Figure 1.

Structural, institutional, and interpersonal racism's effects on biological mediators, surrogate endpoints, and clinical endpoints. This figure demonstrates how structural and institutional racism shape the context in which interpersonal racism occurs. Individual differences are shaped by structural racism, as the meanings for phenotypes in relation to white supremacy, cultural representations of race, racism, and Latinidad are shaped by the structure. Moreover, Latinx life chances, such as their educational attainment and health status, are shaped by the structure. Individual differences in phenotypic features, immigration status, generational status (e.g., first generation), socioeconomic status, language use (indigenous, Spanish, etc.), family history of disease, and accent also shape the ways that structural and institutional racism form experience of interpersonal racism for diverse Latinx persons. Individual differences also influence experience of interpersonal racism from experience. For example, lighter-skinned Latinx person without an accent may not experience interpersonal racism as intensely as a darker-skinned Latinx person. Individual differences, such as family history of disease also play a moderating role on biological mediators, biological surrogates, and clinical endpoints. Dependent on the context and outcomes of interest, these individual differences can directly or indirectly impact the discriminatory experience a Latinx person faces, as well as moderate the link between racism and clinical endpoints. Acute and chronic stress emanating from (a) cultural, environment, and economic deprivation resulting from structural and institutional racism, and (b) experience of interpersonal racism have physiological effects on the body, which manifest as biological mediators [e.g., HPA axis, ANS; see page. 12 of the article and (104)] and surrogate endpoints (e.g., metabolic indices). Over time, as a Latinx child becomes older or an immigrant lives longer in their host society, racial chronic stress can lead to adverse health outcomes and their subsequent clinical endpoints. Protective factors such as familial (e.g., parent-child relationships, social support), race-ethnicity (e.g., identity, cultural orientation, ethnic-racial socialization), and psychosocial and material factors (e.g., coping strategies, health care access), may buffer the impact of structural and institutional racism on biological mediators, which may decrease the likelihood of the development of surrogate endpoints and subsequent subjective (e.g., self-reported depression symptoms) and/or objective (e.g., Type II diabetes) clinical endpoints. The line at the bottom represents time—acute (moments of interpersonal racism) vs. chronic racial stress through ones life course. The institutions capture under structural racism were adapted from Bailey et al. (46) and the biological mediators, surrogate and clinical endpoints were adopted from Robles et al. (104).