Elsevier

Journal of Psychiatric Research

Volume 96, January 2018, Pages 189-195
Journal of Psychiatric Research

An exploratory study of salivary cortisol changes during chamomile extract therapy of moderate to severe generalized anxiety disorder

https://doi.org/10.1016/j.jpsychires.2017.10.011Get rights and content

Abstract

Objectives

Dysfunctions in stress biology are hypothesized to contribute to anxiety disorders, and to be ameliorated during successful treatment, but limited clinical data exist to support this hypothesis. We evaluated whether increases in morning cortisol and the diurnal cortisol slope, markers of stress biology, are associated with clinical response to chamomile therapy among subjects with generalized anxiety disorder (GAD).

Methods

Among 45 subjects with DSM-IV diagnosed GAD in an open-label clinical trial of chamomile, salivary cortisol was assessed for three days each pre- and post-treatment, at 8am, 12pm, 4pm, and 8pm. Mixed model analyses assessed whether GAD symptom change predicted the degree to which cortisol levels changed during treatment.

Results

Symptom improvement during treatment was significantly associated with pre-to-post treatment changes in cortisol. Subjects who experienced more symptomatic improvement experienced significant increases in their morning salivary cortisol (β = 0.48, p < 0.001), and a greater decrease in cortisol from morning to the rest of the day (β = 0.55, p < 0.001). In addition, at baseline a lower cortisol level (β = −0.24, p = 0.023) and a lesser decrease in cortisol after morning (β = 0.30, p = 0.003) were associated with greater symptomatic improvement.

Conclusion

Increases in morning salivary cortisol and the diurnal cortisol slope are associated with symptom improvement in chamomile treatment of GAD. Response to treatment for GAD could partially stem from normalization of stress biology dysfunction, but further work involving establishing abnormalities within-sample, ruling out of confounds (e.g., sleep), and a placebo control is necessary to conclude an amelioration effect.

Registration code

NCT01072344.

Section snippets

Subjects

Subjects were adults (>18 years) with a DSM-IV diagnosis of GAD as a primary disorder recruited from a psychiatric clinic at a major research hospital and from primary care practices. All diagnoses were determined using the MINI-SCID/P structured interview to assess for the presence of specific DSM-IV Axis I disorders (First et al., 2001). Discrepancies in diagnostic assessment for inclusion into the study were resolved by conferencing and consensus between the investigators of the trial.

Demographics and clinical information on subject subsample with CORT measurements

Forty-five subjects were trial completers with pre- and post-treatment measurements of salivary cortisol, and four subjects did not have usable post-treatment cortisol measurements. Of these subjects, two were lost to follow-up, one was withdrawn from the trial due to an unstable preexisting medical condition, and one was withdrawn due to medication non-compliance. The average subject in this subsample experienced a change of 9.4 (SD 5.5) points on the GAD-7, which was the outcome criterion

Discussion

While many researchers hypothesize that stress biology dysregulation is implicated in the etiology of GAD, few data exist to support a relationship between stress biology and clinical response to psychopharmacological drugs (Bandelow et al., 2016, Elnazer and Baldwin, 2014). In this exploratory investigation conducted in the context of a trial of chamomile for patients with GAD, we found that greater symptom improvement was associated with pre-to-post treatment increases in morning cortisol

Disclosures

None of the authors declare any conflicts of interest as regards this manuscript. The parent clinical trial for this study was funded by an NIH/NCCAM R01 grant (AT005074) to Jun J. Mao. This research was also funded in part through the NIH/NCI Cancer Center Support Grant P30 CA008748 and by the Rockefeller Translational and Integrative Medicine Research Fund at the Memorial Sloan-Kettering Cancer Center.

Acknowledgements

We would like to thank Dr. Bernard Carroll for his helpful commentary and review of an earlier version of this manuscript.

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