Socioeconomic status and stress-induced increases in interleukin-6

Brydon, Lena; Edwards, Susan; Mohamed‐Ali, Vidya; Steptoe, Andrew

doi:10.1016/j.bbi.2003.09.011

Cited by 173 publications

(97 citation statements)

References 53 publications

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“…Additionally, there are direct associations between lower SES and disturbed stress-related neuroendocrine and inflammatory processes that could contribute to risk of depression. For example, lower SES is associated with heightened inflammatory responses to acute stress and with cortisol dysregulation, both of which are implicated in the development of depression (Brydon et al 2004 ;Kumari et al 2010). Patients who have experienced acute emotional stress before ACS display heightened platelet activation following acute experimental stress (Strike et al 2006a) and this may also be involved in depressive responses (Nemeroff & Musselman, 2000).…”

Section: Discussionmentioning

confidence: 99%

Emotional triggering and low socio-economic status as determinants of depression following acute coronary syndrome

et al. 2011

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Background. The determinants of depression following acute coronary syndrome (ACS) are poorly understood. Triggering of ACS by emotional stress and low socio-economic status (SES) are predictors of adverse outcomes. We therefore investigated whether emotional triggering and low SES predict depression and anxiety following ACS.Method. This prospective observational clinical cohort study involved 298 patients with clinically verified ACS. Emotional stress was assessed for the 2 h before symptom onset and compared with the equivalent period 24 h earlier using case-crossover methods. SES was defined by household income and education. Depression was measured with the Beck Depression Inventory and the Hamilton Rating Scale for Depression and anxiety with the Hospital Anxiety and Depression Scale 3 weeks after ACS and again at 6 and 12 months. Age, gender, ethnicity, marital status, the Global Registry of Acute Coronary Events risk score, duration of hospital stay and history of depression were included as covariates.Results. Emotional stress during the 2-h hazard period was associated with increased risk of ACS (odds ratio 1.88, 95 % confidence interval 1.01-3.61). Both low income and emotional triggering predicted depression and anxiety at 3 weeks and 6/12 months independently of covariates. The two factors interacted, with the greatest depression and anxiety in lower income patients who experienced acute emotional stress. Education was not related to depression. Conclusions.Patients who experience acute emotional stress during their ACS and are lower SES as defined by current affluence and access to resources are particularly vulnerable to subsequent depression and anxiety.

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Section: Discussionmentioning

confidence: 99%

Emotional triggering and low socio-economic status as determinants of depression following acute coronary syndrome

et al. 2011

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“…16 However, proinflammatory cytokines show circadian rhythms and variations in peripheral blood, and the differences can potentially be related to the following factors: 1) the time of the day at which the blood samples were drawn, based on a study that demonstrated that IL-6 concentrations peaked in the evening; 15 2) IL-6 is a cytokine that increases in concentration in response to stressful conditions and may be affected by any emotional changes or symptom amplification; 26 3) cytokines may be released in a time-ordered sequence; 27 4) when an interleukin binds to its functional receptor, the complex is internalized; 28 and 5) cytokines are also potent stimulators of the hypothalamic-pituitary-adrenal (HPA) axis, either singly or in synergy with other classes of cytokines, thereby causing glucocorticoid release. 29 Thus, a dysfunctional HPA axis response occurring in some patients may result in elevated serum cytokine levels.…”

Section: Discussionmentioning

confidence: 99%

Serum cytokine levels in patients with chronic low back pain due to herniated disc: analytical cross-sectional study

et al. 2010

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CONTEXT AND OBJECTIVE: The role of immune response and proinflammatory cytokines in the pathogenesis of chronic pain has been of growing interest. In order to evaluate whether there is any association between disc herniation and elevated cytokine levels, we measured cytokine levels in patients with chronic low back pain and in healthy subjects. DESIGN AND SETTING:Analytical cross-sectional study at the Pain Clinic of Universidade Federal da Bahia (UFBA). METHODS:Cytokine levels were measured using the enzyme-linked immunosorbent assay (ELISA) technique on 23 patients with low back pain (G1) and on 10 healthy subjects (G2). RESULTS:The levels of tumor necrosis factor-alpha [TNF-alpha] (G1 = 5.6 ± 2.3 pg/ml; G2 = 1.6 ± 0.5 pg/ml; P = 0.01) and interleukin-6[IL-6] (G1 = 4.1 ± 3.0 pg/ml; G2 = 0.9 ± 0.4 pg/ml; P = 0.01) were higher in G1. There were no statistically significant differences in relation to interleukin-1 [IL-1] (G1 = 0.5 ± 0.3 pg/ml; G2 = 0.5 ± 0.1 pg/ml; P = 1) or soluble tumor necrosis factor receptor [sTNF-R] (G1 = 572 pg/ml ± 36; G2 = 581 ± 50 pg/ml; P = 0.87). CONCLUSION:The patients with chronic low back pain due to disc herniation presented higher levels of TNF-alpha and IL-6, but not of IL-1 or sTNF-R. RESUMO CONTEXTO E OBJETIVO:A função da resposta imunológica e das citocinas pró-inflamatórias na patogênese da dor crônica tem tido interesse crescente. Para avaliar se há correlação entre hérnia de disco e aumento de citocinas, foi medida a concentração de citocinas em pacientes com lombalgia crônica e em indivíduos sadios. TIPO DE ESTUDO E LOCAL: Estudo transversal analítico realizado na Clínica de Dor da Universidade Federal da Bahia (UFBA).MÉTODO: As concentrações de citocinas foram medidas pela técnica de ELISA (enzyme linked immunosorbent assay) em 23 pacientes com lombalgia (G1) e 10 sadios (G2). RESULTADOS:As concentrações de fator-alfa de necrose tumoral [TNF-alpha] (G1 = 5.6 ± 2.3 pg/ml; G2 = 1.6 ± 0.5 pg/ml; P = 0,01) e interleucina-6 [IL-6] (G1 = 4.1 ± 3.0 pg/ml; G2 = 0.9 ± 0.4 pg/ml; P = 0,01) foram maiores no G1. Não houve diferença estatisticamente significante para interleucina-1 [IL-1] (G1 = 0.5 ± 0.3 pg/ml; G2 = 0.5 ± 0.1 pg/ml; P = 1) e receptor solúvel do factor de necrose tumoral [sTNF-R] (G1 = 572 pg/ml ± 36; G2 = 581 ± 50 pg/ml; P = 0,87).CONCLUSÃO: Os pacientes com lombalgia crônica por hérnia de disco apresentam concentrações maiores de TNF-alpha e IL-6, mas não de IL-1 ou sTNF-R.

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“…Indeed, mice that are consistently subjected to social defeat (a rodent model of low social status) show greater inflammatory dysregulation (Blanchard et al, 1993;Powell et al, 2009), and lower-ranking female macaques have been shown to have greater expression of genes involved in inflammation than higher-ranking females (Tung et al, 2012). In humans, subjective ratings of social status have been associated with increases in stressor-evoked inflammation, such that lower-status individuals show a more pronounced inflammatory response to a laboratory stressor than individuals who perceive themselves as higher in status (Brydon et al, 2004;Derry et al, 2013). While short-term increases in inflammation in response to injury or infection are an integral part of the innate immune system's response to physical insults, exaggerated inflammatory activation in response to purely psychological threats (Slavich and Cole, 2013) and systemic elevations in inflammation are associated with the development of a number of chronic diseases (Hansson, 2005;, thus providing a possible physiological mechanism linking social status and poor physical and mental health outcomes.…”

Section: Introductionmentioning

confidence: 99%

Neural mechanisms linking social status and inflammatory responses to social stress

Muscatell

Dedovic

Slavich

et al. 2016

Social Cognitive and Affective Neuroscience

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Social stratification has important implications for health and well-being, with individuals lower in standing in a hierarchy experiencing worse outcomes than those higher up the social ladder. Separate lines of past research suggest that alterations in inflammatory processes and neural responses to threat may link lower social status with poorer outcomes. This study was designed to bridge these literatures to investigate the neurocognitive mechanisms linking subjective social status and inflammation. Thirty-one participants reported their subjective social status, and underwent a functional magnetic resonance imaging scan while they were socially evaluated. Participants also provided blood samples before and after the stressor, which were analysed for changes in inflammation. Results showed that lower subjective social status was associated with greater increases in inflammation. Neuroimaging data revealed lower subjective social status was associated with greater neural activity in the dorsomedial prefrontal cortex (DMPFC) in response to negative feedback. Finally, results indicated that activation in the DMPFC in response to negative feedback mediated the relation between social status and increases in inflammatory activity. This study provides the first evidence of a neurocognitive pathway linking subjective social status and inflammation, thus furthering our understanding of how social hierarchies shape neural and physiological responses to social interactions.

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Socioeconomic status and stress-induced increases in interleukin-6

Cited by 173 publications

References 53 publications

Emotional triggering and low socio-economic status as determinants of depression following acute coronary syndrome

Emotional triggering and low socio-economic status as determinants of depression following acute coronary syndrome

Serum cytokine levels in patients with chronic low back pain due to herniated disc: analytical cross-sectional study

Neural mechanisms linking social status and inflammatory responses to social stress

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