BACKGROUND: Fundamental cause theory posits that social conditions strongly influence the risk of health risks. This study identifies risk mechanisms that social conditions associated with socioeconomic status (SES) and race/ethnicity shape in the production of colorectal cancer (CRC) mortality. METHODS: Two large datasets in the United States examining behavioral and medical preventive factors (N = 4.63-million people) were merged with population-level mortality data observing 761,100 CRC deaths among 3.31-billion person-years of observation to examine trends in CRC mortality from 1999-2012. Analyses examined the changing role of medical preventions and health behaviors in catalyzing SES and racial/ethnic inequalities in CRC mortality. RESULTS: Lower SES as well as Black, Hispanic, Asian/Pacific Islander, and Native American race/ethnicity were associated with decreased access to age-appropriate screening and/or increased prevalence of behavioral risk factors. Analyses further revealed that SES and racial/ethnic inequalities were partially determined by differences in engagement in two preventive factors: use of colonoscopy, and participation in physical activity. DISCUSSION: Social inequalities were not completely determined by behavioral risk factors. Nevertheless, a more equitable distribution of preventive medicines has the potential to reduce both the risk of, and social inequalities in, CRC mortality.

PURPOSE: Children of mothers with prenatal depression have elevated risk for depression later in life. Pregnant women are hesitant to use antidepressants due to fear of adverse fetal effects. To inform prevention, this study examined associations between maternal prenatal depression and antidepressant use, and adolescent depressive symptoms and suicidality. PATIENTS AND METHODS: Prospective data from 74,695 mother-adolescent dyads from the Kaiser Permanente Northern California integrated healthcare delivery system were used. Three prenatal exposure groups were examined: maternal depression and antidepressants (Med); depression and no antidepressants (No-Med); neither depression nor antidepressants (NDNM). Adolescent depressive symptoms (Patient Health Questionnaire-2 score ≥3) and suicidality were assessed for 12- to 18-year-olds. Associations were analyzed using mixed effects logistic regression, adjusted for confounders. RESULTS: Maternal prenatal depression was associated with higher odds of adolescent depressive symptoms (Med odds ratio [OR]: 1.50, 95% confidence interval [CI]: 1.23-1.84; No-Med OR: 1.59, CI: 1.34-1.88) and suicidality (Med OR: 2.36, CI: 1.67-3.34; No-Med OR: 1.54, CI: 1.10-2.14) compared to no prenatal depression (NDNM). Adolescents exposed to prenatal depression and antidepressants were not at greater odds of depressive symptoms (Med OR: 0.95, CI: 0.74-1.21) compared to those not exposed to antidepressants (No-Med). However, they showed non-significant but greater odds of suicidality (Med OR: 1.54, CI: 0.99-2.39). CONCLUSION: Our findings suggest that maternal prenatal depression is associated with adolescent depressive symptoms and suicidality, and that exposure to antidepressants in utero does not increase risk of depressive symptoms, specifically. While not statistically significant, the increased odds of suicidality among adolescents exposed to antidepressants suggest a possible association; however, further investigation is needed. After replication, the findings of this study may inform shared clinical decision-making when considering options regarding antidepressant use for the treatment of maternal prenatal depression.

PURPOSE: Early puberty is associated with adverse health outcomes over the life course, and Black and Hispanic girls experience puberty earlier than girls of other racial/ethnic backgrounds. Neighborhood racial and economic privilege may contribute to these disparities by conferring differential exposure to mechanisms (e.g., stress, obesity, endocrine disruptors) underlying early puberty. We examined associations between neighborhood privilege, measured by the Index of Concentration at the Extremes (ICE), and age at pubic hair onset (pubarche) and breast development onset (thelarche) in a large multiethnic cohort. METHODS: A cohort of 46,299 girls born 2005-2011 at Kaiser Permanente Northern California medical facilities were followed until 2021. Pubertal development was assessed routinely by pediatricians using the Sexual Maturity Rating scale. ICE quintiles for race/ethnicity, income, and income + race/ethnicity were calculated using American Community Survey 2010 5-year estimates and linked to census tract at birth. We fit multilevel Weibull regression models accommodating left, right, and interval censoring for all analyses. RESULTS: ICE measures were monotonically associated with pubertal onset, with the strongest associations observed for ICE-race/ethnicity. Adjusting for maternal education, age at delivery, and parity, girls from the least versus most privileged ICE-race/ethnicity quintiles were at increased risk for earlier pubarche (hazard ratio: 1.30, 95% confidence interval: 1.21, 1.38) and thelarche (hazard ratio: 1.45, 95% confidence interval: 1.36, 1.54). These associations remained significant after adjusting for girls race/ethnicity and childhood body mass index. Additionally, adjustment for ICE partially attenuated Black-White and Hispanic-White disparities in pubertal onset. DISCUSSION: Neighborhood privilege may contribute to pubertal timing and related disparities.

In 2017-2019, the March of Dimes convened a workgroup with biomedical, clinical, and epidemiologic expertise to review knowledge of the causes of the persistent Black-White disparity in preterm birth (PTB). Multiple databases were searched to identify hypothesized causes examined in peer-reviewed literature, 33 hypothesized causes were reviewed for whether they plausibly affect PTB and either occur more/less frequently and/or have a larger/smaller effect size among Black women vs. White women. While definitive proof is lacking for most potential causes, most are biologically plausible. No single downstream or midstream factor explains the disparity or its social patterning, however, many likely play limited roles, e.g., while genetic factors likely contribute to PTB, they explain at most a small fraction of the disparity. Research links most hypothesized midstream causes, including socioeconomic factors and stress, with the disparity through their influence on the hypothesized downstream factors. Socioeconomic factors alone cannot explain the disparitys social patterning. Chronic stress could affect PTB through neuroendocrine and immune mechanisms leading to inflammation and immune dysfunction, stress could alter a womans microbiota, immune response to infection, chronic disease risks, and behaviors, and trigger epigenetic changes influencing PTB risk. As an upstream factor, racism in multiple forms has repeatedly been linked with the plausible midstream/downstream factors, including socioeconomic disadvantage, stress, and toxic exposures. Racism is the only factor identified that directly or indirectly could explain the racial disparities in the plausible midstream/downstream causes and the observed social patterning. Historical and contemporary systemic racism can explain the racial disparities in socioeconomic opportunities that differentially expose African Americans to lifelong financial stress and associated health-harming conditions. Segregation places Black women in stressful surroundings and exposes them to environmental hazards. Race-based discriminatory treatment is a pervasive stressor for Black women of all socioeconomic levels, considering both incidents and the constant vigilance needed to prepare oneself for potential incidents. Racism is a highly plausible, major upstream contributor to the Black-White disparity in PTB through multiple pathways and biological mechanisms. While much is unknown, existing knowledge and core values (equity, justice) support addressing racism in efforts to eliminate the racial disparity in PTB.