in the process of allostasis, or maintaining stability during times of change [69]. However, when these stress hormones are not turned off when not needed, are overused, or are not turned on when needed, allostatic load ensues, a wear and tear on the body and the brain that is evident in major depressive illness [70].
Individuals of low socioeconomic status (SES) and racial/ethnic minorities (especially Blacks, Latinos, and American Indians/Alaska Natives) usually live and work in environments with limited material and social resources and increased probability of exposure to threats, and thus report higher levels of stress than high‐SES and White individuals [68]. Moreover, racial and ethnic minorities have a greater likelihood of being exposed to discrimination and discrimination‐related stressors, threats to safety and financial security, violence, and barriers to occupational advancement across their life course than Whites [71]. In fact, WHO has deemed chronic stress as one of the main social determinants of health inequities [68]. The consistent adverse exposures that racial and ethnic minorities experience starting as early as the prenatal period and throughout their adult lives result in the accumulation of chronic stress; this repeated adaptation to stressors and overuse of the stress response systems results in cumulative “wear and tear” or physiological deterioration that contributes to allostatic load, the chronic conditions or diseases caused by persistent allostasis [6]. Depression is one of the chronic diseases whose development has been shown to be associated with disturbance of allostasis and inflammatory activation of the immune system [72]. For example, the HPA axis plays a key role in mediating the relationship between stress and depression through the excessive production of glucocorticoids [73]. Over time, prolonged exposure to adversity and excessive levels of glucocorticoids may have negative effects on areas of the developing brain that pertain to depression [74]. A number of studies have shown an association between elevated allostatic load and depression [75–77]. Moreover, a case control study showed that the effects of childhood physical abuse on adult depression were mediated by allostatic load [78]. Given that racial/ethnic minorities may experience more adversity and stressful circumstances than Whites throughout their life course and thus accumulate higher allostatic load, one would expect that they experience higher prevalence of chronic conditions, including MDDs. However, while racial and ethnic disparities in many physical illnesses have been clearly established, the disparities in depression prevalence present a more complex picture. For example, data (2013–2016) from the National Health and Nutrition Examination Survey (NHANES) show no statistically significant differences in depression prevalence for Hispanic, non‐Hispanic White, and non‐Hispanic Black adults, yet lower depression prevalence for Asian adults [79]. Earlier national studies showed lower rates of lifetime prevalence of depression and lower lifetime risk for depression among Latinos, Blacks, Asian, and Pacific Islanders compared to Whites, and higher rates of lifetime prevalence and risk for American Indians/Alaska Natives [70]. However, compared to Whites, Blacks and Latinos experience higher rates of dysthymia, a persistent depressive disorder characterized by chronic negative mood, and are more likely to characterize their own depressive symptoms as severe [80, 81]. Moreover, once present, depression has been shown to follow a chronic and persistent pattern among Blacks [82]. In addition, the consequences of depression have been shown to be worse and more disabling in Blacks compared to Whites, including lower quality of life, higher severity of symptoms when depression is present, and lower rates of treatment [83]. The underlying assumptions about the rates of depression in racial/ethnic minorities, as established in earlier national studies, coupled with physician–patient communication problems, may lead to discrimination in the detection and diagnosis of depression among minorities. For example, in two mental healthcare studies, clinicians responded with less alacrity to variation in depression severity in minority patients compared to White patients [84]. Moreover, two other studies found that Hispanics and Blacks were less frequently given depression diagnoses than Whites [85].
Given that culture can influence the experience of depression and how patients communicate their symptoms, diagnosis recommendations for depression specific to Latinos state that a somatic presentation pattern of depression is more common in this minority group [83]. Similarly, diagnosis recommendations for Blacks state that somatic and neurovegetative symptoms are more common in this group than mood or cognitive symptoms of depression [86]. These cultural differences may be playing a role in underdiagnosing MDD among racial/ethnic minorities. Interestingly, the literature consistently finds lower lifetime risk for depression among immigrants than the US‐born population, pointing to a potential role of environmental factors and stressors specific to the US context and culture [87]. For example, using data from the Collaborative Psychiatric Epidemiology Surveys, one study examined American‐born and foreign‐born Blacks, Hispanics, Asians, and Afro‐Caribbeans, as well as American‐born Whites and found that immigrants had 37% lower odds of lifetime MDD than those who were American‐born and that foreign‐born Afro‐Carribeans and foreign‐born Asians had the lowest rates of lifetime depression [88]. In addition, some studies point to lower allostatic load among immigrants compared to US‐born racial/ethnic minorities. For instance, one study that used the 2001–2010 NHANES data found a health advantage for foreign‐born Blacks in terms of allostatic load as compared to US‐born Blacks [89]. Two other studies found lower allostatic load among foreign‐born Mexican immigrants compared to US‐born Mexicans [90, 91].
Studies that examine allostatic load as a mediator of racial/ethnic disparities in depression prevalence have shown mixed findings. For example, a study by Rodriquez et al. that used 2005–2012 NHANES data on individuals aged 40–79 years showed that while African Americans and Latinos had higher levels of allostatic load and higher rates of depressive disorder than Whites, there was no association between allostatic load and depressive disorder in either racial/ethnic group [92]. Another study that used 2005–2010 NHANES data on Black and White adults aged 18–64 found that the relationship between allostatic biomarkers and depression varied with gendered race, such that different biomarkers were associated with depression among Black men, Black women, White men, and White women [93]. An Australian study that examined the relationship of two indices of sustained stress, cortisol, and allostatic load with depressive symptoms in Australian Aboriginal and Torres Strait Islander populations found that neither of these two hypothesized mediators were related to depressive symptoms [94]. A review article on 58 studies of allostatic load, health, and health disparities highlighted the heterogeneity in the operationalization of allostatic load and the measurement of its biomarkers, which makes it difficult to compare different studies in this area of research [95]. It also highlighted the importance of moving beyond the simple count‐based index to more complex scoring methods for creating allostatic indices, such as recursive partitioning, canonical correlation analyses, and Grade of Membership (GOM) multivariate methods.
The field of racial/ethnic disparities in depression prevalence still has many unanswered questions. Underdiagnosing depression in racial/ethnic minorities by the healthcare system and cultural differences in experiences of depression may provide some explanations as to why current depression prevalence rates in racial/ethnic minorities are not in line with assumptions of the “weathering hypothesis.” However, studying mediators of the association between stress and depression using the concept of allostatic load shows promise in clarifying the mechanisms through which early life adversity and chronic exposure to stress may affect depression outcomes in different racial/ethnic groups. In addition, future research should examine mechanisms of resilience in immigrant versus US‐born populations given the consistent finding of lower depression prevalence among immigrants. Moreover, research on allostatic load and depression in racial/ethnic minorities may gain from a more unified approach to operationalizing allostatic load and measurement of its biomarkers to enhance comparability of findings. Finally, a focus on identifying key developmental periods in the life course to target the antecedents of allostatic load, in addition to delineating key areas of vulnerability and resilience, may yield effective interventions to decrease depression rates among vulnerable populations.
2.8 Summary
In this chapter, we outline major biological pathways through which environmental, behavioral, and social exposures influence health. We summarize the mechanisms through which disparate exposures to societal inequities and inequalities are manifested in the form of health disparities. The
