Racial differences in links between perceived discrimination, depressive symptoms, and ambulatory working memory.

OBJECTIVES: Perceived discrimination is associated with racial cognitive health disparities. Links between discrimination and cognitive performance, like working memory, in everyday settings (i.e. ambulatory performance) require investigation. Depressive symptoms may be a mechanism through which discrimination relates to ambulatory working memory. METHOD: Discrimination, retrospective and momentary depressive symptoms/mood, and aggregated and momentary working memory performance among older Black and White adults were examined within the Einstein Aging Study. RESULTS: Racially stratified analyses revealed that discrimination did not relate to Black or White adults' ambulatory working memory. Among Black adults, however, more frequent discrimination was associated with greater retrospectively reported depressive symptoms, which related to more working memory errors across two weeks (indirect effect p < 0.05). This path was not significant among White adults. Links between discrimination and momentary working memory were not explained by momentary reports of depressed mood for Black or White adults. CONCLUSION: Depressive symptoms may play an important role in the link between discrimination and ambulatory working memory among Black adults across extended measurements, but not at the momentary level. Future research should address ambulatory cognition and momentary reports of discrimination and depression to better understand how to minimize cognitive health disparities associated with discrimination.

Neighborhood racial composition and experiences of racial discrimination: Associations with cytokines during pregnancy among African American women.

Background: Preterm birth rates are consistently higher in African American (AA) pregnancies compared to White pregnancies in the United States. Neighborhood racial composition, experiences of racial discrimination, and systemic inflammation are factors that have been associated with preterm birth and other adverse pregnancy outcomes that may account for these disparities. Here, we investigated whether perceived neighborhood racial composition and experiences of discrimination were predictive of cytokine levels during pregnancy among AA individuals. Methods: 545 AA individuals completed surveys and had blood samples collected at prenatal clinics in the Midwest at three timepoints (8-18,19-29, and 30-36 weeks gestation) throughout pregnancy. Pro-inflammatory [interferon (IFN)-γ, interleukin (IL)-6, IL-8, tumor necrosis factor (TNF)-α, macrophage migration inhibitory factor (MIF)] and anti-inflammatory cytokines (IL-10) were quantified. Multivariate and multilevel models were used to examine associations of perceived neighborhood racial composition and experiences of racial discrimination with cytokine levels, controlling for relevant covariates. Results: Perceived neighborhood racial composition was significantly associated with MIF at 30-36 weeks gestation in multivariate regression (p < 0.001). Living in neighborhoods with more compared to fewer White people was predictive of higher levels of MIF (b = 0.599, SE = 0.12, p < 0.001). Experiences of discrimination were also associated with higher levels of MIF (ß = 0.141, SE = 0.07, p = 0.036). Neither predictor was associated with other cytokines. Follow-up analyses revealed that neighborhood racial composition was also predictive of higher MIF levels at 8-18 weeks gestation (p = 0.02) and at 19-29 weeks gestation (p = 0.04). Conclusions: Living in neighborhoods with more White individuals and having more lifetime experiences of racial discrimination were positively related to levels of the pro-inflammatory cytokine, MIF, among pregnant AA individuals. MIF's known positive relationships with chronic stress and preterm birth suggest that these elevations in MIF may have negative health consequences. Future studies should explore whether MIF serves as a pathway between neighborhood racial composition or experiences of racial discrimination and preterm birth risk among AA individuals.

Epigenetic Age Acceleration and Chronological Age: Associations With Cognitive Performance in Daily Life.

DNA methylation-derived epigenetic clocks offer the opportunity to examine aspects of age acceleration (ie, the difference between an individual's biological age and chronological age), which vary among individuals and may better account for age-related changes in cognitive function than chronological age. Leveraging existing ambulatory cognitive assessments in daily life from a genetically diverse sample of 142 adults in midlife, we examined associations between 5 measures of epigenetic age acceleration and performance on tasks of processing speed and working memory. Covarying for chronological age, we used multilevel models to examine associations of epigenetic age acceleration (Horvath 1, Horvath 2, Hannum, PhenoAge, and GrimAge clocks) with both average level and variability of cognitive performance. Positive age acceleration (ie, epigenetic age greater than chronological age) was associated with poorer mean processing speed (Horvath 1 and 2) and working memory (GrimAge). Higher chronological age was also associated with poorer mean processing speed and working memory performance. Further, positive age acceleration was generally associated with greater intraindividual variability in working memory and processing speed tasks, whereas being chronologically older was associated with less intraindividual variability. Although further work is needed, our results indicate age acceleration effects have comparable or greater size as those for chronological age differences, suggesting that epigenetic age acceleration may account for additional risk and interindividual variation in cognitive performance above chronological age.

The heart of Detroit study: a window into urban middle-aged and older African Americans' daily lives to understand psychosocial determinants of cardiovascular disease risk.

BACKGROUND: Cardiovascular disease disproportionately affects African Americans. Psychosocial factors, including the experience of and emotional reactivity to racism and interpersonal stressors, contribute to the etiology and progression of cardiovascular disease through effects on health behaviors, stress-responsive neuroendocrine axes, and immune processes. The full pathway and complexities of these associations remain underexamined in African Americans. The Heart of Detroit Study aims to identify and model the biopsychosocial pathways that influence cardiovascular disease risk in a sample of urban middle-aged and older African American adults. METHODS: The proposed sample will be composed of 500 African American adults between the ages of 55 and 75 from the Detroit urban area. This longitudinal study will consist of two waves of data collection, two years apart. Biomarkers of stress, inflammation, and cardiovascular surrogate endpoints (i.e., heart rate variability and blood pressure) will be collected at each wave. Ecological momentary assessments will characterize momentary and daily experiences of stress, affect, and health behaviors during the first wave. A proposed subsample of 60 individuals will also complete an in-depth qualitative interview to contextualize quantitative results. The central hypothesis of this project is that interpersonal stressors predict poor cardiovascular outcomes, cumulative physiological stress, poor sleep, and inflammation by altering daily affect, daily health behaviors, and daily physiological stress. DISCUSSION: This study will provide insight into the biopsychosocial pathways through which experiences of stress and discrimination increase cardiovascular disease risk over micro and macro time scales among urban African American adults. Its discoveries will guide the design of future contextualized, time-sensitive, and culturally tailored behavioral interventions to reduce racial disparities in cardiovascular disease risk.

Older adults' self-reported prospective memory lapses in everyday life: Connections to inflammation and gender.

OBJECTIVE: Limited research has focused on the association between inflammatory markers and features of subjective cognitive functioning among older adults. The present work examined links between inflammation and a specific subjective cognitive report: prospective memory (PM), or our memory for future intentions, such as attending an appointment or taking medication. METHOD: We assessed self-reported PM lapses using a two-week ecological momentary assessment (EMA) diary protocol via smartphone as well as levels of blood-based inflammation among 231 dementia-free older adults (70-90 years, 66% women) enrolled in the Einstein Aging Study. RESULTS: Overall, PM lapses were largely unrelated to inflammatory markers. However, a significant gender difference was observed in the link between basal levels of interleukin (IL)-8 and PM lapses: higher levels of basal IL-8 were associated with more PM lapses among men (estimate = 0.98, 95%CI: [0.43, 1.53], p < .001) but not women (estimate = -0.03, 95%CI: [-0.45, 0.39], p = .826). No other significant relationships between PM lapses and basal or stimulated (ex vivo) cytokine levels (IL-1ß, IL-4, IL-6, IL-8, IL-10, tumor necrosis factor-alpha [TNF-α]) or C-reactive protein (CRP) emerged. CONCLUSION: Elevated levels of IL-8 in older men may possibly be an early indicator of neurodegeneration that relates to PM performance. Future studies should continue to examine PM and inflammation across genders to identify possible mechanisms through which these constructs may indicate neurodegeneration and dementia risk.

The association of epigenetic age acceleration and depressive and anxiety symptom severity among children recently exposed to substantiated maltreatment.

Child maltreatment is a major risk factor for both depressive and anxiety disorders. However, many children exposed to maltreatment never meet diagnostic threshold for either disorder while experiencing only transitory symptoms post-exposure. Recent research suggests DNA methylation adds predictive value in explaining variation in the onset and course of multiple psychiatric disorders following exposure to child maltreatment. Epigenetic age acceleration (EAA), the biological aging of cells not attributable to chronological aging, is a stress-sensitive biomarker capturing genome-wide variation in DNA methylation with the potential to identify children who have been maltreated at greatest risk for depressive and anxiety disorders. The current study examined two EAA clocks appropriate for the pediatric population, the Horvath and Pediatric Buccal Epigenetic (PedBE) clocks, and their associations with depressive and anxiety symptom severity following child maltreatment. Children (N = 71) 8-15 years of age, all of whom were exposed to substantiated child maltreatment in the 12 months prior to study entry, were enrolled. Risk modeling adjusting for several confounders revealed that EAA estimated via the Horvath clock was significantly associated with more severe depressive and anxiety symptoms. The PedBE clock was not associated with either depressive or anxiety symptom severity. Sensitivity analyses demonstrated that EAA via the Horvath clock robustly predicted depressive and anxiety symptom severity across multiple modeling scenarios. Our findings advance existing research suggesting EAA, as estimated with the Horvath clock, may be a promising biomarker for identifying children at greatest risk for more severe depressive and anxiety symptoms following maltreatment.

Heightened inflammation in bipolar disorder occurs independent of symptom severity and is explained by body mass index.

Inflammation is hypothesized to be a key component of bipolar disorder (BP) development and progression. However, findings linking BP prevalence and symptomology to immune functioning have been mixed, with some work suggesting that obesity may play an important role in BP-relevant inflammation. Here we investigate differences in biomarkers of inflammation [C-reactive protein (CRP), interleukin (IL)-1ß, IL-6, IL-8, IL-10] between healthy controls (HC) and individuals with BP or other mental illness (MI). Adults with BP, MI, or HC (n = 545, 70% BP, 21% HC, 9% MI) self-reported depressive and manic symptoms close to a blood draw and physical exam that included measurement of height and weight. A composite score was calculated from the four cytokines measured in plasma; follow-up analyses explored a pro-inflammatory composite and IL-10, individually. BP individuals had elevated cytokine concentrations compared to HC (B = 0.197, [0.062, 0.333], t (542) = 2.855, p = .004); this difference was also evident for the pro-inflammatory composite and for IL-10. Cytokine concentrations were not associated with BP mood states. Body mass index (BMI), an indicator of obesity, was significantly higher in BP compared to HC (B = 3.780, [2.118, 5.443], t (479) = 4.457, p < .001) and differences in cytokines between the two groups was no longer significant after controlling for BMI. No differences in CRP were evident between BP and HC. These results suggest that cytokine concentrations are elevated in BP and this difference from HC is associated with obesity. Interventions targeting immune modulators in BP must carefully consider the complex relationships within the BP-inflammation-obesity triangle.

Greater Ecologically Assessed Positive Experiences Predict Heightened Sex Hormone Concentrations Across Two Weeks in Older Adults.

OBJECTIVES: Sex hormones are important components of healthy aging, with beneficial effects on physical and mental health. Positive experiences such as elevated mood, lowered stress, and higher well-being also contribute to health outcomes and, in younger adults, may be associated with elevated sex hormone levels. However, little is known about the association between positive experiences and sex hormones in older adults. METHODS: In this study, older men and women (N = 224, 70+ years of age) provided blood samples before and after a 2-week period of ecological momentary assessment (EMA) of positive and negative experiences (assessed based on self-reporting items related to affect, stress, and well-being). Concentrations of a panel of steroid sex hormones and glucocorticoids were determined in blood. RESULTS: Higher levels of positive experiences reported in daily life across 2 weeks were associated with increases in free (biologically active) levels of testosterone (B = 0.353 [0.106, 0.601], t(221.3) = 2.801, p = .006), estradiol (B = 0.373 [0.097, 0.649], t(225.1) = 2.645, p = .009), and estrone (B = 0.468 [0.208, 0.727], t(224.3) = 3.535, p < .001) between the start and the end of the 2-week EMA period. DISCUSSION: These findings suggest that sex hormones may be a pathway linking positive experiences to health in older adults.

The longitudinal connection between depressive symptoms and inflammation: Mediation by sleep quality.

Although there is a strong association between depressive symptoms and markers of inflammation, it remains unclear whether depressive symptoms at one point in life may predict inflammation later in life. Moreover, despite extant literature linking sleep with both depressive symptoms and inflammation, there is little research investigating poor sleep as a mechanism linking depressive symptoms with later inflammation. The links between depression and physical health can also vary by gender. In longitudinal analyses with data from the Midlife in the United States (MIDUS) study, we examined whether depressive symptoms were associated with inflammatory markers 11 years later and whether these associations were mediated by sleep disturbances or moderated by gender. Participants reported depressive symptoms and demographic information at baseline. At 11-year follow-up, the same participants (n = 968) reported depressive symptoms, sleep quality and duration using validated scale items, and provided a blood sample from which inflammatory markers interleukin-6 (IL-6) and C-reactive protein (CRP) were quantified. Actigraphy assessment of sleep was obtained in a subsample (n = 276). After adjusting for concurrent depressive symptoms and other relevant covariates, baseline depressive symptoms were associated with CRP 11 years later in the full sample, and with IL-6 among women. Subjective sleep quality mediated the association between depressive symptoms and CRP. Results suggest that depressive symptoms may be longitudinally associated with inflammation; however, directionality issues cannot be determined from the present work, particularly as inflammation markers (which might have been associated with baseline depressive symptoms) were not available at baseline. Findings further suggest that longitudinal associations between depressive symptoms and inflammation may potentially be explained by sleep and may reflect gender specific patterns.

Psychosocial and behavioral factors affecting inflammation among pregnant African American women.

African American women are reported to have greater inflammation compared with women from other racial groups. Higher inflammation during pregnancy has been associated with increased risk of adverse perinatal outcomes. We hypothesized that maternal inflammation is related to depressive symptoms and social and behavioral risk factors among pregnant African American women. Pregnant African American women (n â€‹= â€‹187) were recruited at prenatal clinics in the Midwest. Women completed questionnaires and had blood drawn at a prenatal visit. Plasma levels of cytokines (interferon gamma [IFN]-γ, interleukin [IL]-6, IL-8, IL-10, tumor necrosis factor [TNF]-α) and C-reactive protein (CRP) were measured by multiplex assays. Women had a mean age of 26.58±5.42 years and a mean gestational age at data collection of 16.35±5.95 weeks. Twenty-six percent of women had Center for Epidemiological Studies-Depression (CES-D) scores ≥23 (scores that have been correlated with clinical diagnosis of depression), 15.5% smoked cigarettes, 16.6% used marijuana, and 5.3% reported experiencing intimate partner violence (IPV). Higher CES-D scores were correlated with higher plasma CRP levels (r â€‹= â€‹0.16, p â€‹= â€‹0.046). Women who reported any experiences of IPV during pregnancy had higher levels of IL-8 (p â€‹= â€‹0.018) and lower levels of IFN-γ (p â€‹= â€‹0.012) compared with women who did not report IPV. Cigarette smoking during pregnancy was associated with lower levels of the anti-inflammatory cytokine IL-10 (p â€‹= â€‹0.003). These findings suggest that depressive symptoms, IPV, and cigarette smoking during pregnancy relate to select inflammatory markers in pregnant African American women. The relationships of inflammation with these factors should be further investigated to better understand the mechanisms which influence maternal and fetal health outcomes.

Diminished Cellular Immunity and Executive Cognitive Functioning Among Middle-Aged and Elderly Adults.

OBJECTIVE: Within the field of psychoneuroimmunology, much attention has been given to immune dysregulation and its impact on cognitive functioning. Some of this work has focused on the association between high levels of basal proinflammatory cytokines and poorer performance on measures of executive functioning; however, effect sizes have been quite small in human studies. METHODS: We investigated whether Epstein-Barr virus (EBV) antibody titers, a marker of immune dysregulation related to cellular immunity, may be associated with executive functioning while also attempting to replicate prior studies using two markers of proinflammatory cytokine production (i.e., circulating and lipopolysaccharide [LPS]-stimulated cytokines [interleukin 6, interleukin 1ß, interferon-γ]). A total of 71 community-dwelling adults (mean [standard deviation] age = 60.87 [6.26] years) who were seropositive for EBV infection participated in the study. RESULTS: Findings indicated that greater EBV antibody titers were associated with poorer performance on measures of the executive functions of inhibition ( B = -2.36, standard error = 1.06, p = .028) and cognitive flexibility ( B = -2.89, standard error = 1.13, p = .013) when including circulating and LPS-stimulated cytokines and other relevant covariates (i.e., age, sex, and body mass index) in linear regression analyses. Neither circulating nor LPS-stimulated cytokines were associated with performance on the cognitive tasks in the regression analyses. CONCLUSIONS: These results suggest that EBV antibody titers may be an indicator of immune dysregulation that is more relevant to executive functioning performance than either circulating or stimulated proinflammatory cytokines among community-dwelling adults.

Individuals with both higher recent negative affect and physical pain have higher levels of C-reactive protein.

Conceptualizing physical pain and negative affect as potentially interactive, we hypothesized that higher levels of peripheral inflammatory markers would be observed consistently only among individuals with both higher negative affect and pain symptomatology. Participants were generally healthy midlife adults from the Bronx, NY (N â€‹= â€‹212, M age â€‹= â€‹46.77; 60.8% Black, 25.5% Hispanic/Latina/o) recruited as part of a larger study. Key measures were: reported pain intensity and pain interference at baseline, recent negative affect averaged from self-reports 5x/day for 7 days, and peripheral inflammatory markers (C-reactive protein [CRP] and a composite cytokine measure based on seven cytokines). Controlling for age, BMI, gender, and education, recent negative affect significantly interacted with both pain variables to explain variance in CRP, with higher CRP levels observed only in individuals with both higher negative affect and either higher pain intensity or pain interference. These findings contribute to an emerging literature suggesting that negative affect, pain, and inflammation are related in important and complex ways.

Depressive symptoms and other negative psychological states relate to ex vivo inflammatory responses differently for men and women: Cross-sectional and longitudinal evidence.

An array of negative psychological states - including depressive symptoms, perceived stress, rumination, and negative affect - have been linked to immune function and inflammatory responses. Herein we show evidence of gender-dependent associations between ex vivo lipopolysaccharide (LPS)-stimulated cytokine responses and such psychological states, in both cross-sectional and longitudinal analyses from three annual waves (N = 162 at baseline, 67.3% female). In cross-sectional analyses (at baseline), gender moderated the associations of depressive symptoms (previously reported), perceived stress (B = -0.043, 95%CI [-0.080, -0.015]), rumination (B = -0.500, [-1.015, -0.232]), negative affect (B = -0.020, [-0.020, -0.005]), and positive affect (B = 0.024, [0.008, 0.047]) with LPS-stimulated cytokine responses. In each analysis, negative psychological states were positively associated with LPS-stimulated cytokine responses among men but negatively among women (with associations for positive affect in the opposite direction). In longitudinal analyses (across three annual measurements), similar associations were seen for depressive symptoms (B = -0.024, [-0.059, -0.004]), perceived stress (B = -0.045, [-0.069, -0.024]), and rumination (B = -0.381, [-0.622, -0.120]). These results indicate that gender is a critical factor in associations between a broad array of negative psychological states and inflammatory responses and identify one pathway by which gender may influence psychosomatic health.

Perceived stress is linked to heightened biomarkers of inflammation via diurnal cortisol in a national sample of adults.

Exposure to and perceptions of stress have been associated with altered systemic inflammation, but the intermediate processes by which stress links to inflammation are not fully understood. Diurnal cortisol slopes were examined as a pathway by which self-reported psychosocial stress is associated with inflammation [i.e., C-reactive protein (CRP), interleukin-6 (IL-6), fibrinogen, E-Selectin, and Intercellular Adhesion Molecule-1 (ICAM-1)] in a large sample of adults (the Midlife in the US study; N = 914; 55.9% female; aged 34-84 years). Structural equation modeling indicated that perceived psychological stress was associated with flattened diurnal cortisol slopes and flatter diurnal cortisol slopes were, in turn, associated with heightened inflammation in these cross-sectional analyses (index of indirect pathway, ω = 0.003, 95% CI [0.001, 0.004], ωSTD = 0.027; with covariates, ω = 0.001, [0.0002, 0.002], ωSTD = 0.011). A similar indirect effect was evident for self-reported traumatic life events (ω = 0.007, [0.004, 0.012], ωSTD = 0.030); however, inclusion of covariates (i.e., age, gender, race, ethnicity, body mass index, and other factors associated with physical health) accounted for this finding (ω = 0.001, [-0.001, 0.004], ωSTD = 0.005). These results support an allostatic load model of psychosomatic health, in which cortisol (along with other stress-responsive signaling molecules) is a necessary component for understanding links between stress exposure, perceived stress, and immune functioning.

The Association Between Loneliness and Inflammation: Findings From an Older Adult Sample.

Loneliness has been linked to poor mental and physical health outcomes. Past research suggests that inflammation is a potential pathway linking loneliness and health, but little is known about how loneliness assessed in daily life links with inflammation, or about linkages between loneliness and inflammation among older adults specifically. As part of a larger investigation, we examined the cross-sectional associations between loneliness and a panel of both basal and LPS-stimulated inflammatory markers. Participants were 222 socioeconomically and racially diverse older adults (aged 70-90 years; 38% Black; 13% Hispanic) systematically recruited from the Bronx, NY. Loneliness was measured in two ways, with a retrospective trait measure (the UCLA Three Item Loneliness Scale) and an aggregated momentary measure assessed via ecological momentary assessment (EMA) across 14 days. Inflammatory markers included both basal levels of C-reactive protein (CRP) and cytokines (IL-1ß, IL-4, IL-6, IL-8, IL-10, TNF-α) and LPS-stimulated levels of the same cytokines. Multiple regression analyses controlled for age, body-mass index, race, and depressive symptoms. Moderation by gender and race were also explored. Both higher trait loneliness and aggregated momentary measures of loneliness were associated with higher levels of CRP (ß = 0.16, p = 0.02; ß = 0.15, p = 0.03, respectively). There were no significant associations between loneliness and basal or stimulated cytokines and neither gender nor race were significant moderators. Results extend prior research linking loneliness with systemic inflammation in several ways, including by examining this connection among a sample of older adults and using a measure of aggregated momentary loneliness.

Ex vivo LPS-stimulated cytokine production is associated with cortisol curves in response to acute psychosocial stress.

BACKGROUND: Empirical and theoretical evidence suggest that because of the co-evolution of the endocrine and immune response systems, different types of stressors may lead to similar levels of physiological activation. The present analyses examined associations between two physiological stress responses: the cortisol response to an acute laboratory stressor and ex vivo lipopolysaccharide (LPS) stimulated inflammatory cytokine production. METHODS: Healthy middle-aged adults (N = 65) completed testing at two appointments, two weeks apart. Blood was collected at each appointment to measure circulating inflammatory cytokine levels and stimulated inflammatory cytokine production after 4 and 24 hours of incubation with LPS. A cumulative standardized composite measure of inflammation was calculated using the cytokines interleukin-6 (IL-6), interleukin-1ß (IL-1ß), and interferon-γ (IFN-γ). At visit two, after the blood draw, participants completed the Trier Social Stress Test (TSST); saliva samples were collected before and after to generate cortisol response curves (area under the curve with respect to ground [AUCG] and increase/decrease [AUCI]). RESULTS: AUCG was significantly associated with stimulated cytokine production at visit 2 after both 4 hours (B = 6.89; p = 0.007) and 24 hours (B = 7.50; p = 0.005) of incubation, controlling for age, sex, and BMI. AUCI was also significantly associated with stimulated cytokine production at visit 2 after 4 hours (B = 6.28; p = 0.004) and 24 hours (B = 6.16; p = 0.007) of incubation, controlling for age, sex, and BMI. Stimulated inflammatory cytokine production was strongly correlated across the two visits (2 weeks apart) after 4 hours of incubation (r = 0.80, p < 0.001) and after 24 hours (r = 0.80, p < 0.001). Within each visit, stimulated cytokine production after 4 hours was significantly correlated with stimulated inflammation at 24 hours (r = 0.93-0.94, p < 0.05) CONCLUSIONS: These results suggest that LPS-stimulated inflammatory cytokine production and the cortisol response to the TSST contain comparable information about acute human physiological stress responses. Moreover, measurement of stimulated cytokines was highly stable across a two-week time period whether measured after 4 or 24 hours of incubation with LPS.

Prenatal cigarette smoking as a mediator between racism and depressive symptoms: The Biosocial Impact on Black Births Study.

OBJECTIVE: This study examined whether cigarette smoking mediated the association of racial discrimination with depressive symptoms among pregnant Black women. DESIGN: Cross-sectional. SAMPLE: Two hundred Black women at 8-29 weeks gestation. MEASUREMENTS: Women completed questionnaires including the Experiences of Discrimination and the Center for Epidemiologic Studies-Depression (CES-D) scales, as well as questions about sociodemographic characteristics and cigarette smoking. RESULTS: The mean age of the sample was 26.9 ± 5.7 years and the mean gestational age at data collection was 15.6 ± 5.7 weeks. Approximately 17% of women reported prenatal cigarette smoking; 27% had prenatal CES-D scores ≥23, which have been correlated with depression diagnoses; and 59% reported ever (lifetime) experiencing discrimination in at least one situation (e.g., at work). Path analysis results indicated that the standardized indirect effect of experiences of racial discrimination on CES-D scores through prenatal smoking was statistically significant (standardized indirect effect = 0.03; 95% CI: 0.001, 0.094; p = .042). CONCLUSION: Cigarette smoking during pregnancy partially mediated the association between lifetime experiences of racial discrimination and prenatal depressive symptoms among pregnant Black women. Smoking cessation programs should focus on identifying and treating depressive symptoms among pregnant Black women.

Affect variability and inflammatory markers in midlife adults.

OBJECTIVE: Higher affect variability (the extent to which individuals vary in their affect over time) has been associated with poorer health indicators, but associations with inflammation are less well understood. The purpose of the present study was to examine whether affect variability was associated with inflammation in ways consistent with the stability theory or the fragile positive affect theory, and whether associations were linear or nonlinear. METHOD: In a racially diverse sample (N = 231; Aged 25-65; 65% female; 62% Black; 25% Hispanic), we examined whether positive affect (PA) and negative affect (NA) variability exhibited linear or quadratic associations with circulating inflammatory cytokines (a composite measure comprised of IL-1ß, IL-4, IL-6, IL-8, IL-10, TNF-α, IFN-γ), and C-reactive protein (CRP) and whether person-mean affect moderated these associations. Affective states were assessed using ecological momentary assessments (EMAs) 5 times per day for 2 weeks, with a blood draw at the end of the EMA period. Individual standard deviations of affective states indexed affect variability. RESULTS: A quadratic association indicated that moderate NA variability was associated with lower CRP. There was evidence of significant moderation by linear associations with PA only: For those with higher person-mean PA, PA variability was positively associated with the cytokine composite. Both person-mean PA and person-mean NA moderated quadratic associations, such that for those with high person-mean affect, both high and low affect variability was associated with systemic inflammation. CONCLUSION: Results are in line with fragile affect theory suggesting that associations between affect variability and health indicators may vary by person-mean affect. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

The relationship between diurnal variation of cytokines and symptom expression in mild obstructive sleep apnea.

OBJECTIVES: To identify the relationship between (1) cytokines and everyday symptoms and (2) cytokine diurnal variation and everyday symptoms in mild obstructive sleep apnea (OSA). METHODS: An observational, single-night study of 20 adults with mild to moderate OSA undergoing diagnostic polysomnography. Everyday symptoms included sleepiness measured by Stanford Sleepiness Scale, fatigue and energy levels measured by Lee Fatigue Scale, and cytokine plasma concentrations including interleukin (IL)-1ß, IL-6, IL-8, and tumor necrosis factor-α (TNF-α) measured concurrent with symptoms at presleep (8 pm to 10 pm; time 1) and postsleep (5 am to 6 am; time. 2) Cytokine diurnal variation was calculated as [time 2 - time 1]. Wilcoxon signed-rank tests and Spearman partial rank correlations adjusted for age, body mass index, cardiovascular disease, and type 2 diabetes were used. RESULTS: Twenty patients (50% male, obese, median age = 51.0 years) with mild OSA (apnea-hypopnea index, AHI; median 9.5 events/h) were evaluated. Evening IL-6 was associated with evening symptoms, including sleepiness (r = .69, P = .002) and energy level (r = -0.68, P = .003); morning IL-8 (r = .73, P = .001), and TNF-α (r = .59, P = .015) were associated with morning fatigue. Only morning IL-8 (r = -0.57, P = .022) and diurnal variations in IL-8 (r = -0.60, P = .014) were associated with morning energy level. CONCLUSION: There is scant evidence addressing the diurnal variation of inflammatory biomarkers and the relationship with symptom expression in mild OSA. The present findings provide preliminary mechanistic findings for symptom expression in OSA and contribute insight to mild OSA symptom phenotypes.