Biobehavioral research examining the racism in relation to clinical surrogates and endpoints of Type 2 diabetes mellitus. This figure presents an example of how to examine the biobehavioral response to racism among Latinx persons and its impact on the development of prediabetes and T2DM. Solid arrows represent established associations and dashed arrows represent potential pathways. Curved lines represent correlations. Solid lines are merely descriptive. For example, insulin has a solid arrow to the clinical endpoints, hemoglobin Alc (HbAlc) and fasting plasma glucose (FPG), since it is established that insulin is the key hormone responsible for bringing glucose into cells and controlling the amount of glucose in the blood. Prediabetes is diagnosed with a HbAlc between 5.7 and 6.4% and a FPG of 100–125 mg/dL. T2DM is diagnosed with a HbA1c >6.5% and a FPG >126 mg/dL. Plasma insulin is usually monitored together with HbA1c and FPG to discern insulin resistance and distinguish between TlDM and T2DM. Both structural and institutional racism shape the economic, educational, legal, environmental, and cultural conditions in which Latinx communities are embedded. In turn, this shapes the food environments, health care access, and living conditions that allow Latinx persons to engage in health behaviors and preventive measures. Nevertheless, material and instrumental resources available to Latinx persons, families, and communities may offset the challenges present in a racist society (16, 46). Structural and institutional racism also produce the conditions and settings in which Latinx people experience interpersonal racism. Social support and personal coping can mediate or moderate the effects of interpersonal racism on physiological stress responses in both the ANS and HPAA stress systems. Here, they are displayed as mediators, assuming that this model is using longitudinal data and the temporality precedence is met (136). If assumptions are not met for a mediation analysis, protective factors against interpersonal racism have been examined as moderators [see (137)]. Acute and chronic racial stress activate immune and inflammatory responses related to β-cell production, pro-inflammatory cytokines (e.g., tumor necrosis factor-α, IL-6, IL-8), and abdominal adiposity. The biopsychosocial pathway was adapted from Hackett and Steptoe (118), Joseph and Golden (138), and Tsenkova et al. (135).