13
Apr 23

Mean affect and affect variability may interact to predict inflammation

Introduction Individuals with greater affect variability (i.e., moment-to-moment  fluctuations possibly reflecting emotional dysregulation) are at risk for greater systemic inflammation, which is associated with cardiovascular disease. Some evidence suggests that affect variability is linked with poorer health indicators only among those with higher average levels of affect, particularly for positive affect (PA), and that  associations may be non-linear. The present study sought to examine whether links  between both PA and negative affect (NA) variability and inflammation are moderated  by average level of affect. Methods Participants (N = 300, 50 % female, ages 21–70,  60 % non-Hispanic White, 19 % Hispanic, 15 % non-Hispanic Black) completed a lab  assessment and provided a blood sample to measure systemic inflammation (i.e., TNF-α, IL-6, CRP). Affect was collected via a two-day ecological momentary assessment  protocol where reports were collected about every 45-min during waking hours.  Momentary affect ratings were averaged across both days (i.e., iM), separately for PA  and NA, for each participant. Affect variability was calculated as the person-specific SD  (i.e., iSD) of affect reports, separately for PA and NA. Linear and quadratic interactions  were tested. Models included covariates for sex, race, and body mass index. Results  There were significant interactions between NA iM and NA iSD predicting TNF-α (b =  6.54; p < 0.05) and between PA iM and PA iSD predicting IL-6 (b = 0.45; p < 0.05).  Specifically, the association between these affect variability indicators and inflammatory  markers were suggestive of a positive association among those with higher average affect but a negative association among those with lower average affect. There was no  evidence of non-linear associations between affect and inflammation. Discussion Incorporating interactive effects between affect variability and average affect may be an  important consideration in understanding affective-inflammatory associations.

CITATION: Dusti R. Jones, John M. Ruiz, Hannah M.C. Schreier, Matthew A. Allison, Burt N. Uchino, Michael A. Russell, Daniel J. Taylor, Timothy W. Smith, Joshua M. Smyth, Mean affect and affect variability may interact to predict inflammation, Brain, Behavior, and Immunity, Volume 109, 2023, Pages 168-174, ISSN 0889-1591, https://doi.org/10.1016/j.bbi.2023.01.008. (https://www.sciencedirect.com/science/article/pii/S0889159123000089)


13
Jul 22

First-generation college students have greater systemic inflammation following the initial college transition

Background First-generation college students (“first-gens”) are often at a disadvantage socially and academically; whether they are at risk physiologically is unknown despite the well-established link between greater education and better long-term health. Purpose To examine whether first-gens have higher levels of cardiovascular disease (CVD) risk markers relative to continuing-generation college students (“continuing-gens”). Methods A panel of CVD risk markers was assessed among 87 emerging adults (41 first-gens) twice over their first year of college. Results Compared to continuing-gens, first-gens had greater systemic inflammation (composite of averaged z-scores for C-reactive protein and interleukin-6; B = 0.515, SE = 0.171, p = .003) during the fall but not spring semester (p > .05). Associations were independent of family home ownership and childhood adversity, even though first-gens were more likely to live in rental homes and reported riskier home environments. Lower childhood subjective social status (SSS) accounted for greater systemic inflammation among first-gens as evidenced by an indirect effect of college generation status on systemic inflammation through childhood SSS (a1b1 = 0.261, bootstrapped SE = 0.103, 95% boot CI [0.078, 0.482]). There were no differences in metabolic risk and latent virus regulation by college generation status in either semester (p > .10). Conclusions This is the first study to find that first-gens have higher levels of systemic inflammation than continuing-gens following the college transition and that childhood SSS may be one explanatory pathway. First-gens may benefit from university resources that address social class differences, which should be provided early on so that first-gens can reap the health-relevant benefits of higher education, at least in the short term.

CITATION: Jones E. J., & Schreier H. M. C. First-Generation College Students, Emotional Support, and Systemic Inflammation Following the College Transition. J Adolesc Health. 2023 Jan;72(1):36-43. doi: 10.1016/j.jadohealth.2022.08.012. Epub 2022 Oct 8. PMID: 36220685.


13
Jul 22

The intergenerational interplay of adversity on salivary inflammation in young children and caregivers

Systemic inflammation links exposure to early childhood adversity to later disease. The associations among adversity and disease risk might in part operate through poor oral hygiene and subsequent periodontal inflammation, which can be measured in saliva. Few studies, however, have examined the association between adversity and salivary inflammation in young children. Further, there is a dearth of literature investigating adverse experiences and salivary inflammation in children and caregivers together, limiting our understanding of the intergenerational, dual effects of adversity on inflammation for both members of the caregiver-child dyad. This study tested child and caregiver adversity and their associations with an inflammatory composite (i.e., IL-6, IL-1β, IL-8, TNF-α) and CRP in 93 preschool-age children and their caregivers. Caregivers reported on their child’s experiences of adversity, as well as on their own adverse experiences, using a comprehensive questionnaire synthesized from previous checklists for complete coverage of possible adverse events. Results showed that caregivers’ salivary inflammatory markers (i.e., IL-6, IL-1β, IL-8, TNF-α, and CRP) were not significantly correlated with the same five inflammatory markers in children’s saliva. Among children, adversity was associated with significantly higher levels of the inflammatory composite, though not CRP. This association was amplified among children whose caregivers also experienced more adversity during adulthood. Among caregivers, childhood adversity and adulthood adversity were each independently associated with significantly higher levels of the inflammatory composite and CRP. The association between caregivers’ own childhood adversity and inflammation was amplified among caregivers whose children also experienced more adversity during their childhoods. These findings provide preliminary evidence for the possible dual role of young children’s and caregivers’ adverse experiences in contributing to salivary inflammation for both members of the dyad, suggesting possible implications for systemic inflammation and future disease.

CITATION: Huffhines, L., Jackson, Y., McGuire, A. B. & Schreier, H. M. C. (2021). The intergenerational interplay of adversity on salivary inflammation in young children and caregivers. Psychoneuroendocrinology, 128, 105222.


13
Jul 22

Childhood physical neglect is associated with exaggerated systemic and intracellular inflammatory responses to repeated psychosocial stress in adulthood

Experiences of child maltreatment are associated with a host of adverse mental and physical health outcomes in adulthood. Altered reactivity to psychosocial stress exposure may partially explain known associations between early experiences of maltreatment and later life health. The present study focuses on examining whether experiences of child maltreatment are associated with physiological reactions to initial and repeated psychosocial stress in adulthood. To this end, 44 healthy adults (52% male, aged 18-65) completed the Childhood Trauma Questionnaire to provide information about exposure to child maltreatment and completed the Trier Social Stress Test (TSST) on 2 consecutive days. Peripheral blood was collected prior to as well as 30 and 120 min following the TSST on each day. Plasma Interleukin-6 (IL-6) and gene expression of IL-6, IL-1β, nuclear factor-kB (NF-kB), and inhibitor of kB (IkB) were measured from each blood sample. Total CTQ scores were unrelated to plasma IL-6 and gene expression (ps > .10) but a history of childhood physical neglect was associated with increased interleukin-1β (β =.35; p =.02; R2 =.19) and nuclear factor-kB (β =.30; p =.046; R2 =.13) expression following initial stress. Following repeated exposure to the TSST, childhood physical neglect was associated with increased plasma IL-6 reactivity (β =.34; p =.02; R2 =.16) and increased expression of nuclear factor-kB (β =.31; p =.04; R2 =.08). Finally, childhood physical neglect was associated with decreased habituation following repeated exposure to the TSST. Other CTQ subscales were not related to plasma IL-6 and gene expression when considered individually. Results from this study are suggestive of a unique effect of childhood physical neglect on the physiological stress response following initial and repeated exposure to a common psychosocial stressor. This provides important directions for future research because the effect of childhood physical neglect on long-term neglect are not well understood and in need of further investigation.

CITATION: Schreier, H. M. C., Kuras, Y. I., McInnis, C. M., Thoma, M. V., Gianferante, D., Hanlin, L., Chen, X., Wang, D., Goldblatt, D. & Rohleder, N. (2020). Childhood physical neglect is associated with exaggerated systemic and intracellular inflammatory responses to repeated psychosocial stress in adulthood. Frontiers Psychiatry, 11, 504.


03
Oct 18

Chronic Family Stress and Adolescent Health: The Moderating Role of Emotion Regulation

Objective The aim of the study was to assess whether the association between chronic family stress and physiological measures is moderated by emotion regulation strategies in an adolescent sample. Methods Chronic family stress was assessed via a semi-structured interview and emotion regulation strategies (cognitive reappraisal and suppression) via questionnaire among 261 adolescents (14.57 (1.07) years). Several metabolic (waist-hip ratio, systolic and diastolic blood pressure) and inflammatory markers (basal and stimulated pro-inflammatory cytokine production in response to bacterial challenge) as well as glucocorticoid sensitivity were assessed. Results There were no main effects of chronic family stress, cognitive reappraisal, or suppression on physiological measures (all p’s > .10). Emotion regulation moderated the association between chronic family stress and physiological measures. As chronic family stress increased, adolescents higher in cognitive reappraisal had smaller waist-hip ratios (B = −.003, SE = .001, p = .015) and lower systolic blood pressure (B = −.303, SE = .143, p = .035), although no moderation was found with respect to inflammatory markers and glucocorticoid sensitivity (all p’s > .30). In addition, as chronic family stress increased, adolescents higher in suppression showed evidence of higher stimulated pro-inflammatory cytokine production (B = .046, SE = .020, p = .021) and lower glucocorticoid sensitivity (B = .051, SE = .021, p = .015), although basal inflammation and metabolic measures were not moderated by suppression (all p’s > .50). Conclusions This study suggests that the types of emotion regulation strategies used by adolescents may affect the extent to which chronic family stress affects important metabolic and immune processes.

CITATION: Jones, E. J., Lam, P.H., Hoffer, L.C., Chen, E., & Schreier, H.M.C. (2018). Chronic stress and adolescent health: the moderating role of emotion regulation. Psychosomatic Medicine, 80(8), 764-773.


27
Aug 16

Low-Grade Inflammation and Ambulatory Cortisol in Adolescents: Interaction Between Interviewer-Rated Versus Self-Rated Acute Stress and Chronic Stress

Objective: To determine whether the association between self-rated or interviewer-rated recent acute stress exposures and low-grade inflammation and daily cortisol production in adolescents is moderated by chronic stress ratings. Methods: Acute and chronic stress exposures were assessed in 261 adolescents aged 13 to 16 years using a semistructured life stress interview. The negative impact of acute stressors was independently rated by both adolescents (self-rated) and interviewers (interviewer-rated). Markers of inflammation (interleukin (IL)-6, IL-1ra, C-reactive protein) were measured from peripheral blood samples obtained via antecubital venipuncture. Participants collected 4 saliva samples at home on each of 6 consecutive days for the analysis of diurnal salivary cortisol profiles. Results: There were no main effects of acute stressors (self- and interviewer-rated) and chronic family or peer stress on adolescent inflammation markers and cortisol (p values > .10). However, the interaction between interviewer-rated acute stress and chronic family stress was significantly associated with adolescent inflammation markers (IL-6, IL-1ra). Specifically, as chronic family stress increased, the association between acute stressor impact (interviewer-rated) and inflammation markers became more positive (IL-6 (B = .054, SE = .023, p = .022); IL-1ra (B = .030, SE = .014, p = .034)). Interactions between self-rated acute stress and chronic family stress were not associated with any biological measures (p values > .10). Interactions between acute stressor impact (both self- and interviewer-rated) and chronic peer stress were also not significantly associated with any biological measures (p values > .05). Conclusions: Among adolescents, interviewer-based ratings of acute stressor impact may allow for better prediction of health-relevant inflammation markers than adolescents’ own ratings.

CITATION: Schreier, H. M. C. & Chen, E. (2016). Low-Grade Inflammation and Ambulatory Cortisol in Adolescents: Interaction Between Interviewer-Rated Versus Self-Rated Acute Stress and Chronic Stress. Psychosomatic Medicine.


27
Aug 16

Social role conflict predicts stimulated cytokine production among men, not women

Objective: To assess whether perceived role conflict is associated with stimulated pro-inflammatory cytokine production and glucocorticoid sensitivity, and whether these associations are moderated by sex. Methods: 153 healthy adults (aged 45.8±5.5years, 78% female) listed their 3 main social roles and indicated the amount of role conflict they perceived between each pair of social roles. Subsequently, participants underwent blood draws and leukocyte response to microbial challenge and glucocorticoid sensitivity were assessed by incubating whole blood with lipopolysaccharide (LPS) in the presence or absence of hydrocortisone. Stimulated levels of Interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor alpha (TNFα) were measured. Results: Multiple regression analyses controlling for sociodemographics revealed significant sex×role conflict interactions for LPS-stimulated production of IL-1β, IL-6, and TNFα (all interaction ps<0.05), and a marginal interaction on LPS-stimulated IL-8 production (interaction p<0.10). Greater perceived role conflict was associated with greater pro-inflammatory cytokine production in response to microbial stimulation only among men, not women. There also were significant sex×role conflict interactions with respect to glucocorticoid sensitivity for IL-1β, IL-6, and TNFα production (all interaction ps<0.05) and a marginal interaction for IL-8 (interaction p<0.10). Greater perceived role conflict was unrelated to glucocorticoid sensitivity among women, but associated with less sensitivity to glucocorticoid signaling among men. Conclusions: Perceived social role conflict, indicating greater perceived demand across multiple social roles, may take a greater toll on the regulation of inflammatory processes among men compared to women.

CITATION: Schreier, H. M. C, Hoffer, L. C. & Chen, E. (2016). Social role conflict predicts stimulated cytokine production among men, not women. Brain, Behavior, & Immunity.


15
Sep 15

Chronic traffic-related air pollution and stress interact to predict biologic and clinical outcomes in asthma

Background: Previous research has documented effects of both physical and social environmental exposures on childhood asthma. However, few studies have considered how these two environments might interact to affect asthma. Objective: This study aimed to test interactions between chronic exposure to traffic-related air pollution and chronic family stress in predicting biologic and clinical outcomes in children with asthma. Method: Children with asthma (n = 73, 9-18 years of age) were interviewed about life stress, and asthma-relevant inflammatory markers [cytokine production, immunoglobulin E (IgE), eosinophil counts] were measured. Parents reported on children’s symptoms. Children completed daily diaries of symptoms and peak expiratory flow rate (PEFR) measures at baseline and 6 months later. Exposure to traffic-related air pollution was assessed using a land use regression model for nitrogen dioxide concentrations. Results: NO(2) by stress interactions were found for interleukin-5 (beta for interaction term = -0.31, p = 0.02), IgE (interaction beta = -0.29, p = 0.02), and eosinophil counts (interaction beta = -0.24, p = 0.04). These interactions showed that higher chronic stress was associated with heightened inflammatory profiles as pollution levels decreased. Longitudinally, NO(2) by stress interactions emerged for daily diary symptoms (interaction beta = -0.28, p = 0.02), parent-reported symptoms (interaction beta = -0.25, p = 0.07), and PEFR (interaction beta = 0.30, p = 0.03). These interactions indicated that higher chronic stress was associated with increases over time in symptoms and decreases over time in PEFR as pollution levels decreased. Conclusions: The physical and social environments interacted in predicting both biologic and clinical outcomes in children with asthma, suggesting that when pollution exposure is more modest, vulnerability to asthma exacerbations may be heightened in children with higher chronic stress.

CITATION: Chen, E., Schreier, H. M. C., Strunk, R. C., & Brauer, M. (2008). Chronic traffic-related air pollution and stress interact to predict biologic and clinical outcomes in asthma. Environmental Health Perspectives, 116(7), 970-975.


15
Sep 15

Resilience in low socioeconomic status children with asthma: adaptations to stress

Background: Low socioeconomic status (SES) is a strong predictor of many health problems, including asthma impairment; however, little is understood about why some patients defy this trend by exhibiting good asthma control despite living in adverse environments. Objective: This study sought to test whether a psychological characteristic, the shift-and-persist strategy (dealing with stressors by reframing them more positively while at the same time persisting in optimistic thoughts about the future), protects low-SES children with asthma. Methods: One hundred twenty-one children aged 9 to 18 years with a physician’s diagnosis of asthma were recruited from medical practices and community advertisements (mean age, 12.6 years; 67% male; 61% white). Shift-and-persist scores and asthma inflammation (eosinophil counts and stimulated IL-4 cytokine production) were assessed at baseline, and asthma impairment (daily diary measures of rescue inhaler use and school absences) and daily peak flow were monitored at baseline and at a 6-month follow-up. Results: Children who came from low-SES backgrounds but who engaged in shift-and-persist strategies displayed less asthma inflammation at baseline (β = 0.19, P < .05), as well as less asthma impairment (reduced rescue inhaler use and fewer school absences; β = 0.32, P < .01) prospectively at the 6-month follow-up period. In contrast, shift-and-persist strategies were not beneficial among high-SES children with asthma. Conclusion: An approach that focuses on the psychological qualities that low-SES children develop to adapt to stressors might represent a practical and effective starting point for reducing health disparities. Moreover, the approaches that are effective in low-SES communities might be different from those that are optimal in a high-SES context.

CITATION: Chen, E., Strunk, R. C., Threthewey, A., Schreier, H. M. C., Maharaj, N., & Miller, G. E. (2011). Resilience in low socioeconomic status children with asthma: adaptations to stress. Journal of Asthma and Clinical Immunology, 128(5), 970-976.


15
Sep 15

Longitudinal relationships between family routines and biological profiles among youth with asthma

Objective: To investigate whether longitudinal trajectories of inflammatory markers of asthma can be predicted by levels of family routines in youth with asthma. Design: Family routines were assessed through parent questionnaires and peripheral blood samples obtained from youth every 6 months throughout the 18-month study period. Longitudinal relationships were evaluated using hierarchical linear modeling. Main Outcome Measures: Mitogen-stimulated production of cytokines implicated in asthma, specifically IL-4, IL-5, and IL-13. Results: Youth with more family routines in their home environment showed decreases in IL-13 (but not IL-4 or IL-5) over the course of the study period. In turn, within-person analyses indicated that at times when stimulated production of IL-13 was high, asthma symptoms were also high, pointing to the clinical relevance of changes in IL-13 over time. A variety of child and parent psychosocial as well as child behavioral characteristics could not explain these effects. However, medication use eliminated the relationship between family routines and stimulated production of IL-13. Conclusion: Our study suggests that family routines predict asthma outcomes at the biological level, possibly through influencing medication use. Considering daily family behaviors when treating asthma may help improve both biological and clinical profiles in youth with asthma.

CITATION: Schreier, H. M. C. & Chen, E. (2010). Longitudinal relationships between family routines and biological profiles among youth with asthma. Health Psychology, 29(1), 82-90.


09
Sep 15

Family chaos and adolescent inflammatory profiles: the moderating role of socioeconomic status

Objective: To test whether family chaos influences adolescents’ inflammatory profiles and whether adolescents from low socio- economic status (SES) environments are at higher risk for experiencing adverse inflammatory profiles from living in chaotic family environments. Methods: A total of 244 families with an adolescent aged 13 to 16 years participated. Parents completed measures of family SES and family chaos. Both systemic inflammation and stimulated proinflammatory cytokine production in response to bacterial challenge were assessed in adolescents. Results: Our results suggest that SES moderates the detrimental effect of family chaos on systemic inflammation and interleukin-6 (B = -0.010, standard error [SE] = 0.004, p = .026), but not C-reactive protein (B = 0.009, SE = 0.006, p = .11), and on stimulated proinflammatory cytokine production (B = -0.098, SE = 0.044, p = .026) in adolescents, such that a chaotic family environment is positively associated with greater systemic inflammation and greater stimulated proinflammatory cytokine production in adolescents as family SES declines. Conclusions: These findings indicate that living in chaotic family environments places youth who may be vulnerable based on socioeconomic factors at a potentially higher risk for inflammation-related diseases. Key words: inflammation, family chaos, adolescents, socioeconomic status.

CITATION: Schreier, H. M. C., Roy, L. B., Frimer, L., & Chen, E. (2014). Family chaos and adolescent inflammatory profiles: the moderating role of socioeconomic status. Psychosomatic Medicine, 76(6), 460-467.


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