Racial discrimination, educational attainment, and biological dysregulation among midlife African American women

Highlights

• There was a non-linear association between discrimination and allostatic load.

• The association between discrimination and allostatic load varied by education.

• A U-shaped relationship emerged among those with lower education.

• High discrimination had a buffering effect among those with higher education.

• Associations were found for allostatic load and in system-specific analyses.

Abstract

Objective

To examine the association between self-reported racial discrimination and allostatic load, and whether the association differs by socioeconomic position.

Methods

We recruited a purposive cross-section of midlife (ages 30–50) African American women residing in four San Francisco Bay area counties (n = 208). Racial discrimination was measured using the Experience of Discrimination scale. Allostatic load was measured as a composite of 15 biomarkers assessing cardiometabolic, neuroendocrine, and inflammatory activity. We calculated four composite measures of allostatic load and three system-specific measures of biological dysregulation. Multivariable regression was used to examine associations, while adjusting for relevant confounders.

Results

In the high education group, reporting low (b = −1.09, P = .02, 95% CI = −1.99, −0.18) and very high (b = −1.88, P = .003, 95% CI = −3.11, −0.65) discrimination was associated with lower allostatic load (reference=moderate). Among those with lower education, reporting low (b = 2.05, P = .008, 95% CI = 0.55,3.56) discrimination was associated with higher allostatic load. Similar but less consistent associations were found for poverty status. Associations were similar for cardiometabolic functioning, but not for neuroendocrine or inflammatory activity.

Conclusions

Racial discrimination may be an important predictor of cumulative physiologic dysregulation. Factors associated with educational attainment may mitigate this association for African American women and other groups experiencing chronic social stress.

Introduction

In the U.S., experiences of social stress associated with race and gender intersect to perpetuate and exacerbate poor health outcomes for women of color, particularly African Americans (Geronimus, 1996; Jackson, 2005; Jackson et al., 2001). African American (AA) women are disproportionately burdened by the simultaneous dysregulation of multiple physiologic systems (Chyu and Upchurch, 2011; Duru et al., 2012; Geronimus et al., 2006; Upchurch et al., 2015), commonly referred to as allostatic load or cumulative biological risk. Allostatic load has been associated with numerous negative health outcomes including decreased cognitive and physical function, heart disease, stroke, diabetes, and mortality (Beckie, 2012; Borrell et al., 2010; Habib et al., 2001; McEwen, 1998; Seeman et al., 1997). The association between social stress and cumulative biological risk is now well accepted. Though early studies focused on age-related changes in physiologic function (Crimmins et al., 2003; Karlamangla et al., 2002; Seeman et al., 2001, 1997), more recent studies have demonstrated associations with explicit forms of social stress that appear to be unrelated to chronological age. In particular, numerous studies show an association between chronic (i.e., ongoing or repeated) social stress and allostatic load, which may help explain the heightened risk of poor health among AA women (Beckie, 2012; Borrell et al., 2010; Carlson and Chamberlain, 2005; Habib et al., 2001; Kessler et al., 1999; McEwen, 1998; Seeman et al., 1997).

Chronic stress plays a critical role in the progression of multiple disease states via prolonged activation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympatho-adrenal-medullary (SAM) axis, the body’s primary stress response systems (Borrell et al., 2010; Karlamangla et al., 2002; McEwen, 1998; Seeman et al., 1997). Activation of these neuroendocrine systems results in a cascade of physiologic events including the secretion of pro-inflammatory cytokines, catecholamines, and acute phase proteins, all of which have deleterious effects on the body with sustained elevation (Karlamangla et al., 2002; McEwen, 1998; Seeman et al., 1997). When stress exposure is chronic, the negative feedback loops that typically shut-off the neuroendocrine stress response are dysregulated resulting in a chronic pro-inflammatory state (Karlamangla et al., 2002; Seeman et al., 1997), heightened and extended autonomic reactivity (Karlamangla et al., 2002; McEwen, 1998; Seeman et al., 1997), and a variety of other impairments (e.g., tissue damage, receptor desensitization) (Crimmins et al., 2003; McEwen, 1998; Miller et al., 2002). Although helpful in the short term (i.e., when responding to more mild and transient forms of stress) chronic hyperactivity of various systems can compromise the body’s ability to regulate the internal physiologic environment resulting in cumulative biological dysregulation (Karlamangla et al., 2002; McEwen, 1998; Seeman et al., 1997).

Perception of mistreatment has been associated with pronounced and sustained arousal across a number of physiologic systems including the HPA axis, autonomic nervous system, immune, metabolic and cardiovascular systems (Adam et al., 2015; Busse et al., 2017; Cooper et al., 2009; Cunningham et al., 2012; Dickerson et al., 2009; Friedman et al., 2009; Fuller-Rowell et al., 2012; Hill et al., 2017; Hoggard et al., 2015; Huynh et al., 2017; Lewis et al., 2010; Mays et al., 2007; Mendes et al., 2008; Myers, 2009; Wagner et al., 2015; Zeiders et al., 2014). Studies have also provided evidence of a more buffered stress response among those reporting chronic unfair treatment. For example, numerous studies have shown associations between reports of unfair treatment and a blunted cortisol response as well as overall poor HPA flexibility (e.g., flatter diurnal slope), especially among AAs (Adam et al., 2015; Busse et al., 2017; Fuller-Rowell et al., 2012; Hill et al., 2017; Huynh et al., 2016; Skinner et al., 2011; Zeiders et al., 2014). This heightened dysregulation observed among AAs may be at least partially explained by their histories of past exposures and their perception of the potential impact of these events (Zeiders et al., 2014)—getting hired and work settings, more generally, are among the most commonly reported sources of discrimination among AAs (Brondolo et al., 2011; Karlsen and Nazroo, 2002; Krieger et al., 2011).

Several studies show that the majority of AA women report racial discrimination as a unique and chronic social stressor (Cunningham et al., 2012; Fuller-Rowell et al., 2012; Krieger and Sidney, 1996; Lewis et al., 2010), evoking negative affective states that have been linked with biological alterations characteristic of the stress response (Nuru-Jeter et al., 2009; Tomfohr et al., 2016). Moreover, it is generally widely accepted that the nature of the threat matters for evoking particular stress responses (Dickerson et al., 2009; Kemeny, 2003; Miller et al., 2007; Plummer and Slane, 1996). Social evaluative threat, such as that experienced with racial discrimination, is a particular form of stress that studies show is associated with heightened inflammation via dysregulation of both the HPA and SAM axes (Kemeny, 2003). A strong body of research has shown adverse effects of discrimination on mental health outcomes including depression, anxiety, psychological distress, hypervigilance, and various health behaviors (Borrell et al., 2006; Brown et al., 2000; Landrine and Klonoff, 1996; Lorenzo-Blanco et al., 2011; Robinette et al., 2016; Sellers et al., 2006; Tomfohr et al., 2016; Williams and Mohammed, 2013; Williams et al., 1997), all of which have been linked with subsequent poor physical health outcomes via neurobiological stress responses (Brown et al., 2000; Chae et al., 2012b; Gee et al., 2006; Pieterse et al., 2012). Those neurobiological pathways include, among others, impaired hippocampal learning and activity, which has deleterious effects on HPA functioning; a hyperactive amygdala, which compromises memory and the body’s ability to predict threat and prepare the body for adaptive regulation (i.e., allostasis); and overall reduced neuroplasticity which promotes wear and tear due to the inability of the brain to respond adaptively to both anticipated and unanticipated stressors (Berger and Sarnyai, 2015; Carlson and Chamberlain, 2005; Fossion and Linkowski, 2007; Logan and Barksdale, 2008; Lucas et al., 2016; Lupien et al., 2015; McEwen, 2003; McEwen et al., 2015; Ziabreva et al., 2003). One of the amygdala’s primary roles is to regulate the fight or flight response. Notably, studies have shown enhanced amygdala activity—especially the left amygdala, which is associated with recall of events—among women than among men, suggesting that women may be more vulnerable to emotionally threatening events (Hamann, 2005).

Evidence suggests that rather than having uniform effects on physiology, stressors are met with integrated cognitive, affective, and behavioral responses that determine the psychobiological response to stress (i.e., integrated specificity) (Kemeny, 2003). In particular, studies suggest that how people appraise and cope with specific stressors differs by socioeconomic position (SEP). Lower socioeconomic groups are more likely to minimize attributions to discrimination and internalize their discrimination experiences (Crocker et al., 1991), both of which have been associated with poorer health (Chae et al., 2012a). Lower socioeconomic groups also report greater stress exposure, and hence may face depletion of health-protective resources and a lower sense of control over stressful life situations, increasing the likelihood of appraising stressors as threatening (Gallo and Matthews, 2003).

Geronimus proposed the “weathering hypothesis” to explain the accelerated physiologic deterioration experienced among black women due to the repeated stress associated with cumulative social disadvantage, including chronic experiences of racial discrimination (Geronimus, 1996; Geronimus et al., 2006). Several studies show heightened allostatic load among AA women relative to other race-gender groups (Chyu and Upchurch, 2011; Duru et al., 2012; Geronimus et al., 2006; Upchurch et al., 2015), which may help explain their elevated risk of poor health especially during midlife where differences are most pronounced (Borrell et al., 2010; Chyu and Upchurch, 2011). However, no studies to our knowledge have examined whether racial discrimination may account for the higher levels of allostatic load observed among this group. The purpose of this study was two-fold: To (1) examine the association between level of reported racial discrimination and allostatic load among a community-sample of midlife AA women, and (2) assess whether two commonly used indicators of SEP (i.e., educational attainment and poverty status) modify this association. We hypothesized that the association between racial discrimination and allostatic load would be greatest among lower socioeconomic groups.