Salivary Cortisol Response During Exposure Treatment in Driving Phobics

Alpers, Georg W.; Abelson, James L.; Wilhelm, Frank H.; Roth, Walton T.

doi:10.1097/01.psy.0000073872.85623.0c

Cited by 89 publications

(56 citation statements)

References 47 publications

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“…Further, panic attacks themselves do not lead to increased cortisol levels (Hollander et al 1989;Liebowitz et al 1985;Woods et al 1987). In driving phobics, cortisol levels are elevated one hour prior to driving exposure, without further increase during an actual driving test (Alpers et al 2003).…”

Section: A Working Hypothesis: Role Of Glucocorticoids In Anxietymentioning

confidence: 99%

“…There are numerous reports of increased physiological arousal or subjective anxiety in anxious patients during conditions of distal threat, for example, during the period that precedes a future psychological or chemical challenges (Alpers et al 2003;Braune et al 1994;Charney et al 1984;Coplan et al 1998;Hoehn et al 1997;Parente et al 2005). Similarly, mere participation in an experiment involving the future delivery of aversive stimuli can generate substantial anticipatory anxiety that can be measured with the startle reflex (Bocker et al 2004;Grillon and Ameli 1998).…”

Section: Clinical Anxietymentioning

confidence: 99%

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Models and mechanisms of anxiety: evidence from startle studies

2007

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Rationale-Preclinical data indicates that threat stimuli elicit two classes of defensive behaviors, those that are associated with imminent danger and are characterized by avoidance or fight (fear), and those that are associated with temporally uncertain danger and are characterized by sustained apprehension and hypervigilance (anxiety).Objective-To 1) review evidence for a distinction between fear and anxiety in animal and human experimental models using the startle reflex as an operational measure of aversive states, 2) describe experimental models of anxiety, as opposed to fear, in humans, 3) examine the relevance of these models to clinical anxiety.Results-The distinction between phasic fear to imminent threat and sustained anxiety to temporally uncertain danger is suggested by psychopharmacological and behavioral evidence from ethological studies and can be traced back to distinct neuroanatomical systems, the amygdala and the bed nucleus of the stria terminalis. Experimental models of anxiety, not fear, are relevant to nonphobic anxiety disorders.Conclusions-Progress in our understanding of normal and abnormal anxiety is critically dependent on our ability to model sustained aversive states to temporally uncertain threat.

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Section: A Working Hypothesis: Role Of Glucocorticoids In Anxietymentioning

confidence: 99%

Section: Clinical Anxietymentioning

confidence: 99%

Models and mechanisms of anxiety: evidence from startle studies

2007

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“…Cortisol is excreted primarily in urine in an unbound (free) form. Salivary cortisol measurement is reliable indicator of free cortisol or biologically active cortisol (Alpers et al 2003), whereas serum cortisol measurement assesses total cortisol (bound and free) (Ritsner et al 2007).…”

Section: Methodsmentioning

confidence: 99%

Increased Anxiety Level and High Salivary and Serum Cortisol Concentrations in Patients with Recurrent Aphthous Stomatitis

Albanidou-Farmaki

Poulopoulos

Epivatianos

et al. 2008

Tohoku J. Exp. Med.

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Recurrent aphthous stomatitis (RAS) is one of the most common oral mucosal disorders. The aim of the study was to determine any association between anxiety levels and concentrations of salivary and serum cortisol in patients with RAS. It has been suggested that stress with its presumed effects on the immune system, constitutes one of the major causative agents of RAS. The concentrations of salivary and serum cortisol were measured in 38 patients with recurrent aphthous stomatitis, and 38 healthy controls. Salivary and serum cortisol levels were measured using a Luminenscent Immunoassay (LIA) method. Anxiety levels were evaluated using Spielberger's State-Trait Anxiety Inventory which measures both trait anxiety as a general aspect of personality (STAI-T) and state anxiety as a response to a specific situation (STAI-S). The salivary cortisol levels were 1.44 (± 0.58) μ g dl -1 in RAS patients and 0.91 (± 0.56) μ g dl -1 in controls ( p = 0.001), while the serum cortisol levels were 3.13 (± 1.59) μ g dl -1 in RAS patients and 1.89 (± 1.11) μ g dl -1 in controls ( p = 0.001). The state anxiety levels (STAI-S) were 48.85 (± 9.7) in RAS group and 39.45 (± 7.5) in control group ( p = 0.001). The trait anxiety levels (STAI-T) were 49.78 (± 13.02) in RAS group and 38.49 (± 10.31) in control group ( p = 0.001). Salivary and serum cortisol concentrations and state and trait anxiety levels in RAS were significantly higher than those in the control group. Our results suggest that stress may be involved in the pathogenesis of RAS. recurrent aphthous stomatitis; anxiety; salivary cortisol; serum cortisol; pathogenesis.Tohoku

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“…Although it is well established that phobic stimuli trigger the release of cortisol (7)(8)(9)(10), it has not been investigated whether cortisol feeds back to influence fear symptoms. In contrast to the enhancing effects of glucocorticoids on memory consolidation (11), we have shown previously that pretest administration of glucocorticoids inhibits the retrieval of previously acquired information in animals (12) and humans (13).…”

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confidence: 99%

Glucocorticoids reduce phobic fear in humans

Soravia

Heinrichs

Aerni

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

325

245

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Phobias are characterized by excessive fear, cued by the presence or anticipation of a fearful situation. Whereas it is well established that glucocorticoids are released in fearful situations, it is not known whether these hormones, in turn, modulate perceived fear. As extensive evidence indicates that elevated glucocorticoid levels impair the retrieval of emotionally arousing information, they might also inhibit retrieval of fear memory associated with phobia and, thereby, reduce phobic fear. Here, we investigated whether acutely administrated glucocorticoids reduced phobic fear in two double-blind, placebo-controlled studies in 40 subjects with social phobia and 20 subjects with spider phobia. In the social phobia study, cortisone (25 mg) administered orally 1 h before a socioevaluative stressor significantly reduced self-reported fear during the anticipation, exposure, and recovery phase of the stressor. Moreover, the stress-induced release of cortisol in placebo-treated subjects correlated negatively with fear ratings, suggesting that endogenously released cortisol in the context of a phobic situation buffers fear symptoms. In the spider phobia study, repeated oral administration of cortisol (10 mg), but not placebo, 1 h before exposure to a spider photograph induced a progressive reduction of stimulus-induced fear. This effect was maintained when subjects were exposed to the stimulus again 2 days after the last cortisol administration, suggesting that cortisol may also have facilitated the extinction of phobic fear. Cortisol treatment did not reduce general, phobia-unrelated anxiety. In conclusion, the present findings in two distinct types of phobias indicate that glucocorticoid administration reduces phobic fear.cortisol ͉ memory ͉ cortisone ͉ extinction

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Salivary Cortisol Response During Exposure Treatment in Driving Phobics

Abstract: The data demonstrate that the HPA axis can be strongly activated by exposure to, and anticipation of, a phobic situation.

Cited by 89 publications

References 47 publications

Models and mechanisms of anxiety: evidence from startle studies

Models and mechanisms of anxiety: evidence from startle studies

Increased Anxiety Level and High Salivary and Serum Cortisol Concentrations in Patients with Recurrent Aphthous Stomatitis

Glucocorticoids reduce phobic fear in humans

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