Race, Genes and Preterm Delivery: Heritability and PTD
Evidence implicating genetic factors in PTD has been summarized elsewhere. It includes the tendency of PTD to recur and familial aggregation. A prior history of PTD is one of the most powerful risk factors for future PTD. Recurrent PTD contributes to a sizable proportion of all PTDs. While risk of recurrence is consistent with a biological predisposition, it is also consistent with continued exposure to environmental risk factors, such as chronic stress or subclinical infection. For example, bacterial vaginosis (BV), subclinical endometritis, stress from poverty, or racism may predispose women to recurrent PTD due to their continued exposure.
A family history of PTD is also associated with increased risk of PTD. This holds for both white and black women. Maternal, but not paternal, intermarriage among Amish groups has been linked to PTD. Risk of recurrent PTD is less strongly associated with paternal factors. Familial clustering is suggestive of genetic effects but also consistent with shared behavioral factors between family members. Reports of greater immune responsiveness to infection or inflammation among women with a history of PTD suggest biological, though not necessarily genetically mediated, susceptibility to PTD.
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Quantitative genetic analysis of Australian twins estimated that PTD was 17% heritable in the first pregnancy and 27% overall. A Swedish twin study estimated the heritability for two proximal causes of PTD—PIH and preeclampsia—as 24% and 54%, respectively. Estimates of heritability of PTD are somewhat smaller than those for polygenic conditions, such as osteoarthritis, obesity and hypertension. However, genetic factors may be stronger for extremely PTD; women with a history of extremely PTD have a 22-fold increased risk of a subsequent PTD. In contrast, the most potent identified environmental risk factors for PTD typically show relative risks of <7.0 and more often <3.0.
However, establishing that genetics contributes to PTD by no means proves that genetic mechanisms contribute to racial disparities in PTD. Simply because a condition is heritable does not imply that population differences in that condition are attributable to genetics. Height is 90% heritable, yet environment, not genetics, caused the large difference in heights between whites and African-American slaves. Similarly, obesity is roughly 50% heritable, but the recent emergence of racial disparity in child and adolescent obesity is due to environmental, not genetic, change. Viagra Super Active
Findings from quantitative genetic analyses provide little insight regarding the impact of genetics on disparity in PTD. A study of a national sample of children and their half-siblings showed that shared environments (including similar intrauterine environments), but not fetal genes, contributed to racial disparity in birthweight and gestation length. Parental history of low birthweight (LBW) contributes to the black-white gap in LBW, although the relative risk is lower for blacks than whites. Higher household income improves birthweight only in the presence of parental LBW, suggesting a potential genetic-environmental interaction. However, genetic effects on LBW may differ from those for PTD.
