fully account for it. This unexplained gap has led to speculation that genetic factors contribute to racial disparity in PTD.
In order to examine this hypothesis, it is essential to first clarify use of the term “race.” Race is defined as a social construct that categorizes groups of people based upon self-identification, common continental ancestry and arbitrary physical characteristics, such as skin color, hair texture and facial features. False biological attributions of racial inferiority have been used to rationalize slavery and continued racial injustice. The simplistic and flawed notion that black women are inherently predisposed to PTD reinforces such racial stereotypes.
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If race has little biological basis, how could genetic factors contribute to racial disparity in any health outcome? On one hand, rates of uncommon polymorphisms (gene variants), including some related to immune modulation and drug metabolism, differ between populations with disparate, continental ancestry. Continental ancestry is associated with self-identified race.
On the other hand, differences in the frequency of these polymorphisms between continental groups are too small to establish a biological basis for race. Genetic variation is much greater within racial groups than between them and greater among persons of African ancestry than among those of European ancestry. Nonetheless, subtle variation in polymorphism frequency between groups could conceivably contribute to disparity in uncommon adverse outcomes between groups with differing continental ancestry within specific environmental contexts.
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The sickle cell gene’s association with race is purely incidental. Sickle cell trait (AS) is associated with a survival advantage in geographic regions with high prevalence of malaria. However, unlike sickle cell anemia, which results from a single-gene polymorphism, PTD presumably results from complex interactions of multiple genes and environmental factors. Thus, any contribution of genetics to disparity in PTD is likely to involve extensive interactions with environmental factors. Whether a polymorphism is favorable or deleterious may depend on past or present environmental factors (and other genes).
To address the question of the role of genes in racial disparity in PTD, a review of the literature was undertaken. Evidence was reviewed related to the heritability of PTD, contribution of environmental factors to PTD, gene-environment interactions (differential genetic effects depending on environmental exposure), physiological pathways mediating disparity in PTD and candidate polymorphisms. buy protonix online
