Depression, evening salivary cortisol and inflammation in chronic fatigue syndrome: A psychoneuroendocrinological structural regression model

Sara F. Milrad; Daniel L. Hall; Devika R. Jutagir; Emily G. Lattie; Sara J. Czaja; Dolores M. Perdomo; Mary Ann Fletcher; Nancy Klimas; Michael H. Antoni

doi:10.1016/j.ijpsycho.2017.09.009

Depression, evening salivary cortisol and inflammation in chronic fatigue syndrome: A psychoneuroendocrinological structural regression model

Sara F. Milrad, Daniel L. Hall, Devika R. Jutagir, Emily G. Lattie, Sara J. Czaja, Dolores M. Perdomo, Mary Ann Fletcher, Nancy Klimas, Michael H. Antoni^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

29 Scopus citations

Abstract

Introduction: Chronic Fatigue Syndrome (CFS) is a poorly understood illness that is characterized by diverse somatic symptoms, hypothalamic pituitary adrenal (HPA) axis dysfunction and heightened inflammatory indicators. These symptoms are often exacerbated and accompanied by psychological distress states and depression. Since depression is known to be associated with HPA axis dysfunction and greater inflammation, a psychoneuroendocrinological (PNE) model of inflammation was examined in persons diagnosed with CFS in order to uncover underlying biopsychosocial mechanisms in this poorly understood chronic illness. Methods: Baseline data were drawn from two randomized controlled trials testing the efficacy of different forms of psychosocial intervention, and included psychological questionnaires, di-urnal salivary cortisol, and blood samples. Data were analyzed with structural equation modeling (SEM). Results: The sample (N = 265) was mostly middle-aged (M _age = 49.36 ± 10.9, range = 20–73 years), Caucasian (67.7%), female (81.7%), highly educated (85.5% completed some college, college, or graduate program), and depressed (CES-D M = 23.87 ± 12.02, range 2–57). The SEM supporting a psychoneuroendocrinological model of immune dysregulation in CFS fit the data χ ² (12) = 17.725, p = 0.1243, RMSEA = 0.043, CFI = 0.935, SRMR = 0.036. Depression was directly related to evening salivary cortisol and inflammation, such that higher evening cortisol predicted greater depressive symptoms (β = 0.215, p < 0.01) and higher pro-inflammatory cytokines (interleukin-2 [IL-2], IL-6, and tumor necrosis factor-alpha [TNF-α] levels (β = 0.185, p < 0.05), when controlling for covariates. Discussion: Results highlight the role of depression, cortisol and inflammation in possible biological mechanisms involved in the pathophysiology of CFS. Time-lagged, longitudinal analyses are needed to fully explore these relationships.

Original language	English (US)
Pages (from-to)	124-130
Number of pages	7
Journal	International Journal of Psychophysiology
Volume	131
DOIs	https://doi.org/10.1016/j.ijpsycho.2017.09.009
State	Published - Sep 2018

Funding

The authors report no conflicts of interest. This research was supported by the NIH grant 1R01 NS055672 . DLH was also supported by an Institutional National Research Service Award ( T32AT000051 ) from the National Center for Complementary and Integrative Health at the National Institutes of Health.

Keywords

Chronic fatigue syndrome (CFS)
Depression
Evening cortisol
Inflammation
Structural equation modeling

ASJC Scopus subject areas

General Neuroscience
Neuropsychology and Physiological Psychology
Physiology (medical)

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10.1016/j.ijpsycho.2017.09.009

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Milrad, S. F., Hall, D. L., Jutagir, D. R., Lattie, E. G., Czaja, S. J., Perdomo, D. M., Fletcher, M. A., Klimas, N., & Antoni, M. H. (2018). Depression, evening salivary cortisol and inflammation in chronic fatigue syndrome: A psychoneuroendocrinological structural regression model. International Journal of Psychophysiology, 131, 124-130. https://doi.org/10.1016/j.ijpsycho.2017.09.009

@article{e6e2aec2bf2c41e4971e179215d87a8f,

title = "Depression, evening salivary cortisol and inflammation in chronic fatigue syndrome: A psychoneuroendocrinological structural regression model",

abstract = " Introduction: Chronic Fatigue Syndrome (CFS) is a poorly understood illness that is characterized by diverse somatic symptoms, hypothalamic pituitary adrenal (HPA) axis dysfunction and heightened inflammatory indicators. These symptoms are often exacerbated and accompanied by psychological distress states and depression. Since depression is known to be associated with HPA axis dysfunction and greater inflammation, a psychoneuroendocrinological (PNE) model of inflammation was examined in persons diagnosed with CFS in order to uncover underlying biopsychosocial mechanisms in this poorly understood chronic illness. Methods: Baseline data were drawn from two randomized controlled trials testing the efficacy of different forms of psychosocial intervention, and included psychological questionnaires, di-urnal salivary cortisol, and blood samples. Data were analyzed with structural equation modeling (SEM). Results: The sample (N = 265) was mostly middle-aged (M age = 49.36 ± 10.9, range = 20–73 years), Caucasian (67.7%), female (81.7%), highly educated (85.5% completed some college, college, or graduate program), and depressed (CES-D M = 23.87 ± 12.02, range 2–57). The SEM supporting a psychoneuroendocrinological model of immune dysregulation in CFS fit the data χ 2 (12) = 17.725, p = 0.1243, RMSEA = 0.043, CFI = 0.935, SRMR = 0.036. Depression was directly related to evening salivary cortisol and inflammation, such that higher evening cortisol predicted greater depressive symptoms (β = 0.215, p < 0.01) and higher pro-inflammatory cytokines (interleukin-2 [IL-2], IL-6, and tumor necrosis factor-alpha [TNF-α] levels (β = 0.185, p < 0.05), when controlling for covariates. Discussion: Results highlight the role of depression, cortisol and inflammation in possible biological mechanisms involved in the pathophysiology of CFS. Time-lagged, longitudinal analyses are needed to fully explore these relationships.",

keywords = "Chronic fatigue syndrome (CFS), Depression, Evening cortisol, Inflammation, Structural equation modeling",

author = "Milrad, {Sara F.} and Hall, {Daniel L.} and Jutagir, {Devika R.} and Lattie, {Emily G.} and Czaja, {Sara J.} and Perdomo, {Dolores M.} and Fletcher, {Mary Ann} and Nancy Klimas and Antoni, {Michael H.}",

note = "Publisher Copyright: {\textcopyright} 2017 Elsevier B.V.",

year = "2018",

month = sep,

doi = "10.1016/j.ijpsycho.2017.09.009",

language = "English (US)",

volume = "131",

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Milrad, SF, Hall, DL, Jutagir, DR, Lattie, EG, Czaja, SJ, Perdomo, DM, Fletcher, MA, Klimas, N & Antoni, MH 2018, 'Depression, evening salivary cortisol and inflammation in chronic fatigue syndrome: A psychoneuroendocrinological structural regression model', International Journal of Psychophysiology, vol. 131, pp. 124-130. https://doi.org/10.1016/j.ijpsycho.2017.09.009

TY - JOUR

T1 - Depression, evening salivary cortisol and inflammation in chronic fatigue syndrome

T2 - A psychoneuroendocrinological structural regression model

AU - Milrad, Sara F.

AU - Hall, Daniel L.

AU - Jutagir, Devika R.

AU - Lattie, Emily G.

AU - Czaja, Sara J.

AU - Perdomo, Dolores M.

AU - Fletcher, Mary Ann

AU - Klimas, Nancy

AU - Antoni, Michael H.

PY - 2018/9

Y1 - 2018/9

N2 - Introduction: Chronic Fatigue Syndrome (CFS) is a poorly understood illness that is characterized by diverse somatic symptoms, hypothalamic pituitary adrenal (HPA) axis dysfunction and heightened inflammatory indicators. These symptoms are often exacerbated and accompanied by psychological distress states and depression. Since depression is known to be associated with HPA axis dysfunction and greater inflammation, a psychoneuroendocrinological (PNE) model of inflammation was examined in persons diagnosed with CFS in order to uncover underlying biopsychosocial mechanisms in this poorly understood chronic illness. Methods: Baseline data were drawn from two randomized controlled trials testing the efficacy of different forms of psychosocial intervention, and included psychological questionnaires, di-urnal salivary cortisol, and blood samples. Data were analyzed with structural equation modeling (SEM). Results: The sample (N = 265) was mostly middle-aged (M age = 49.36 ± 10.9, range = 20–73 years), Caucasian (67.7%), female (81.7%), highly educated (85.5% completed some college, college, or graduate program), and depressed (CES-D M = 23.87 ± 12.02, range 2–57). The SEM supporting a psychoneuroendocrinological model of immune dysregulation in CFS fit the data χ 2 (12) = 17.725, p = 0.1243, RMSEA = 0.043, CFI = 0.935, SRMR = 0.036. Depression was directly related to evening salivary cortisol and inflammation, such that higher evening cortisol predicted greater depressive symptoms (β = 0.215, p < 0.01) and higher pro-inflammatory cytokines (interleukin-2 [IL-2], IL-6, and tumor necrosis factor-alpha [TNF-α] levels (β = 0.185, p < 0.05), when controlling for covariates. Discussion: Results highlight the role of depression, cortisol and inflammation in possible biological mechanisms involved in the pathophysiology of CFS. Time-lagged, longitudinal analyses are needed to fully explore these relationships.

AB - Introduction: Chronic Fatigue Syndrome (CFS) is a poorly understood illness that is characterized by diverse somatic symptoms, hypothalamic pituitary adrenal (HPA) axis dysfunction and heightened inflammatory indicators. These symptoms are often exacerbated and accompanied by psychological distress states and depression. Since depression is known to be associated with HPA axis dysfunction and greater inflammation, a psychoneuroendocrinological (PNE) model of inflammation was examined in persons diagnosed with CFS in order to uncover underlying biopsychosocial mechanisms in this poorly understood chronic illness. Methods: Baseline data were drawn from two randomized controlled trials testing the efficacy of different forms of psychosocial intervention, and included psychological questionnaires, di-urnal salivary cortisol, and blood samples. Data were analyzed with structural equation modeling (SEM). Results: The sample (N = 265) was mostly middle-aged (M age = 49.36 ± 10.9, range = 20–73 years), Caucasian (67.7%), female (81.7%), highly educated (85.5% completed some college, college, or graduate program), and depressed (CES-D M = 23.87 ± 12.02, range 2–57). The SEM supporting a psychoneuroendocrinological model of immune dysregulation in CFS fit the data χ 2 (12) = 17.725, p = 0.1243, RMSEA = 0.043, CFI = 0.935, SRMR = 0.036. Depression was directly related to evening salivary cortisol and inflammation, such that higher evening cortisol predicted greater depressive symptoms (β = 0.215, p < 0.01) and higher pro-inflammatory cytokines (interleukin-2 [IL-2], IL-6, and tumor necrosis factor-alpha [TNF-α] levels (β = 0.185, p < 0.05), when controlling for covariates. Discussion: Results highlight the role of depression, cortisol and inflammation in possible biological mechanisms involved in the pathophysiology of CFS. Time-lagged, longitudinal analyses are needed to fully explore these relationships.

KW - Chronic fatigue syndrome (CFS)

KW - Depression

KW - Evening cortisol

KW - Inflammation

KW - Structural equation modeling

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Depression, evening salivary cortisol and inflammation in chronic fatigue syndrome: A psychoneuroendocrinological structural regression model

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