Skip to main content
NCBI home page
NIHPA Author Manuscripts logoLink to NIHPA Author Manuscripts
. Author manuscript; available in PMC: 2014 Aug 1.
Published in final edited form as: J Clin Psychopharmacol. 2013 Aug;33(4):556–560. doi: 10.1097/JCP.0b013e3182968962

The association of dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS) with anxiety sensitivity and electronic diary negative affect among smokers with and without posttraumatic stress disorder

Elizabeth E Van Voorhees 1,2,3, Michelle F Dennis 3, F Joseph McClernon 1,2,3, Patrick S Calhoun 1,2,3, Natalie A Buse 3, Jean C Beckham 1,2,3
PMCID: PMC3896952  NIHMSID: NIHMS538654  PMID: 23771199

Abstract

Posttraumatic stress disorder (PTSD) is associated with increased smoking initiation, maintenance and relapse. Dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS) are neurosteroids that have been associated with mood measures as well as smoking status, and nicotine is associated with increased DHEA and DHEAS levels. Given the difficulties with mood experienced by smokers with PTSD, the purpose of the current study was to evaluate the association between negative affect and anxiety sensitivity with DHEA and DHEAS levels. Ninety-six smokers with and without PTSD provided blood samples for neurosteroid analyses, and completed self-report measures of anxiety sensitivity and electronic diary ratings of negative affect. As expected, PTSD smokers reported higher levels of anxiety sensitivity (F[1,94]=20.67, partial η2= 0.18, p<.0001) and negative affect (F[1,91]=7.98, partial η2= .08, p=.006). After accounting for age and gender, DHEAS was significantly inversely associated with both anxiety sensitivity (F[3,92]=6.97, partial η2= 0.07, p=.01) and negative affect (F[3,87]=10.52, partial η2= 0.11, p=.002) across groups. Effect sizes indicated that these effects are moderate to high. No significant interactions of diagnosis and DHEA(S) levels with mood measures were detected. Given that nicotine is known to elevate DHEA(S) levels, these results suggest that DHEAS may serve as a biomarker of the association between mood and nicotine among smokers. Implications for the results include 1) the use of DHEAS measurement across time and across quit attempts; and 2) the potential for careful use of DHEA supplementation to facilitate abstinence during smoking cessation.

Posttraumatic stress disorder (PTSD) is significantly associated with smoking initiation and maintenance 1,2. Individuals with posttraumatic stress disorder (PTSD) endorse rates two to three times higher of smoking and heavy smoking, and have more difficultly quitting than non-PTSD samples 3,4. Research has implicated the hypothalamic-pituitary-adrenal (HPA) axis in both PTSD and smoking, suggesting that acute and chronic smoking-related HPA axis changes may be related to nicotine dependence 5–10, and particularly to the higher addiction vulnerability among those with PTSD 11.

Dehydroepiandrosterone (DHEA) and its sulfated metabolite DHEAS (often referred to together as DHEA[S]) are neuroendocrine hormones of the HPA axis that appear to have protective antiglucocorticoid effects on brain functioning upon exposure to severe or chronic stress 12,13. Higher DHEA(S) levels have been associated with increased resiliency or coping among individuals with PTSD 14–16 and cocaine dependence 17. There is some evidence that supplementation with DHEA may improve mood in individuals with depression 18,19.

Studies have demonstrated that baseline DHEA(S) levels are higher in smokers than non-smokers 11,20,21, and that acute smoking of a single cigarette induces increases in DHEA that are greater than those observed after weeks of DHEA supplementation treatment for depression 8,18. In one study with 28 male smokers, DHEAS was significantly inversely correlated with the negative affect subscale of a smoking withdrawal measure and a craving item 6, and in another study DHEA levels were found to drop 18% in postsmenopausal smokers 6 weeks after smoking cessation 9. PTSD and smoking relapse during quit attempts are both associated with anxiety sensitivity and high negative affect 5,22–26, and expectations of relief from negative affect are associated with smoking relapse in those high in anxiety sensitivity generally 27 and in those with PTSD specifically 28,29.

Given the association of DHEA(S) with lower negative affect, improved mood, and smoking 6–9,19,30, and the positive association of DHEA(S) levels and coping among those with PTSD 13–16, it is possible that smoking-induced increases in DHEA(S) contribute to higher levels of smoking and greater difficulty quitting in individuals with PTSD. The following hypotheses were developed to test in a sample of PTSD and non-PTSD smokers: 1) PTSD status will be associated with increased anxiety sensitivity and negative affect; 2) DHEA and DHEAS will be negatively related to anxiety sensitivity and negative affect; and 3) there will be an interaction of PTSD and neurosteroid levels, such that compared to those without PTSD, smokers with PTSD will have a stronger negative association between DHEA and DHEAS, and anxiety sensitivity and negative affect.

Materials and Methods

Participants and Procedures

Data presented here are baseline measures administered as part of a larger smoking cessation study investigating mechanisms of relapse in smokers with and without PTSD. Neuroendocrine and anxiety sensitivity measures were available for 41 smokers with PTSD and 55 smokers without PTSD; of these participants, five did not have electronic diary negative affect data. Eligible participants were between 18 and 65 years of age and currently smoking at least10 cigarettes/day. Because the larger smoking cessation study focused on a counseling intervention (Beckham et al., 2012), participants were excluded if they were using non-cigarette forms of nicotine or bupropion. In addition, participants were excluded for major unstable medical problems (because this could affect quitting smoking); using non-cigarette forms of nicotine; current alcohol or drug abuse/dependence (as this can effect smoking craving and behavior); schizophrenia or current manic syndrome (as these psychiatric disorders are associated with additional difficulty with quitting smoking); and lifetime but not current PTSD (because these individuals would not have been representative of a non-PTSD group). In addition, because acoustic startle responses and prepulse inhibition measures were evaluated in the larger trial, individuals with current benzodiazepine use were excluded. This study was approved by the Durham Veterans Affairs Institutional Review Board (IRB) and Research and Development Committees and the Duke University School of Medicine IRB.

Measures

Clinician-Administered PTSD Scale (CAPS) and Structured Clinical Interview for DSM-IV Disorders (SCID)

The CAPS 31 was used to determine PTSD diagnosis during a screening visit. This instrument is a clinical structured interview that is considered the “gold standard” for PTSD assessment. PTSD symptoms were considered present based on the CAPS frequency ≥1/intensity ≥2 rule 31,32. The Structured Clinical Interview for DSM-IV33 was used to determine Major Depressive Disorder (MDD) diagnosis. The CAPS and the SCID were administered by clinical raters trained using standardized SCID training. Inter-rater reliability for diagnoses based on videotapes of patient interviews was high (kappa = .96).

The Anxiety Sensitivity Index-R (ASI)

The ASI-R 34 is a 36-item measure that assesses an individual's concerns about the emotional and physical consequences of experiencing anxiety symptoms. Participants rate each item on a 5-point Likert scale, with total scores ranging from 0 to 144. AS is considered to be a stable endophenotypic trait associated with the development of anxiety disorders 35. The ASI has demonstrated excellent psychometric properties in both clinical and nonclinical samples 34,36–39. The ASI-R was administered at the baseline visit.

Positive and Negative Affect Schedule (PANAS)

Negative affect was measured over a 7-day baseline using the PANAS 40,41, a10-item positive affect and 10-item negative affect scale designed to measure both types of affect. The two scales are largely uncorrelated with one another and are reliable over a two-month period 40. Participants used electronic diaries to complete mood ratings several times daily upon randomly administered alarm cues, for an average of 22 PANAS ratings over the 7 days (range of 1 to 49 ratings, SD = 11.2).

Fagerström Test of Nicotine Dependence (FTND)

Baseline nicotine dependence was assessed with the FTND, which has been shown to be a valid assessment of heaviness of smoking as reflected in biochemical measures such as cotinine levels 42.

Endocrine testing

Blood for serum analyses was drawn between 10am and 2pm on the day of screening. Samples were centrifuged at 3000 rpm for 15 minutes and frozen within 60 minutes of venipuncture, and were stored in at −80 degree C until they were shipped on dry ice to the Clinical Assay Ligand Service Satellite (CLASS) Laboratory in the School of Public Health, Department of Epidemiology, at the University of Michigan for analysis.

DHEAS levels were measured using the ADVIA Centaur DHEA-S assay, a competitive immunoassay using direct chemiluminescent technology. CLASS lab DHEAS analyses are automated and are therefore conducted in singleton; in-house intra- and inter-assay CV’s for DHEAS are between 3.2% - 6.5% and 3.3% - 5.8%, respectively. Plasma DHEA samples were analyzed in duplicate using the DRG DHEA ELISA Kit, a solid phase enzyme-linked immunosorbent assay (ELISA); intra-assay CV for DHEA was 4.5%.

Statistical Analysis

Log transformations were used to normalize the distributions for DHEA and DHEAS. General linear models were used to evaluate all hypotheses. Both DHEA and DHEAS are age and gender dependent: secretion levels of both hormones decline from early adulthood through old age, and the ratio of DHEA to DHEAS is higher in women than in men 12. Therefore, age and gender were entered as covariates in all models. Bonferroni corrections were applied to account for multiple comparisons, and p<.0125 (.05/4 comparisons) was adopted as the significance threshold.

To test hypothesis 1, two general linear models (GLM) were conducted with age and gender as covariates and PTSD status as the independent variable. For the first model the outcome variable was the total ASI score, and for the second the outcome variable was the total PANAS negative affect score. To test hypothesis 2, two GLM analyses with age and gender as covariates, and DHEA as the independent variable were conducted: in the first model total ASI score was the dependent variable, and in the second mean negative affect across the seven days was the dependent variable. The same models were then re-run with DHEAS as the independent variable. As a test of hypothesis 3, the models were re-run with the addition of the interaction term of PTSD × DHEA and PTSD × DHEAS.

Results

Clinical and Demographic Characteristics

Gender distribution, age, minority status, education level, employment status, and veteran status are presented in Table 1. No significant differences were detected between participants with and without PTSD on these variables other than employment status. Most participants in the sample had experienced at least one significant trauma accompanied by fear, helplessness, and horror at some time in their lives; however, participants with PTSD had experienced significantly more such traumas compared to those without.

Table 1.

Demographics and Clinical Characteristics

PTSD (n=41) W/out PTSD (n=55) Test Statistic Effect Size
Gender (female) 51.2% 41.8% Χ2=.83, p=.36, ns V=.09
Age (years) 42.9 (9.5) 41.9 (10.0) t=−.48, p=.63, ns d=.10
Minority 70.7% 69.1% χ2=.03, p=.86, ns V=.02
Education 12.3 (1.8) 12.6 (2.9) t=.50, p=.62, ns d=−.12
Employed 34.1% 60% χ2=6.3, p=.01 V=−.26
Veteran 26.8% 21.8% χ2=.32, p=.57, ns V=.06
# Trauma types with fear, helplessness, or horror 9.8 (3.4) 4.4 (3.9) t=−7.08, p<.0001 d=1.48
Current MDD diagnosis 26.8% 3.6% χ2=10.8, p=.001 V=.34
FTND score 6.0 (1.9) 5.3 (2.1) t=−1.47, p=.14, ns d=.35
ASI Total score 69.2 (32.8) 38.3 (32.9) t=−4.55, p<.0001 d=.94
Negative affect 14.2 (4.3) 12.0 (3.0) t=−2.7, p=.001 d=.59
DHEA level* 5.8 (3.3) 6.5 (3.4) t=.98, p=.33, ns d=−.21
DHEAS level* 139.5 (73.9) 180.7 (110.7) t=.97, p=.33, ns d=−.44
Open in a new tab
*

DHEA and DHEAS levels reported here are raw values; statistical analyses to address hypotheses were conducted on log values.

Key clinical characteristics and mean hormone levels for PTSD and non-PTSD groups are also presented in Table 1. Participants with PTSD were significantly more likely to have current MDD, though no significant differences were observed between the groups on comorbid anxiety disorder diagnoses. As expected, the PTSD group had significantly higher scores for ASI Total and PANAS negative affect. There were no significant differences in FTND scores, and the groups did not differ on DHEA or DHEAS levels. As DHEA(S) may be impacted by antidepressant use 43 and possibly by lifetime substance use via dopamanergic mechanisms 44, we examined the correlation of DHEA and DHEAS levels with these two variables (22% of the sample endorsed current antidepressant use; 50% of the sample met lifetime criteria for substance abuse/dependence). These correlations failed to be significant.

Results examining the association of DHEA(S) with anxiety sensitivity and negative affect revealed that after accounting for age and gender, DHEAS was significantly associated with both ASI total score, F(3,92)=6.97, partial η2= 0.07, p=.01, and with PANAS negative affect, F(3,87)=10.52, partial η2= 0.11, p=.002. DHEA was associated with PANAS negative affect, F(3,87)=6.25, partial η2= 0.07, p=.014, but this did not survive Bonferroni corrections. DHEA was not significantly associated with ASI total score.

The hypothesis that there would be a stronger negative association of DHEA(S) with anxiety sensitivity and negative affect among participants with PTSD was not supported. Consistent with the significant differences in means reported in Table 1, GLM analyses revealed significant main effects in the association between PTSD and ASI total score, F(1,94)=20.67, partial η2= 0.18, p<.0001, and between PTSD and PANAS negative affect, F(1,91)=7.98, partial η2= .08, p=.006. Those with PTSD reported higher anxiety sensitivity and experienced more negative affect during the baseline monitoring period than those without PTSD. Though there was an interaction between DHEA and PTSD and ASI sensitivity (p=.02), this did not survive Bonferroni corrections. No other interactions were detected.

Discussion

This study examined the association of dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS) with anxiety sensitivity and negative affect in smokers with and without PTSD. As predicted, PTSD was positively associated with both anxiety sensitivity and negative affect, and DHEAS levels were significantly inversely associated with anxiety sensitivity and negative affect. Effect sizes were in the moderate to high range 45. However, the interaction hypothesis was not supported: The negative association between DHEAS, anxiety sensitivity and negative affect was similar across both PTSD and non-PTSD smoker groups. DHEA levels were not significantly associated with either of the mood measures after Bonferroni corrections.

The observation that PTSD was positively associated with anxiety sensitivity and negative affect in smokers replicates previous findings 46,47. Among all smokers, the negative association of DHEAS with anxiety sensitivity and negative affect is consistent with and extends previous findings of an inverse relationship between DHEAS and the negative affect scale of a smoking withdrawal measure 6. Taken together, these findings suggest that DHEAS levels may be associated with increased coping among smokers. Increased DHEA(S) levels and associated improvement in functioning have been observed in response to both psychotherapy and DHEA supplementation. As cigarette smoking is related to increased DHEA(S) levels 7, DHEAS elevations may reflect one of the reinforcing effects of smoking.

Contrary to hypotheses, DHEA(S) levels were not more strongly inversely associated with mood measures in smokers with versus without PTSD. This suggests that smokers use smoking to improve mood across a range of dimensions and levels of functioning, and that this is not limited to those who meet a clinical threshold. Such an interpretation would be consistent with findings of the association of smoking with subthreshold symptoms of attention-deficit/hyperactivity disorder, which is also linked to high rates of nicotine dependence 48. As such, smokers with subthreshold symptoms of a range of psychiatric disorders may derive mood-related benefits associated with smoking-related elevations in DHEA(S) levels. Taken together, these results and the literature suggest that DHEA(S) may serve as a biomarker for the association of nicotine and mood across smokers, and that varying levels are quantitative rather than qualitative.

Inverse correlations of negative affect and craving with DHEA levels in smokers have led researchers to suggest that supplementation with DHEA may help mitigate mood-related withdrawal symptoms in smokers during a cessation attempt 6. Our findings support this conclusion. However, the timing and context of DHEA supplementation may be important if used to facilitate abstinence. For example, DHEA supplementation with individuals in an outpatient cocaine dependence treatment program resulted in increased cocaine use, and the authors suggested that this may have been due to the augmentation by DHEA of cocaine’s euphoric effects during lapses 49. As such, it will be important to determine whether such effects also occur with nicotine, and to carefully consider when and under what circumstances DHEA may be helpful or harmful in the treatment of nicotine dependence.

Though we found DHEAS levels to be inversely associated with both negative affect and anxiety sensitivity, we did not find an association of DHEA levels with our mood measures. Circulating levels of DHEAS are 250 times higher than levels of DHEA in women, and 500 times higher than levels of DHEA in men 12, potentially allowing for a more sensitive measure of association. As such, DHEAS may be a more sensitive biomarker of mood among smokers than DHEA.

These findings must be considered in light of the study’s limitations. Even though the DHEA(S) measurement was restricted to a four hour window, it is possible that there was unintended diurnal variation during the restricted time period. Other variables known to affect DHEA(S), such as exercise 50 and previous treatment with serotonergic compounds 51, were unavailable for evaluation. Further, because there are varying trajectories associated with PTSD 52, different PTSD symptom patterns across time could potentially have some effect on the associations reported here. In future research it may be useful to monitor DHEA(S) levels across baseline smoking, quit attempts and relapse periods to determine how the association may vary. Finally, it could be helpful to investigate DHEA(S) supplementation and the effect of antidepressant medications on the association between DHEA(S) and negative affect/anxiety sensitivity to explore improved methods for smoking cessation interventions.

Acknowledgements

Preparation of this work was supported by the National Cancer Institute (2R01CA081595); the National Institute on Drug Abuse (2K24DA016388); the Durham, NC Veterans Affairs Medical Center; and the Department of Veterans Affairs office of Research and Development Clinical Science. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Cancer Institute or the National Institutes of Health, the Department of Veterans Affairs, or the United States Government.

Footnotes

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

References

  • 1.Feldner MT, Babson KA, Zvolensky MJ. Smoking, traumatic event exposure, and post-traumatic stress: a critical review of the empirical literature. Clin Psychol Rev. 2007 Jan;27(1):14–45. doi: 10.1016/j.cpr.2006.08.004. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2.Fu SS, McFall M, Saxon AJ, et al. Post-traumatic stress disorder and smoking: a systematic review. Nicotine Tob Res. 2007 Nov;9(11):1071–1084. doi: 10.1080/14622200701488418. [DOI] [PubMed] [Google Scholar]
  • 3.Beckham JC, Roodman AA, Shipley RH, et al. Smoking in Vietnam combat veterans with posttraumatic stress disorder. J Trauma Stress. 1995 Jul;8(3):461–472. doi: 10.1007/BF02102970. [DOI] [PubMed] [Google Scholar]
  • 4.Breslau N, Davis GC, Schultz LR. Posttraumatic stress disorder and the incidence of nicotine, alcohol, and other drug disorders in persons who have experienced trauma. Arch Gen Psychiatry. 2003 Mar;60(3):289–294. doi: 10.1001/archpsyc.60.3.289. [DOI] [PubMed] [Google Scholar]
  • 5.Evatt DP, Kassel JD. Smoking, arousal, and affect: the role of anxiety sensitivity. J Anxiety Disord. 2010 Jan;24(1):114–123. doi: 10.1016/j.janxdis.2009.09.006. [DOI] [PubMed] [Google Scholar]
  • 6.Marx CE, Trost WT, Shampine L, et al. Neuroactive steroids, negative affect, and nicotine dependence severity in male smokers. Psychopharmacology (Berl) 2006 Jun;186(3):462–472. doi: 10.1007/s00213-005-0226-x. [DOI] [PubMed] [Google Scholar]
  • 7.Mello NK. Hormones, nicotine, and cocaine: clinical studies. Horm Behav. 2010 Jun;58(1):57–71. doi: 10.1016/j.yhbeh.2009.10.003. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8.Mendelson JH, Sholar MB, Goletiani N, et al. Effects of low- and high-nicotine cigarette smoking on mood states and the HPA axis in men. Neuropsychopharmacology. 2005 Sep;30(9):1751–1763. doi: 10.1038/sj.npp.1300753. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.Oncken C, Prestwood K, Cooney JL, et al. Effects of smoking cessation or reduction on hormone profiles and bone turnover in postmenopausal women. Nicotine Tob Res. 2002 Nov;4(4):451–458. doi: 10.1080/1462220021000018399. [DOI] [PubMed] [Google Scholar]
  • 10.Rasmusson AM, Wu R, Paliwal P, et al. A decrease in the plasma DHEA to cortisol ratio during smoking abstinence may predict relapse: a preliminary study. Psychopharmacology (Berl) 2006 Jun;186(3):473–480. doi: 10.1007/s00213-006-0367-6. [DOI] [PubMed] [Google Scholar]
  • 11.Rasmusson AM, Picciotto MR, Krishnan-Sarin S. Smoking as a complex but critical covariate in neurobiological studies of posttraumatic stress disorders: a review. J Psychopharmacol. 2006 Sep;20(5):693–707. doi: 10.1177/0269881106060193. [DOI] [PubMed] [Google Scholar]
  • 12.Kroboth PD, Salek FS, Pittenger AL, et al. DHEA and DHEA-S: a review. J Clin Pharmacol. 1999 Apr;39(4):327–348. doi: 10.1177/00912709922007903. [DOI] [PubMed] [Google Scholar]
  • 13.Maninger N, Wolkowitz OM, Reus VI, et al. Neurobiological and neuropsychiatric effects of dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS) Front Neuroendocrinol. 2009 Jan;30(1):65–91. doi: 10.1016/j.yfrne.2008.11.002. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14.Olff M, de Vries GJ, Guzelcan Y, et al. Changes in cortisol and DHEA plasma levels after psychotherapy for PTSD. Psychoneuroendocrinology. 2007 Jul;32(6):619–626. doi: 10.1016/j.psyneuen.2007.04.001. [DOI] [PubMed] [Google Scholar]
  • 15.Rasmusson AM, Vasek J, Lipschitz DS, et al. An increased capacity for adrenal DHEA release is associated with decreased avoidance and negative mood symptoms in women with PTSD. Neuropsychopharmacology. 2004 Aug;29(8):1546–1557. doi: 10.1038/sj.npp.1300432. [DOI] [PubMed] [Google Scholar]
  • 16.Yehuda R, Brand SR, Golier JA, et al. Clinical correlates of DHEA associated with post-traumatic stress disorder. Acta Psychiatr Scand. 2006 Sep;114(3):187–193. doi: 10.1111/j.1600-0447.2006.00801.x. [DOI] [PubMed] [Google Scholar]
  • 17.Wilkins JN, Majewska MD, Van Gorp W, et al. DHEAS and POMS measures identify cocaine dependence treatment outcome. Psychoneuroendocrinology. 2005 Jan;30(1):18–28. doi: 10.1016/j.psyneuen.2004.04.006. [DOI] [PubMed] [Google Scholar]
  • 18.Schmidt PJ, Daly RC, Bloch M, et al. Dehydroepiandrosterone monotherapy in midlife-onset major and minor depression. Arch Gen Psychiatry. 2005 Feb;62(2):154–162. doi: 10.1001/archpsyc.62.2.154. [DOI] [PubMed] [Google Scholar]
  • 19.Wolkowitz OM, Reus VI, Keebler A, et al. Double-blind treatment of major depression with dehydroepiandrosterone. Am J Psychiatry. 1999 Apr;156(4):646–649. doi: 10.1176/ajp.156.4.646. [DOI] [PubMed] [Google Scholar]
  • 20.Baron JA, Comi RJ, Cryns V, et al. The effect of cigarette smoking on adrenal cortical hormones. J Pharmacol Exp Ther. 1995 Jan;272(1):151–155. [PubMed] [Google Scholar]
  • 21.Field C. Examining factors that influence the uptake of smoking in women. Br J Nurs. 2008 Aug-Sep;17(15):980–985. doi: 10.12968/bjon.2008.17.15.30703. [DOI] [PubMed] [Google Scholar]
  • 22.Ceballos NA, al'Absi M. Dehydroepiandrosterone sulfate, cortisol, mood state and smoking cessation: relationship to relapse status at 4-week follow-up. Pharmacol Biochem Behav. 2006 Sep;85(1):23–28. doi: 10.1016/j.pbb.2006.06.021. [DOI] [PubMed] [Google Scholar]
  • 23.Cook JW, McFall MM, Calhoun PS, et al. Posttraumatic stress disorder and smoking relapse: A theoretical model. J Trauma Stress. 2007 Dec;20(6):989–998. doi: 10.1002/jts.20275. [DOI] [PubMed] [Google Scholar]
  • 24.Perkins KA, Karelitz JL, Giedgowd GE, et al. Differences in negative mood-induced smoking reinforcement due to distress tolerance, anxiety sensitivity, and depression history. Psychopharmacology (Berl) 2010 May;210(1):25–34. doi: 10.1007/s00213-010-1811-1. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 25.Shiffman S, Waters AJ. Negative affect and smoking lapses: a prospective analysis. J Consult Clin Psychol. 2004 Apr;72(2):192–201. doi: 10.1037/0022-006X.72.2.192. [DOI] [PubMed] [Google Scholar]
  • 26.Berenz EC, Vujanovic AA, Coffey SF, et al. Anxiety sensitivity and breath-holding duration in relation to PTSD symptom severity among trauma exposed adults. J Anxiety Disord. 2012;26(1):134–139. doi: 10.1016/j.janxdis.2011.10.004. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 27.Zvolensky MJ, Stewart SH, Vujanovic AA, et al. Anxiety sensitivity and anxiety and depressive symptoms in the prediction of early smoking lapse and relapse during smoking cessation treatment. Nicotine Tob Res. 2009 Mar;11(3):323–331. doi: 10.1093/ntr/ntn037. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 28.Calhoun PS, Levin HF, Dedert EA, et al. The relationship between posttraumatic stress disorder and smoking outcome expectancies among U.S. military veterans who served since September 11 2001. J Trauma Stress. 2011 Jun;24(3):303–308. doi: 10.1002/jts.20634. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 29.Carmody TP, McFall M, Saxon AJ, et al. Smoking Outcome Expectancies in Military Veteran Smokers With Posttraumatic Stress Disorder. Nicotine Tob Res. doi: 10.1093/ntr/ntr304. [published online ahead of print Jan 23 2012] [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 30.Morales AJ, Nolan JJ, Nelson JC, et al. Effects of replacement dose of dehydroepiandrosterone in men and women of advancing age. J Clin Endocrinol Metab. 1994 Jun;78(6):1360–1367. doi: 10.1210/jcem.78.6.7515387. [DOI] [PubMed] [Google Scholar]
  • 31.Blake DD, Weathers FW, Nagy LM, et al. The development of a Clinician-Administered PTSD Scale. J Trauma Stress. 1995 Jan;8(1):75–90. doi: 10.1007/BF02105408. [DOI] [PubMed] [Google Scholar]
  • 32.Weathers FW, Keane TM, Davidson JR. Clinician-administered PTSD scale: a review of the first ten years of research. Depress Anxiety. 2001;13(3):132–156. doi: 10.1002/da.1029. [DOI] [PubMed] [Google Scholar]
  • 33.First MB, Spitzer RL, Williams JBW, et al. Structured Clinical Interview for DSM-IV-TR (SCID-I)- Research Version. New York: Biometrics Research; 2002. [Google Scholar]
  • 34.Deacon BJ, Abramowitz JS, Woods CM, et al. The Anxiety Sensitivity Index - Revised: psychometric properties and factor structure in two nonclinical samples. Behav Res Ther. 2003 Dec;41(12):1427–1449. doi: 10.1016/s0005-7967(03)00065-2. [DOI] [PubMed] [Google Scholar]
  • 35.Stein MB, Schork NJ, Gelernter J. Gene-by-environment (serotonin transporter and childhood maltreatment) interaction for anxiety sensitivity, an intermediate phenotype for anxiety disorders. Neuropsychopharmacology. 2008 Jan;33(2):312–319. doi: 10.1038/sj.npp.1301422. [DOI] [PubMed] [Google Scholar]
  • 36.Maller RG, Reiss S. Anxiety sensitivity in 1984 and panic attacks in 1987. J Anxiety Disord. 1992;6(3):241–247. [Google Scholar]
  • 37.Taylor S, Cox BJ. An expanded anxiety sensitivity index: evidence for a hierarchic structure in a clinical sample. J Anxiety Disord. 1998 Sep-Oct;12(5):463–483. doi: 10.1016/s0887-6185(98)00028-0. [DOI] [PubMed] [Google Scholar]
  • 38.Telch MJ, Lucas JA, Nelson P. Nonclinical panic in college students: an investigation of prevalence and symptomatology. J Abnorm Psychol. 1989 Aug;98(3):300–306. doi: 10.1037//0021-843x.98.3.300. [DOI] [PubMed] [Google Scholar]
  • 39.Peterson RA, Reiss S. Test manual for the Anxiety Sensitivity Index. Orlando Park, IL: International Diagnostic Systems; 1992. [Google Scholar]
  • 40.Watson D, Clark LA, Carey G. Positive and negative affectivity and their relation to anxiety and depressive disorders. J Abnorm Psychol. 1988 Aug;97(3):346–353. doi: 10.1037//0021-843x.97.3.346. [DOI] [PubMed] [Google Scholar]
  • 41.Watson D, Clark LA, Tellegen A. Development and validation of brief measures of positive and negative affect: the PANAS scales. J Pers Soc Psychol. 1988 Jun;54(6):1063–1070. doi: 10.1037//0022-3514.54.6.1063. [DOI] [PubMed] [Google Scholar]
  • 42.Heatherton TF, Kozlowski LT, Frecker RC, et al. The Fagerstrom Test for Nicotine Dependence: a revision of the Fagerstrom Tolerance Questionnaire. Br J Addict. 1991 Sep;86(9):1119–1127. doi: 10.1111/j.1360-0443.1991.tb01879.x. [DOI] [PubMed] [Google Scholar]
  • 43.Deuschle M, Luppa P, Gilles M, et al. Antidepressant treatment and dehydroepiandrosterone sulfate: different effects of amitriptyline and paroxetine. Neuropsychobiology. 2004;50(3):252–256. doi: 10.1159/000079980. [DOI] [PubMed] [Google Scholar]
  • 44.Van den Berghe G, de Zegher F, Wouters P, et al. Dehydroepiandrosterone sulphate in critical illness: effect of dopamine. Clin Endocrinol (Oxf) 1995 Oct;43(4):457–463. doi: 10.1111/j.1365-2265.1995.tb02618.x. [DOI] [PubMed] [Google Scholar]
  • 45.Cohen J. Statistical Power Analysis for the Behavioral Sciences. 2nd ed. Hillsdale, New Jersey: Lawrence Erlbaum Associates; 1988. [Google Scholar]
  • 46.Beckham JC, Feldman ME, Vrana SR, et al. Immediate antecedents of cigarette smoking in smokers with and without posttraumatic stress disorder: a preliminary study. Exp Clin Psychopharmacol. 2005 Aug;13(3):219–228. doi: 10.1037/1064-1297.13.3.219. [DOI] [PubMed] [Google Scholar]
  • 47.Beckham JC, Wiley MT, Miller SC, et al. Ad lib smoking in post-traumatic stress disorder: An electronic diary study. Nicotine Tob Res. 2008 Jul;10(7):1149–1157. doi: 10.1080/14622200802123302. [DOI] [PubMed] [Google Scholar]
  • 48.Kollins SH, McClernon FJ, Fuemmeler BF. Association between smoking and attentiondeficit/ hyperactivity disorder symptoms in a population-based sample of young adults. Arch Gen Psychiatry. 2005 Oct;62(10):1142–1147. doi: 10.1001/archpsyc.62.10.1142. [DOI] [PubMed] [Google Scholar]
  • 49.Shoptaw S, Majewska MD, Wilkins J, et al. Participants receiving dehydroepiandrosterone during treatment for cocaine dependence show high rates of cocaine use in a placebo-controlled pilot study. Exp Clin Psychopharmacol. 2004 May;12(2):126–135. doi: 10.1037/1064-1297.12.2.126. [DOI] [PubMed] [Google Scholar]
  • 50.Gatti R, De Palo EF. An update: salivary hormones and physical exercise. Scand J Med Sci Sports. 2011 Apr;21(2):157–169. doi: 10.1111/j.1600-0838.2010.01252.x. [DOI] [PubMed] [Google Scholar]
  • 51.Perez-Neri I, Montes S, Ojeda-Lopez C, et al. Modulation of neurotransmitter systems by dehydroepiandrosterone and dehydroepiandrosterone sulfate: mechanism of action and relevance to psychiatric disorders. Prog Neuropsychopharmacol Biol Psychiatry. 2008 Jul 1;32(5):1118–1130. doi: 10.1016/j.pnpbp.2007.12.001. [DOI] [PubMed] [Google Scholar]
  • 52.Dickstein BD, Suvak M, Litz BT, et al. Heterogeneity in the course of posttraumatic stress disorder: trajectories of symptomatology. J Trauma Stress. 2010 Jun;23(3):331–339. doi: 10.1002/jts.20523. [DOI] [PubMed] [Google Scholar]

RESOURCES