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. Author manuscript; available in PMC: 2021 Feb 1.
Published in final edited form as: Health Psychol. 2019 Nov 7;39(2):107–115. doi: 10.1037/hea0000812

Depression, Perceived Social Control, and Hypothalamic-Pituitary-Adrenal Axis Function in African-American Adults

Ezemenari M Obasi a,b, Tzu-An Chen b, Lucia Cavanagh a, B Katherine Smith a, Kristin A Wilborn a,b, Lorna H McNeill c, Lorraine R Reitzel b,d
PMCID: PMC6957753  NIHMSID: NIHMS1064482  PMID: 31697108

Abstract

Objective:

Social determinants may negatively affect health via Hypothalamic-Pituitary-Adrenal (HPA) axis dysfunction. The potential contribution of social determinants and related factors to HPA-axis functioning is important to study among African American adults, who are more likely to experience societal inequities and health disparities relative to other racial/ethnic groups. This study examined the relationship between depressive symptoms and perceived social control on HPA-axis functioning among African American adults.

Methods:

Participants (N=107; Mage=50, 79% female) were administered measures including the Center for Epidemiologic Studies–Depression and Informal (neighborhood) Social Control. Study procedures included the provision of six saliva samples for cortisol analysis (at wakeup, 30 and 90 minutes post-wakeup, 2:00 PM, 5:00 PM, and pre-bedtime). The relationship between depression and social control on the functioning of the HPA-axis were simultaneously examined within a two-level hierarchical linear model.

Results:

Variability in the Cortisol Awakening Response (CAR) was accounted for by depressive symptomatology (p = .023) and perceived social control (p = .016), whereby greater depression was associated with a blunted CAR (less awakening cortisol production) and greater perceptions of neighborhood social control with a higher CAR.

Conclusions:

Elevated depressive symptoms and low perceptions of neighborhood social control may serve as mechanisms that help to explain within-group variability in the functioning of stress physiology among African American adults. Findings enhance understanding of how social determinants may affect African Americans’ health.

Keywords: HPA axis, cortisol, social control, depression, African Americans

INTRODUCTION

African Americans suffer disproportionate rates of disease-related morbidity and mortality. When compared to European Americans, African Americans have a 41% higher mortality for stroke, 30% higher mortality for heart disease, and 25% higher mortality for cancer (CDC 2011). African Americans are also eight times more likely to be diagnosed with HIV and at 60% higher risk of developing diabetes (CDC 2011). The economic burden associated with these health disparities amounts to more than $100 billion annually (LaVeist et al. 2011). Social determinants, such as perceptions of little to no social control, can negatively affect health outcomes. Among African Americans, social inequities such as financial strain, lack of access to care, marginalization by providers, chronic poverty and neighborhood disorganization are disproportionately higher than other racial/ethnic groups (Appel et al. 2002; Downey 2013; Hartley 2004). Furthermore, these health risk-factors are generally experienced across generations with minimal perception of being under one’s control. The perceived impact of these social inequities can have a deleterious effect on the regulation of the Hypothalamic-Pituitary-Adrenal (HPA)-axis, and in turn contribute to disease vulnerability. The present study examined the relationship between depressive symptoms and perceived social control on HPA-axis functioning among a sample of African-American adults.

It is important to note that there are several studies have investigated the relationship between diurnal cortisol and global assessments of perceived or chronic stress (i.e., Obasi et al. 2015). However, there is a dearth in the amount of studies that have investigated the relationship between specific sources of stress and HPA-axis functioning with an older community sample of African American adults. Indeed, we are unaware of research that has tested the relationship between depressive symptomatology and perceived social control on HPA-axis functioning in this population. This is supported by research data finding depressive symptoms to be related to stress and immune physiology (Fagundes, Glaser, Hwang, Malarkey, & Kiecolt-Glaser 2013; Liu & Alloy 2010; Stetler & Miller 2011). Moreover, this study is novel in its investigation into the relationship that perceived social control might have as a protective factor in explaining within-group variation in HPA-axis functioning.

Physiology of Stress

When exposed to real or perceived threats in the environment, the body activates the HPA axis, which in turn initiates the release of glucocorticoids that mobilize a fight-or-flight response (Sapolsky et al. 2000). In acute conditions, activation of the HPA-axis is adaptive and enables survival in the face of threat. According to McEwen’s model of Allostatic Load (McEwen 1998), incessant exposure to stress and subsequent activation of the HPA-axis can result in wear and tear on the body, which is manifested in dysregulations of the HPA-axis. HPA-axis dysregulations can be marked by various patterns, including heightened and blunted activity, and may be influenced by adaptive capacities inherent to the individual’s experience (Del Giudice et al. 2011; McEwen 2003). Nevertheless, these dysregulations compromise allostasis (i.e., the body’s capacity to effectively recover from stressful experiences), which ultimately increases susceptibility to disease (McEwen 1998).

Cortisol is the primary hormonal marker of the HPA-axis. As a glucocorticoid produced in the adrenal cortex, it is characterized by a sharp increase within 20–40 minutes of waking (known as the Cortisol Awakening Response: CAR), followed by a gradual decline during the course of the day (Shirtcliff et al. 2012). This diurnal pattern is an important component of HPA-axis regulation and health maintenance, as it is hypothesized that high morning cortisol levels mobilize the individual for the day’s events, and low evening levels enable critical immune and tissue repair (Dallman et al. 2002). The CAR, specifically, is thought to be a reliable indicator of HPA-axis functioning. Variations in CAR have been associated with both sociodemographic factors as well as negative mental and physical health outcomes (Champaneri et al. 2013; Cohen et al. 2006; Chida & Steptoe 2009; Steptoe et al. 2003; Zeiders et al. 2014). For instance, when compared to European Americans, African-American adults exhibited higher evening cortisol and blunted CAR, with a flatter curve among those with lower levels of education (Cohen et al. 2006; Bennett et al. 2004). Because coordination of fight-or-flight responses (i.e., HPA-axis reactivity) is ultimately rooted in individual appraisals of threat, the level of perceived psychosocial distress may in fact be a more robust predictor of regulatory outcomes than objective measures of social inequities, such as income or education (McEwen 1998; Lupien et al. 2009). As such, this study investigates the relationship that perceived social control and depressive symptoms might have on HPA-axis functioning among African-American adults.

Conceptual Framework

McEwen’s concept of allostasis, maintaining stability in the context of change, characterizes people as being capable of adapting or changing to meet the demands of a changing environment or social context (McEwen 1998). As the individual is consistently exposed to their environment over time, the inherent variability may become less malleable. Investigating hormonal changes in cortisol could provide some insight into the match between our biology and social context. For example, a meta-analysis found clinical depression to be related to dysregulated basal cortisol (Stetler & Miller 2011). Moreover, there is emerging data linking a dysregulated cortisol awakening response to the development of major depressive disorder downstream (Adam et al. 2010; Vrshek-Schallhorn et al. 2013). Indeed, the chronic activation of the stress responsive systems (i.e., HPA-axis) by ongoing experiences associated with depressive symptomatology (e.g., sadness, guilt, loss of pleasure, low energy, worthlessness, negative self-talk, changes in appetite, etc.) can cause ‘wear and tear’ on regulatory systems via allostatic load. Conversely, having the capacity to exert a sense of social control (e.g., influence over stressful contextual events) could serve as a protective factor on social and psychological determinants of health. By extension, it is reasonable to hypothesize that a greater sense of perceived social control might be related to a healthy regulatory system. Ultimately, the dysregulation of the HPA-axis represents an understudied endophenotype in African American adults that could be linked to known health disparities that continue to plague this community.

Dysregulation of the HPA-axis has been linked to one’s experience of depressive symptomatology. While both hyperactive and hypoactive CAR has been linked to depression and psychological distress (Chida & Steptoe 2009; Holland et al. 2014; Knight et al. 2010; Dedovic & Ngiam 2015; DeSantis et al. 2007), it is unclear if the discordant findings are a function of chronicity – meaning depressive symptoms initially lead to a hyperactive CAR and then evolve to a more blunting effect across time – or of variability in measurement tools, analytical strategies, conceptualizations of stress (Holland et al. 2014; Hjortskov et al. 2004; Stetler & Miller, 2011; Wilcox et al. 2014) or sample characteristics. Since epidemiological data suggest that African Americans are more likely to report depressive symptoms and are less likely to receive treatment for it (CDC 2010), it is reasonable to expect untreated depressive symptoms to begin to have a ‘wear and tear’ on HPA-axis functioning across time.

While depressive symptomatology is likely related to stress-related outcomes, it is also imperative to identify and investigate potential protective factors like informal neighborhood social control. Informal social control is a dimension of social capital that refers to an individual’s perceptions of the willingness of their neighbors to intervene in the event of various potentially threatening situations (e.g., physical altercation on the sidewalk in front of “your” house) (Sampson et al.1997). Higher perceived social control has shown to attenuate the impact of neighborhood deprivation on depression (Diez Roux & Mair 2010) and physical health (Diez Roux & Mair 2010; Feldman, & Steptoe 2004). Additionally, greater reported fear of crime has been associated with poorer mental health, physical functioning and quality of life (Stafford et al. 2007). These findings suggest that social control may play a central role in mediating physiological responses to neighborhood stress. For instance, in a sample of European adults, social control was associated with greater cortisol reactivity to acute stress among women (Barrington et al. 2014). Moreover, in a study of metropolitan-dwelling American adults, individuals who reported high perceived neighborhood stress and low social support experienced a flatter diurnal cortisol curve and lower overall mean cortisol levels (Karb et al. 2012). Collectively, these findings garner support for a simultaneous investigation into within-group variation depressive symptomatology and perceived neighborhood social control might have on HPA-axis regulation in the African American community.

The Present Study

Given the clear gaps in the literature relating social determinants of health to stress physiology in African-American adults, this study sought to characterize the diurnal regulation of cortisol among a vulnerable and understudied population. The present study also aimed to identify the unique and collective relationship psychosocial factors may have on HPA-axis regulation, namely depressive symptoms and perceived social control in the neighborhood context. This study provides novelty by incorporating subjective perceptions of neighborhood social control. Moreover, this study focused its recruitment on an understudied population that is frequently underrepresented in biobehavioral research, but which bears a large burden of health related-disparities in the U.S. Based on previous research findings and allostatic load models of stress dysregulation, the following hypotheses were made: 1) The presence of depressive symptoms (risk-factor) will explain within-group variation in CAR. More specifically, higher depressive symptoms will be associated with a dysregulated HPA-axis as measured by a blunted CAR; and 2) Greater perceived social control (protective-factor) will also explain within-group variation in CAR. More specifically, greater perceived social control will not be associated with a dysregulated HPA-axis as measured by a blunted CAR.

METHODS

Participants and Procedures

Participants were recruited from a large African-American church in Houston, Texas, with over 17,000 members. Recruitment was accomplished via email describing the study whereby interested individuals could call a devoted study line for more information. Participation was not restricted to church members, and directions indicated that the recruitment materials could be forwarded to others. Individuals were eligible to participate if: 1) they were at least 18 years of age; 2) self-identified as African-American; 3) could provide valid contact information; and 4) were willing to comply with the study protocol. Data collection was completed on-site at the church, with sample size informed by an a priori power analysis. More specifically, with power of 0.8, alpha of 0.05, moderate correlation among repeated measures of 0.2, and 6 repeated measures, a sample size greater than 100 would provide adequate power to detect a small to moderate effect size (f=0.13). Following informed consent, participants were enrolled in this study and completed computerized study questionnaires. Following competition of study questionnaires, participants were introduced to a saliva collection kit. The saliva collection kit contained all the necessary materials and instructions for collecting diurnal samples of salivary cortisol. Participants were instructed to provide 6 saliva samples, using a passive drool protocol not to exceed 15 minutes, in their home on a single day using the following schedule: 1) wakeup – before getting out of bed; 2) 30 min post wakeup; 3) 90 min post wakeup; 4) 2:00 PM or an hour after lunch; 5) 5:00 PM or before dinner; and 6) immediately prior to going to sleep. Samples 1–3 were required as an assessment of the cortisol response to awakening. More specifically, sample 2 represented the cortisol awakening response (CAR). Samples 4–6 provided assessments of the diurnal down-regulation of the HPA-axis on a typical day. Participants were encouraged to collect the samples on a non-work day and instructed not to eat, drink, brush their teeth or smoke cigarettes 30 minutes prior to sample collection. The saliva collection kit also contained collection instructions and a collection diary for the purpose of modeling systematic variation (i.e., time) in our analyses. Participants were also instructed to freeze the saliva samples in the provided kit immediately upon completion. They were welcome to choose a day of convenience on which to collect the samples, based on ready access to a freezer for storage. Participants returned to the church for a second visit following saliva collection to drop off their saliva cooler and diary with study personnel. Frozen saliva samples were transported daily to the Hwemudua Addictions and Health Disparities Laboratory (HAHDL) in sealed coolers filled with freezer bricks in order to prevent a freeze-thaw cycle. Study procedures were approved by the Institutional Review Boards at the primary institution (University of Houston) and collaborating institution (University of Texas MD Anderson Cancer Center) and participants were compensated up to $100 for compliance with all study procedures.

Measures

Depressive symptoms.

Depressive symptoms were assessed via the Center for Epidemiologic Studies Depression scale (CESD). The 20-item CESD was developed to assess symptoms indicative of depression, such as restless sleep, poor appetite, feeling blue, over the last week in community, non-clinical populations (Radloff 1977). Higher scores are associated with greater depressive symptoms. The Cronbach’s alpha for the CESD in this sample was .93.

Perceived social control.

Perceived neighborhood social control was measured with a 5-item Informal Social Control (ISC) scale that asked participants to indicate on a Likert scale from very unlikely to very likely the extent to which their neighbors could be counted on to intervene in various situations including if a fight broke out in front of [the respondent’s house] of if children were showing disrespect to an adult (Sampson et al. 1997). The ISC taps into how effective informal strategies for social control and reflects the general well-being of a neighborhood setting, with higher scores indicating greater perceived informal social control in the neighborhood. This construct was included in this study as a potential protective factor. The Cronbach’s alpha for the ISC in this sample was .91.

Salivary cortisol.

All saliva samples were stored immediately in a laboratory freezer (−30°C). On the day of assay, samples were thawed and cortisol was assayed in duplicate using a well-established enzyme-linked immunosorbent assay (ELISA) kit specifically designed for use with saliva (Salimetrics, State College, PA). Samples were reanalyzed if the CV for the duplicate measurements were ≥15%. This was the case for less than 5% of the samples and the average CV was 5.46. Samples from the same individual were all assayed on the same plate. To normalize distributions, extreme values of raw cortisol were Winsorized. The production of cortisol across the day was measured using area under the cortisol curve (AUC). AUC was operationalized with respect to the last time point (as the majority has the lowest cortisol level just before the bedtime), AUC6, and was calculated using the trapezoid formula (Pruessner et al. 2003), with subtraction of last cortisol secretion. The average cortisol level (Cortisolmean) throughout the day was computed as well. These measures are considered summary parameters of the repeated measurements of cortisol production throughout the day, and allow a sensitive measure of physiological changes over time (Pruessner et al. 2003).

Analytic Strategy

The pattern of missingness was assessed to evaluate whether the missing cortisol values were “missing at random (MAR)” or “missing completely at random (MCAR)”. MCAR means the reason why the participants had missing cortisol values at some assessments is independent of other variables, and MAR is a special case of MCAR where missing cortisol values are not related to other observed cortisol values but can depend on covariates. Hierarchical linear models (HLMs), which allow for variability in the number and spacing of timepoints, were used to estimate the trajectory of cortisol throughout the day with multiple observations (i.e., saliva samples) being treated as nested within participants (n = 107). The effects of depressive symptoms and perceived social control were specifically modeled as main effects on the CAR at level 2 in order to test the proposed research hypotheses. HLM allows for the inclusion of participants with missing cortisol values if the missing pattern is MAR or MCAR. The Little’s MCAR test (Little 1988) suggested that these data were MCAR (χ2(115) = 124.39, p = 0.266; therefore, missing cortisol values were not imputed. We also leveraged additional indicators of repeated cortisol assessments (i.e., AUC6 and Cortisolmean) to provide summary scores that could be related to depressive symptoms and perceived social control.

The dependent variable consisted of six samples of salivary cortisol measured at waking (Mtime = 7:14 AM; Time since waking (TSW) = 0), 30 minutes after waking (Mtime = 7:48 AM, MTSW = 36.9 min, SD = 18.5), 90 minutes after waking (Mtime = 9:03 AM, MTSW = 123.3 min, SD = 83.0), 2:09 PM (MTSW = 440.4 min, SD = 123.3), 5:30 PM (MTSW = 636.3 min, SD = 124.2), and 7:44 PM (MTSW = 921.6 min, SD = 141.3). At level 1, two predictors of cortisol level accounted for the trajectory of cortisol throughout the day. First, self-reported time since waking (TSW; β1 TSW) was modeled in minutes and used to capture the passage of time associated with the collection of six saliva samples from waking to bedtime. Assuming a diurnal slope of cortisol throughout the day, the slope of TSW would reflect a curvilinear decrease in cortisol from waking to bedtime. However, it is likely that the participants would experience a peak cortisol response approximately 30 minutes after waking up. Therefore, we included a second variable to capture the CAR (β2 car), which was modeled using a dummy variable that was coded 1 for Sample #2 (30 min after waking) and 0 for the remaining samples. The intercept (β0) therefore represents cortisol level at baseline.

An advantage of HLM is that these predictors of level 1 cortisol functioning can become outcomes of interest using a slopes-as-outcomes approach (Snijders & Bosker 1999). Individual differences in these terms were modeled to allow for each individual to have different cortisol levels at baseline (U0); different levels of cortisol down-regulation across the day (U1); or different rises in cortisol in response to waking (U2)The equations below illustrate that depression (CESD) and social control (ISC) were were entered as main effects on CAR. Age and sex were included in the model as covariates. All the HLM analyses were conducted using HLM 7.01 (Raudenbush et al. 2013).

Level 1 (within-individual) Cortisolij = β0j + β1j (TSW) + β2j(CAR) + rij
Level 2 (between-individual) β0j = γ00 + γ01(SEX) + γ02(AGE) + U0j
β1j = γ10 + U1j
β2j = γ20 + γ21(SEX) + γ22 (AGE) + γ23(CESD) + γ24 (ISC) + U2j
where i indicates Level 1 unit (e.g., cortisol values); j indicates Level 2 unit (e.g., participant).
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Spearman correlation analyses were conducted to assess the intercorrleation among key study variables. In addition, partial Spearman rank correlation analyses were performed to assess the relation of cortisol indices for the cortisol response to awakening (i.e., AUC6, and Cortisolmean) with stressor including CESD and ISC. Because age and sex were related to the outcomes of interest, the Spearman correlation was adjusted by both of them.

RESULTS

Participant Characteristics

Participants (N = 107; 78.5% female) consisted of African-American adults between the ages of 22 and 75 (Mean= 50.08, SD = 11.15); not including 15 participants removed in the analyses due to missing (i.e., participant did not provide saliva samples, n = 8) or outlier (i.e., participant had cortisol data that was greater than 3 SD from the mean; n = 7) data. Mean scores on main variables of interest were as follows: ISC = 15.29 (SD = 6.09) and CES-D = 9.21 (SD = 9.83). See Table 1 for additional sample characteristics.

Table 1.

Participant Characteristics (N=107).

N (%) /M [SD]
Age 50.08 [11.15]
Sex
 Male 23 (21.5)
 Female 84 (78.5)
Partner Status
 Not Partnered 60 (56.1)
 Partnered 47 (43.9)
Educational Achievement
 < Bachelors 56 (52.3)
 ≥ Bachelors 51 (47.7)
Employment
 Employed Full Time 64 (59.8)
 Not Employed or Employed Full Time 43 (40.2)
Perceived Social Control (range = 5–25) 15.29 [6.09]
Depressive Symptoms (range = 0–48) 9.21 [9.83]
Waking Cortisol 0.29 [0.15]
CAR 0.10 [0.22]
AUC6 165.79 [71.34]
Cortisolmean 0.22 [0.07]
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Note: Perceived Social Control was measured using the Informal Social Control scale. Depressive Symptoms were measured via the Center for Epidemiologic Studies Depression scale. CAR = Cortisol Awakening Response. AUC6 = Area Under the Curve using the last sample as the reference point.

Sex and Age

Prior to running the primary analyses, sex and age were tested as main effects on cortisol level at baseline and the CAR. Sex (Baseline: γ01 = −0.02, t(100) = −1.01, p = .317; CAR: γ21 = −0.01, t(100) = −0.18, p = .859) and age (Baseline: γ02 = 7.06×10−4, t(100) = 1.12, p = .267; CAR: γ22 = 2.65×10−3, t(100) = 1.76, p = .082) were not a significant predictor of either outcome variable. That being said, they were entered as covariates when testing the relationship of depressive symptoms and social control on the CAR.

Depressive Symptoms and Social Control on the CAR

We tested to see if some of the variability in the CAR could be accounted for by depressive symptomatology over the past week and perceived neighborhood social control. To minimize the effect of chance, we ran one omnibus model depicted by the equations listed above. Depressive symptoms (see Figure 1; plotted one SD above and below the mean) had a significant inverse relationship with CAR (γ23 = −2.840×10−3, t(98) = −2.32, p = .023). More specifically, participants had a blunted cortisol awaking response when experiencing higher levels of depression. Furthermore, having a greater perception of social control (see Figure 2; plotted one SD above and below the mean) was positively associated with CAR (γ24 = 7.060×10−3, t(98) = 2.46, p = .016) such that the CAR was larger for those reporting residence in neighborhoods with greater informal social control. Of note, the interaction between depressive symptoms and perceived social control was not associated with CAR (γ25 = −2.33×10−5, t(420) = −0.08, p = .930). This suggests that depressive symptoms and perceived social control represented two unique constructs that were related with the CAR. Given these findings, we then investigated unique models where depressive symptoms and the perception of social control were not tested together. The relationship between depressive symptoms and CAR (γ21 = −3.405×10−3, t(101) = −2.50, p = .014), and the perception of social control and CAR (γ21 = 7.084×10−3, t(101) = 2.35, p = .021), both remained and in the same directions. Ultimately, participants experiencing higher levels of depression or a reduced perception of social control, were likely to have more blunted CAR levels after controlling for sex and age.

Figure 1.

Figure 1.

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Depiction of the association between depressive symptoms and the Cortisol Awakening Response among African-American adults (N = 107).

Note: Depressive Symptoms were measured using the Center for Epidemiologic Studies Depression (CESD) scale. Higher values of CESD indicate greater depressive symptoms. γ21 = −3.405×10–3, t(101) = −2.50, p = .014.

Figure 2.

Figure 2.

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Depiction of the association between perceived neighborhood social control and the Cortisol Awakening Response among African-American adults (N = 107).

Note: Perceived Informal Neighborhood Social Control (SC) was measured using the Informal Social Control scale. Higher values of SC indicate greater perceived informal social control. γ21 = 7.084×10−3, t(101) = 2.35, p = .021.

Cortisol Profile and Stressors

Intercorrelations between the study variables are presented in Table 2. Older participants were associated with lower CESD (r=−0.205, p=0.034). ISC was positively associated with AUC6 (r=0.222, p=0.031) and Cortisolmean (r= 0.383, p<0.001). Waking cortisol, CAR, AUC6 and Cortisolmean were significantly related to each other except the association between waking cortisol and AUC6. Partial spearman rank correlation analyses (data not shown) adjusted for age and sex showed that AUC6 and Cortisolmean were significantly positively related to ISC at similar magnitude (r=0.235, p=0.024; r=0.363, p=0.0004, respectively). That is, the greater perceived informal social control in the neighborhood, the higher cortisol index level. Also, these two cortisol indices were negatively associated with CESD, but none of the associations were significant.

Table 2.

Intercorrelations of Key Study Variables.

1 2 3 4 5 6 7 8 9 10
1. Age 1 −0.05 −0.049 0.272** −0.032 −0.205* 0.091 0.038 0.137 0.157
2. Sexa 1 0.044┼ 0.104┼ 0.051╪ −0.019╪ −0.026╪ 0.015╪ −0.12╪ −0.072╪
3. Educational Achievementb 1 −0.172┼ −0.043╪ −0.111╪ 0.002╪ 0.148╪ 0.153╪ 0.116╪
4. Employmentc 1 −0.033╪ −0.026╪ 0.183╪ 0.044╪ 0.083╪ 0.172╪
5. ISC 1 0.022 0.172 0.151 0.222* 0.383***
6. CESD 1 −0.009 −0.174 −0.093 −0.093
7. Waking Cortisol 1 −0.406*** 0.125 0.460***
8. CAR 1 0.421*** 0.377***
9. AUC6 1 0.827***
10. CortSiolmean 1
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Note: All correlation are Spearman’s correlation except as indicated with symbols ┼ (Phi coefficients) and ╪ (Point-biserial correlation).

*

p<0.05;

***

p<0.001.

a

Dummy coded, with 1=Male; 2=Female.

b

Dummy coded, with 0: < Bachelors; 1: ≥ Bachelors.

c

Dummy coded, with 0=Employed full time; 1= Not employed or employed full time. ISC = Informal Social Control. CESD = Center for Epidemiologic Studies – Depression. CAR = Cortisol Awakening Response. AUC6 = Area Under the Curve using the last sample as the reference point.

DISCUSSION

This is the first known study to concurrently investigate the effects of depressive symptomology and perceived neighborhood social control on stress physiology in African-American adults. More specifically, it was hypothesized that the negative effects of depressive symptomology would have a blunting effect on the CAR. Moreover, living in a neighborhood with greater informal social control was theorized to serve as a protective factor and not be associated with a blunted CAR. These hypotheses were supported within the present study.

The data suggested that an increase in depressive symptoms was associated with a blunted CAR. This supports our contention that African Americans who experience depressive symptomatology are likely struggling with stressors that are having a deleterious effect on the CAR. It is important to note that this finding challenges previous research that found a hyperactive CAR in a community population of depressed individuals (Bhagwagar et al. 2005) and males from a university population with clinical and subclinical depression (Pruessner et al. 2002). Differences for these findings may be accounted for by the causes and chronicity of the depression symptomology and the fact that this study only focused on exploring within-group variation in a community sample of African American adults. We were unable to find published research in this area with a comparable sample. It would make sense to see a hyperactive CAR if the precipitating stressors were acute and recent in onset. However, African Americans are disproportionately subjected to chronic experiences of stress, financial strain, poverty and neighborhood disorganization, which concomitantly provides a context for a more chronic experience of stress (Williams 1999). Indeed, previous research has shown chronic stress and an attenuated CAR to be associated with depressive symptomatology in marginalized and vulnerable populations (Pascoe & Smart Richman 2009; Mangold et al. 2011). This finding is especially concerning given the fact that a blunted CAR could affect one’s energy and motivation to get up and address the challenges of the day – thus potentially providing a physiological feedback loop to support a range of symptoms associated with depression.

In contrast to depressive symptomatology, the data independently suggested that individuals with a higher sense of perceived neighborhood social control tended to have a more robust CAR. This is consistent with previous research that found higher perceived social control to be positively related to robust cortisol reactivity to a laboratory stressor (Barrington et al. 2014), though the present study did not measure reacitivty to acute stress. Although beyond the scope of this study, it is possible that informal social control may serve as a mechanism that protects against the detrimental effects of exposure to stressors in this population. Appraisal of personal control has long been associated with the ability to cope with a problem (Folkman 1984) and could be reasonably connected to a person’s sense of agency to effectively manage stressful situations. Such associations may extend to perceptions of social control within the neighborhood as well.

While this study provides a significant contribution to the literature on stress and health, it is not without limitations. For example, this study consisted of a predominately female community sample that may not have been representative of the broader African-American population. In addition, participant recruitment originated from, and data collection occurred within, a megachurch setting. Although the majority of African-American adults attend church regularly (Newport 2010), results may not be generalizable to non-church attending or affiliated persons. However, it is important to note that the proportion of the sample that actually attended church was unknown, as this particular church functioned as a community center as well (e.g., sponsored health fairs for the broader community, etc.) and because recruitment was also accomplished by word of mouth. While participants were encouraged to collect saliva samples on one non-working day, this cannot be corroborated since this study relied on self-report data. The use of an objective assessment (i.e., MEMS cap), or the collection of saliva across multiple days, would have been cost-prohibitive. Furthermore, important covariates like substance use, medications, sleep, exercise, food consumption, and indicators of health status or other potential stressors were not collected and could have affected cortisol production. Finally, it is important to note that this study utilized a correlational research design. As a result, causal relationships between depressive symptoms and perceived social control on the CAR cannot be inferred. Future research might consider the inclusion of a more representative sample of African American adults, collection of saliva samples across multiple days, and a more comprehensive assessment battery that includes indicators of health status and exposure to stress that could have a bearing on the HPA Axis. Furthermore, it might be informative to study these constructs longitudinally in order to better understand the directionality of the relationships investigated in this study.

In summary, the current study characterizes the diurnal regulation of cortisol among a sample of African-American adults, who are understudied in stress physiology research but who are of particular interest given the potential for increased risk of individual and contextual stressors that influence HPA-axis functioning relative to European-American counterparts (Williams 1999). Results highlight the unique and collective association of psychosocial contributors to HPA-axis dysregulation and suggest that elevated depressive symptoms and low perceived neighborhood social control, may serve as mechanisms that help to explain within-group variability in the functioning of stress physiology among African-American adults. This is consistent with McEwen’s allostatic load model while enhancing our understanding of how social determinants may affect African Americans’ health in the context of perceived neighborhood social control and depressive symptomology.

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