Medical Inspection – Health Blog

Search for candidate polymorphisms should focus on those affecting the pathways described above that differ in frequency between the white and black populations. Definitive evidence that genetic factors contribute to racial disparity in PTD requires identification of polymorphisms that: 1) differ in frequency by race among representative populations, 2) are independently associated with PTD for both blacks and/or whites, and 3) explain racial disparity in PTD in representative samples after adjustment for confounding.

The best-studied genes are single-nucleotide polymorphisms (SNPs). Table 1 summarizes findings for these polymorphisms. These include those regulating maternal inflammatory response, vascular tone, thrombosis and coagulation, stress response, and metabolic pathways.

Table 1. Genes putatively implicated in PTD-related conditions by race

A review of Table 1 seemingly shows no consistent pattern in frequency by race, but others have noted that several polymorphisms linked to proinflammatory response are more prevalent among per­sons of African ancestry. Theoretically, upregula-tion of immune response, particularly in the presence of infection, could increase risk of PTD.
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Table 1 also summarizes studies linking these polymorphisms to PTD. Few definitive conclusions can be drawn regarding the etiological significance of these polymorphisms. Findings are limited by small case-control samples involving selected racial/ethnic populations. Many findings have yet to be replicated. Interpretation is complicated by gene-environment, gene-gene and maternal-fetal genetic interactions. Moreover, the overall contribution of these polymorphisms to racial disparity in PTD has not been directly assessed through large, carefully controlled prospective studies. This is a key point. It is quite possible that differences in polymorphism frequency by race are sufficiently random so that the net overall effect of these differences on disparity in PTD is negligible.

CONCLUSION

The contribution of genetic factors to racial disparity in PTD is unproven. There is evidence that genetic factors contribute to PTD, but this does not mean that genetic factors contribute significantly to differences in rates of PTD by race. There is substantial evidence that environmental factors influence PTD through complex pathways. Many of

these factors disproportionately affect African Americans. However, inferring genetic effects by attempting to control for environmental factors that differ by race is flawed due to limitations in measurement, omitted variables and the cumulative effects of poverty and racism across the life course.

Nonetheless, there is some evidence that polymorphisms potentially related to PTD, particularly those regulating immune responsiveness, differ in frequency by race. However, PTD likely results from complex interactions between multiple maternal and fetal genes and environmental factors. It is therefore unlikely that racial difference in the frequency of any single polymorphism or contiguous group of polymorphisms (haplotypes) contribute substantially to racial disparity in PTD. However, there is emerging but preliminary evidence of gene-environment interactions for PTD that disproportionately affect African Americans. Potentially, the effects of seemingly trivial differences in gene frequency could be amplified through these gene-environmental interactions, but further study is required.
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These findings are similar to those for other polygenic conditions, including hypertension and diabetes mellitus, where despite initial reports of racial differences in candidate polymorphisms, the contribution of genetic factors to racial disparity in outcomes remains unproven. Given daunting methodological challenges and the complexity and social significance of race, a definitive answer regarding the contribution of genetics to racial disparity in PTD is unlikely soon.

Elucidation of gene-environmental interactions in racial disparity in PTD offers a potential means towards addressing this disparity. Such research is not without risks. It may divert public attention away from critical social factors implicated in PTD, such as poverty, segregation, discrimination and stress.

Furthermore, suggesting that genetic factors contribute to racial disparity in PTD may mistakenly imply that racial disparity in PTD is immutable. Moreover, given the longstanding legacy of genetic explanations for racial disparities, it is too easy to prematurely ascribe racial disparity in PTD to potentially trivial differences in polymorphisms between groups of differing continental ancestry and disparate social conditions. Such simplistic genetic explanations may inadvertently reinforce racial stereotypes of biological inferiority. Thus, it is incumbent upon researchers working in this area to distinguish between race (as a social construct) and continental ancestry, avoid overstating preliminary findings and appropriately frame their findings.

Related Posts

• Race, Genes and Preterm Delivery: Gene-Environment Interactions
• Race, Genes and Preterm Delivery: Environmental Explanations
• Race, Genes and Preterm Delivery: Heritability and PTD
• Race, Genes and Preterm Delivery