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.
N1 - Funding Information:
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.
Publisher Copyright:
© 2017 Elsevier B.V.
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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U2 - 10.1016/j.ijpsycho.2017.09.009
DO - 10.1016/j.ijpsycho.2017.09.009
M3 - Article
C2 - 28918107
AN - SCOPUS:85029564678
SN - 0167-8760
VL - 131
SP - 124
EP - 130
JO - International Journal of Psychophysiology
JF - International Journal of Psychophysiology
ER -