Women with PTSD have lower basal salivary cortisol levels later in the day than do men with PTSD: A preliminary study

Freidenberg, Brian M.; Gusmano, Rebecca; Hickling, Edward J.; Blanchard, Edward B.; Bremner, J. Douglas; Frye, Cheryl A.

doi:10.1016/j.physbeh.2009.06.002

Cited by 30 publications

(17 citation statements)

References 39 publications

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“…Differences in inflammatory cytokine levels in trauma survivors with PTSD have previously been reported (Gill et al, 2009). Discrepancies may potentially reflect different degrees of HPA axis response suppression to glucocorticoid activation (Freidenberg et al, 2010), or alternatively, differences associated with the duration since the traumatic experience as well as other confounding factors. One study examining the levels of inflammatory markers within a refugee population with PTSD postulated that differences could partly be explained by a variable environmental component associated with less antigen exposure (Söndergaard et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

PTSD Blood Transcriptome Mega-Analysis: Shared Inflammatory Pathways across Biological Sex and Modes of Trauma

Breen

Tylee

Maihofer

et al. 2017

Neuropsychopharmacol.

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Transcriptome-wide screens of peripheral blood during the onset and development of posttraumatic stress disorder (PTSD) indicate widespread immune dysregulation. However, little is known as to whether biological sex and the type of traumatic event influence shared or distinct biological pathways in PTSD. We performed a combined analysis of five independent PTSD blood transcriptome studies covering seven types of trauma in 229 PTSD and 311 comparison individuals to synthesize the extant data. Analyses by trauma type revealed a clear pattern of PTSD gene expression signatures distinguishing interpersonal (IP)-related traumas from combat-related traumas. Co-expression network analyses integrated all data and identified distinct gene expression perturbations across sex and modes of trauma in PTSD, including one wound-healing module downregulated in men exposed to combat traumas, one IL-12-mediated signaling module upregulated in men exposed to IP-related traumas, and two modules associated with lipid metabolism and mitogen-activated protein kinase activity upregulated in women exposed to IP-related traumas. Remarkably, a high degree of sharing of transcriptional dysregulation across sex and modes of trauma in PTSD was also observed converging on common signaling cascades, including cytokine, innate immune, and type I interferon pathways. Collectively, these findings provide a broad view of immune dysregulation in PTSD and demonstrate inflammatory pathways of molecular convergence and specificity, which may inform mechanisms and diagnostic biomarkers for the disorder.

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Section: Discussionmentioning

confidence: 99%

PTSD Blood Transcriptome Mega-Analysis: Shared Inflammatory Pathways across Biological Sex and Modes of Trauma

Breen

Tylee

Maihofer

et al. 2017

Neuropsychopharmacol.

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“…Some have reported that women with PTSD have lower cortisol levels than their healthy counterparts, an effect not observed in men [67; 68]. Although not always replicated, these results do suggest that, in some cases, low cortisol levels distinguish women with PTSD from those without [69; 70].…”

Section: Sex Differences In Neuroendocrine Responses To Stressmentioning

confidence: 95%

Sex differences in stress-related psychiatric disorders: Neurobiological perspectives

Bangasser

Valentino

2014

Frontiers in Neuroendocrinology

558

398

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Stress is associated with the onset and severity of several psychiatric disorders that occur more frequently in women than men, including posttraumatic stress disorder (PTSD) and depression. Patients with these disorders present with dysregulation of several stress response systems, including the neuroendocrine response to stress, corticolimbic responses to negatively valenced stimuli, and hyperarousal. Thus, sex differences within their underlying circuitry may explain sex biases in disease prevalence. This review describes clinical studies that identify sex differences within the activity of these circuits, as well as preclinical studies that demonstrate cellular and molecular sex differences in stress responses systems. These studies reveal sex differences from the molecular to the systems level that increase endocrine, emotional, and arousal responses to stress in females. Exploring these sex differences is critical because this research can reveal the neurobiological underpinnings of vulnerability to stress-related psychiatric disorders and guide the development of novel pharmacotherapies.

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“…Decreased basal levels of circulating (Yehuda et al, 2005) and urinary free cortisol (Mason et al, 1986) have been described in individuals with PTSD. However, studies have also found increased or no differences in basal glucocorticoid levels (Meewisse et al, 2007) and diurnal cortisol rhythms in individuals with PTSD (Freidenberg et al, 2010;Maes et al, 1998), suggesting that other factors maybe be contributing to HPA dysregulation in PTSD, such as sex (Freidenberg et al, 2010), type and duration of trauma exposure, and severity of PTSD symptoms (Shea et al, 2005). Regardless of the equivocal nature of findings describing differences in basal cortisol levels in individuals with PTSD, more consistent are the findings that PTSD is associated with enhanced glucocorticoid negative-feedback inhibition of the HPA axis as evidenced by increased suppression of cortisol levels following a dexamethasone-suppression test (Yehuda et al, 1995).…”

Section: Mechanisms Of Increased Inflammation In Fearand Anxiety-basementioning

confidence: 99%

Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond

Michopoulos

Powers

Gillespie

et al. 2016

Neuropsychopharmacol

520

376

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The study of inflammation in fear-and anxiety-based disorders has gained interest as growing literature indicates that proinflammatory markers can directly modulate affective behavior. Indeed, heightened concentrations of inflammatory signals, including cytokines and C-reactive protein, have been described in posttraumatic stress disorder (PTSD), generalized anxiety disorder (GAD), panic disorder (PD), and phobias (agoraphobia, social phobia, etc.). However, not all reports indicate a positive association between inflammation and fear-and anxiety-based symptoms, suggesting that other factors are important in future assessments of inflammation's role in the maintenance of these disorders (ie, sex, co-morbid conditions, types of trauma exposure, and behavioral sources of inflammation). The most parsimonious explanation of increased inflammation in PTSD, GAD, PD, and phobias is via the activation of the stress response and central and peripheral immune cells to release cytokines. Dysregulation of the stress axis in the face of increased sympathetic tone and decreased parasympathetic activity characteristic of anxiety disorders could further augment inflammation and contribute to increased symptoms by having direct effects on brain regions critical for the regulation of fear and anxiety (such as the prefrontal cortex, insula, amygdala, and hippocampus). Taken together, the available data suggest that targeting inflammation may serve as a potential therapeutic target for treating these fear-and anxiety-based disorders in the future. However, the field must continue to characterize the specific role pro-inflammatory signaling in the maintenance of these unique psychiatric conditions.

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Women with PTSD have lower basal salivary cortisol levels later in the day than do men with PTSD: A preliminary study

Cited by 30 publications

References 39 publications

PTSD Blood Transcriptome Mega-Analysis: Shared Inflammatory Pathways across Biological Sex and Modes of Trauma

PTSD Blood Transcriptome Mega-Analysis: Shared Inflammatory Pathways across Biological Sex and Modes of Trauma

Sex differences in stress-related psychiatric disorders: Neurobiological perspectives

Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond

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