The impact of devaluing Women of Color: stress, reproduction, and justice.

This commentary is in response to the Call for Papers put forth by the Critical Midwifery Studies Collective (June 2022). We argue that due to a long and ongoing history of gendered racism, Women of Color are devalued in U.S. society. Devaluing Women of Color leads maternal healthcare practitioners to miss and even dismiss distress in Women of Color. The result is systematic underdiagnosis, undertreatment, and the delivery of poorer care to Women of Color, which negatively affects reproductive outcomes generally and birth outcomes specifically. These compounding effects exacerbate distress in Women of Color leading to greater distress. Stress physiology is ancient and intricately interwoven with healthy pregnancy physiology, and this relationship is a highly conserved reproductive strategy. Thus, where there is disproportionate or excess stress (distress), unsurprisingly, there are disproportionate and excess rates of poorer reproductive outcomes. Stress physiology and reproductive physiology collide with social injustices (i.e., racism, discrimination, and anti-Blackness), resulting in pernicious racialized maternal health disparities. Accordingly, the interplay between stress and reproduction is a key social justice issue and an important site for theoretical inquiry and birth equity efforts. Fortunately, both stress physiology and pregnancy physiology are highly plastic-responsive to the benefits of increased social support and respectful maternity care. Justice means valuing Women of Color and valuing their right to have a healthy, respected, and safe life.

Why Causation Matters: Rethinking "Race" as a Risk Factor.

Although it is tempting to construe the correlation between Black "race" and higher rates of preterm birth as causal, this logic is flawed. Worse, the continued use of Black "race" as a risk factor for preterm birth is actively harmful. Using Black "race" as a risk factor suggests a causal relationship that does not exist and, critically, obscures what actually causes Black patients to be more vulnerable to poorer maternal and infant outcomes: anti-Black racism. Failing to name anti-Black racism as the root cause of Black patients' vulnerability conceals key pathways and tempts us to construe Black "race" as immutably related to higher rates of preterm birth. The result is that we overlook two highly treatable pathways-chronic stress and implicit bias-through which anti-Black racism negatively contributes to birth. Thus, clinicians may underuse important tools to reduce stress from racism and discrimination while missing opportunities to address implicit bias within their practices and institutions. Fortunately, researchers, physicians, clinicians, and medical staff can positively affect Black maternal and infant health by shifting our causal paradigm. By eliminating the use of Black "race" as a risk factor and naming anti-Black racism as the root cause of Black patients' vulnerability, we can practice anti-racist maternity care and take a critical step toward achieving birth equity.

Understanding and Reducing Persistent Racial Disparities in Preterm Birth: a Model of Stress-Induced Developmental Plasticity.

Preterm birth is a leading cause of neonatal mortality and is characterized by substantial racial disparities in the US. Despite efforts to reduce preterm birth, rates have risen and racial disparities persist. Maternal stress is a risk factor for preterm birth; however, often, it is treated as a secondary variable rather than a primary target for intervention. Stress is known to affect several biological processes leading to downstream sequelae. Here, we present a model of stress-induced developmental plasticity where maternal stress is a key environmental cue impacting the length of gestation and therefore a primary target for intervention. Black women experience disproportionate and unique maternal stressors related to perceived racism and discrimination. It is therefore not surprising that Black women have disproportionate rates of preterm birth. The downstream effects of racism on preterm birth pathophysiology may reflect an appropriate response to stressors through the highly conserved maternal-fetal-placental neuroendocrine stress axis. This environmentally sensitive system mediates both maternal stress and the timing of birth and is a mechanism by which developmental plasticity occurs. Fortunately, stress does not appear to be an all-or-none variable. Evidence suggests that developmental plasticity is dynamic, functioning on a continuum. Therefore, simple, stress-reducing interventions that support pregnant women may tangibly reduce rates of preterm birth and improve birth outcomes for all women, particularly Black women.

A Nested Case-Control Study of Allopregnanolone and Preterm Birth in the Healthy Start Cohort.

Context: Chronic stress is a risk factor for preterm birth; however, objective measures of stress in pregnancy are limited. Maternal stress biomarkers may fill this gap. Steroid hormones and neurosteroids such as allopregnanolone (ALLO) play important roles in stress physiology and pregnancy maintenance and therefore may be promising for preterm birth prediction. Objective: We evaluated maternal serum ALLO, progesterone, cortisol, cortisone, pregnanolone, and epipregnanolone twice in gestation to evaluate associations with preterm birth. Methods: We performed a nested case-control study using biobanked fasting serum samples from the Healthy Start prebirth cohort. We included healthy women with a singleton pregnancy and matched preterm cases with term controls (1:1; N = 27 per group). We used a new HPLC-tandem mass spectrometry assay to quantify ALLO and five related steroids. We used ANOVA, Fisher exact, χ2, t test, and linear and logistic regression as statistical tests. Results: Maternal serum ALLO did not associate with preterm birth nor differ between groups. Mean cortisol levels were significantly higher in the preterm group early in pregnancy (13w0d-18w0d; P < 0.05) and higher early pregnancy cortisol associated with increased odds of preterm birth (at 13w0d; odds ratio, 1.007; 95% CI, 1.0002-1.014). Progesterone, cortisone, pregnanolone, and epipregnanolone did not associate with preterm birth. Conclusion: The findings from our pilot study suggest potential utility of cortisol as a maternal serum biomarker for preterm birth risk assessment in early pregnancy. Further evaluation using larger cohorts and additional gestational timepoints for ALLO and the other analytes may be informative.