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ORIGINAL ARTICLES |
From the Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California (J.G.-D., M.Y., E.N., C.B.T., H.C.K., D.S.); the Department of Clinical Psychology and Psychotherapy, Institute for Psychology, University of Basel, Basel, Switzerland (F.H.W.); the Department of Veterans Affairs Health Care System, Palo Alto, California (A.C.); the Department of Psychiatry, University of Wisconsin Medical School, Madison, Wisconsin (H.C.A.); and the Department of Psychological and Brain Sciences, University of Louisville, Louisville, Kentucky (S.S.).
Address correspondence and reprint requests to Janine Giese-Davis, PhD, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 401 Quarry Road, Stanford, CA 94305. E-mail: jgiese{at}stanford.edu
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODRESULTSDISCUSSIONCONCLUSIONSNOTESREFERENCES |
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Method: Forty-five nondepressed and 45 depressed patients with MBC underwent a modified Trier Social Stress Test (TSST) while affect, cardiovascular, respiratory, and cortisol responses were measured.
Results: At study entry, depressed compared with nondepressed patients had significantly lower log cortisol waking rise levels (p = .005) but no other HPA differences. Positive affect (p = .025) and high-frequency heart-rate variability (lnHF) (p = .002) were significantly lower at TSST baseline in depressed patients. In response to the TSST, depressed patients reported significantly lower positive (p = .050) and greater negative affect (p = .037) and had significantly reduced lnHF (p = .031). In secondary analyses, at TSST baseline both low-frequency (lnLF) (p = .002) and very-low-frequency (lnVLF) (p = .0001) heart rate variability were significantly lower in the depressed group. In secondary analyses during the TSST, those who were depressed had significantly lower lnVLF (p = .008) and did not increase aortic impedance reactivity as much as did the nondepressed during the stressor (p = .005).
Conclusion: Depression in patients with MBC was associated with alterations in autonomic regulation, particularly reductions in respiratory sinus arrhythmia, a measure of cardiac vagal control, at baseline and during the TSST. In addition, depression was associated with blunted HPA response to awakening. Both MBC groups had relative cortisol hyporesponsiveness to acute stress.
Key Words: breast cancer • major depressive disorder • psychological stress • autonomic nervous system • cortisol • HPA axis
Abbreviations: ANS = autonomic nervous system; BMI = body mass index; BP = blood pressure; BRC = baroreflex control of heart rate; CO = cardiac output; CVD = cardiovascular disease; DBP = diastolic blood pressure; ECG = electrocardiogram; HDL = high-density lipoprotein; HPA axis = hypothalamic–pituitary–adrenal axis; HR = heart rate; HRSD = Hamilton Rating Scale of Depression; HRV = heart rate variability; ICG = impedance cardiogram; lnHF = natural log of high-frequency HRV; lnLF = natural log of low-frequency HRV; lnVLF = natural log of very low frequency HRV; LDL = low-density lipoprotein; MBC = metastatic breast cancer; MDD = major depressive disorder; ND = nondepressed; PANAS = Positive and Negative Affect Schedule; pCO2 = partial pressure of carbon dioxide; PEP = preejection period; RR interval = time between two consecutive R waves of the ECG; RSA = respiratory sinus arrhythmia; RSATF = transfer function respiratory sinus arrhythmia; SBP = systolic blood pressure; SNRI = serotonin–norepinephrine reuptake inhibitor; SSRI = selective serotonin reuptake inhibitor; TSST = Trier Social Stress Test; VLDL = very-low-density lipoprotein.
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INTRODUCTION |
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Breast Cancer, Depression, and Survival
Depression may adversely affect cancer survival (6), so understanding its impact on physiology is important. Of 24 published studies, 15 find a significant association between higher depression and shorter time to recurrence or survival (7). Depression is also associated with aberrations in hypothalamic–pituitary–adrenal (HPA) function (8–11), which in turn has been linked with shorter survival in patients with MBC (12). Responses of depressed patients with MBC to acute stress in not only HPA, but parasympathetic, and sympathetic systems will increase our understanding of any additional physiological burden.
Abnormalities in the regulation of HPA function have been linked to depression (10,13), shorter cancer survival (12), and also poorer recovery from acute myocardial infarction (14). Although no known studies examine respiratory sinus arrhythmia (RSA) and cancer survival, depression (15,16) and shorter survival in patients with heart disease (17) have been associated with abnormalities in cardiovascular regulation, particularly lower levels of RSA. Depressed patients may also have less sensitivity to the anti-inflammatory aspects of cortisol, possibly leading to greater circulating levels of anti-inflammatory cytokines (18). Patients with primary breast cancer who are fatigued have greater cytokines (19), chronic cellular immune response (20), and flatter cortisol response to stress (21).
Depression and Autonomic Nervous System Function
Little research links MBC, depression, and autonomic nervous system (ANS) function. However, in other populations, depression is moderately associated with reduced parasympathetic control of cardiac activity (vagal withdrawal in depression across 13 studies [Cohen's d = 0.33]) (22). Depression is slightly associated with increased sympathetic control in a recent meta-analysis (systolic blood pressure [SBP]: d = 0.13; diastolic blood pressure [DBP]: d = 0.17) (23). Increased heart rate (HR), being dually influenced by sympathetic and parasympathetic factors, was moderately associated with depression (d = 0.37) (23).
Because many cardiovascular and hemodynamic functions are jointly influenced by sympathetic and parasympathetic input, it is necessary to use measures that tease apart the two branches: a) preejection period (PEP) is the interval between the onset of the electrocardiogram (ECG) Q wave to onset of left ventricular ejection time, which is inversely related to the amount of sympathetic activation of the heart (24); and b) RSA quantified by natural log of high-frequency heart rate variability (lnHF) corresponds to the magnitude of rhythmic oscillations in heart rate accompanying breathing, which is related to the amount of vagal activation of the heart (25) and parasympathetic function. Thus, PEP and lnHF were chosen as our primary ANS measures.
Depression and Hypothalamic–Pituitary–Adrenal Axis Function
Depression has been characterized by a state of chronic HPA activation in other populations (13,26,27) with flattening of diurnal variation (8–10). Some patients with major depressive disorder (MDD) have high basal glucocorticoid levels when compared with nondepressed patients (4,13), although recent evidence suggests that those with nonpsychotic depression have low cortisol levels (28,29), and other studies have found no differences (4).
In a recent meta-analysis of stress tasks (4), patients with MDD more often had blunted cortisol and/or ACTH responses (18,30), although not always, and greater depression severity was associated with elevated cortisol during recovery (4,31). Thus, if depressed patients with MBC respond similarly to stress, it may reduce their capacity to mobilize an adequate cortisol response and to recover in the face of stressors.
Based on these mixed results, we hypothesized that depressed patients with MBC would show flattened diurnal cortisol levels, higher waking level, aberrations in waking rise, decreases in cortisol reactivity to social stress, with increased sympathetic (PEP) and decreased parasympathetic (RSA) tone. Patients were studied during baseline rest and Trier Social Stress Test (TSST) reactivity (32). We also explored a wide variety of hemodynamic, autonomic, and respiratory measures and cortisol recovery after the TSST to generate hypotheses for further study.
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METHOD |
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TOPABSTRACTINTRODUCTIONMETHODRESULTSDISCUSSIONCONCLUSIONSNOTESREFERENCES |
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Inclusion criteria were metastatic or recurrent breast cancer, a Karnofsky rating of at least 70%, residence within the Greater San Francisco Bay Area, and proficiency in English to be able to complete questionnaires and the TSST. Exclusion criteria were other active cancers within 10 years (excepting basal cell or squamous cell carcinomas of the skin or in situ cancer of the cervix), positive supraclavicular lymph nodes as the only metastatic lesion, a concurrent medical condition likely to influence short-term survival, utilization of a corticosteroid within the preceding month, or a history of major psychiatric illness for which the patient was hospitalized or medicated (with the exception of depression or anxiety).
Procedure
Patients with MBC participated in the TSST (32), a standardized social and cognitive stressor. On arrival, participants were fitted with physiological recording equipment. After a 5-minute baseline and calibration procedure for respiration belts, participants were told they would have 5 minutes to prepare a speech for a job interview. This was immediately followed by a 5-minute speech and 5 minutes of mental math. A panel of two evaluators provided no facial feedback in response to participants. Participants were then instructed to sit quietly for an hour without moving or speaking much. This procedure was modified from the original TSST to include a 5- (rather than 10-) minute speech preparation, calibration for respiration belts, and a 60- rather than 30-minute recovery. Patients also stayed in the same room (rather than changing rooms) throughout the procedure. They completed the state Positive and Negative Affect Schedule (PANAS) at baseline and after each test segment. We debriefed following saliva collection the next day.
Demographics and medical status were assessed by self-report. Medical status information was collected from both patients and their physicians.
Psychological Measures
Depression
Depression was assessed using the SCID (33). We included in our depressed group those with current diagnoses of MDD, dysthymia, and depressive disorder not otherwise specified (N = 17). We also included those women currently taking antidepressants except those prescribed primarily for sleep, even if they were not currently diagnosable with depression based on the SCID (N = 28). All but nine of those women met the SCID lifetime threshold for a diagnostic depression category. These nine women may have received a diagnosis of depression from a physician who prescribed the medication. In our depressed sample, so many of the women were taking antidepressants (77.8%) that we could not definitively examine those effects: 31.1% selective serotonin reuptake inhibitor (SSRI), 4.4% tricyclic, 2.2% bupropion, 24.4% serotonin–norepinephrine reuptake inhibitor (SNRI), 2.2% SSRI + tricyclic, 4.4% SSRI + bupropion, 2.2% SNRI + tricyclic, 4.4% SNRI + bupropion, and 2.2% St. John's Wort. Self-reported depression severity was measured with the Beck Depression Inventory (BDI) (34).
Perceived Stress Scale
The Perceived Stress Scale (PSS) measured global perception of stress during the previous month (35). We used a short version comprised of 10 5-point Likert-type items (0 = never to 4 = very often).
MOS-SF 36 Health Survey
The MOS-SF 36 Health Survey (36) assessed overall perceived health. It consists of 36 items representing eight health concepts: physical function, role disability resulting from physical health problems, bodily pain, general health perceptions, vitality, social functioning, role disability resulting from emotional problems, and general mental health.
Traumatic Events
Using the traumatic event screening query from the posttraumatic stress disorder (PTSD) SCID, each reported event was judged by two independent raters with expertise in traumatic stress. Overall coding designations based on the SCID included a) none = no report of experiences in response to the prompt, b) stressful = only events that were judged to not meet DSM-IV-TR A1 criteria for PTSD, and c) traumatic = one or more reported events was judged to meet PTSD A1 criteria. Events were coded separately and participants received the life event code reflective of the highest level of exposure they reported.
Positive and Negative Affect Scale
State emotions were measured with the PANAS (37), a Likert-type adjective list of emotions (1–5 = slightly to extremely).
Cardiovascular Risk Factors
Participants were assessed on common cardiovascular risk factors. These included self-report questions on history of heart disease, high blood pressure, stroke, and smoking. Blood panel tests included low-density lipoprotein (LDL; mg/dl), high-density lipoprotein (HDL; mg/dL), LDL/HDL, triglycerides (mg/dL), and cholesterol. We assessed lipid-lowering and antihypertensive medication by self-report. Body weight (in kilograms) and height (in meters) were obtained in a standing position with shoes removed and subjects wearing street clothes. These were used to calculate body mass index (BMI; in kg/m2). Waist/hip ratio was also assessed (38).
Physiological Measurements and Data Reduction
Cortisol
Saliva was collected at waking, 30 minutes later, and at 12:00 PM, 5:00 PM, and 9:00 PM for 2 consecutive days at study entry (at least 1 week before the TSST), the day of the TSST, and the day after the TSST. Patients were offered wrist-worn timers to prompt them at scheduled saliva collection times. Saliva collection swabs (Sarstedt, Inc., Newton, NC) were stored in medication event monitoring system bottles from AARDEX Ltd. so that exact times could be recorded electronically. The TSST was run in the late afternoon between 4:00 PM and 7:00 PM because past research demonstrates greater TSST HPA effect sizes for late afternoon sessions (39). Saliva samples during TSST were collected 10 times: on arrival before hookup, after hookup, after 5 minutes of baseline quiet sitting and 5 minutes of paced breathing before the speech instructions, after speech preparation, after speech and math stressors, and during recovery at 10, 20, 30, 45, and 60 minutes.
During home-based collections, participants were instructed to refrigerate samples. They were advised not to eat, drink, smoke, brush teeth, or use mouthwash for 30 minutes before collections and to postpone collection if they had mouth wounds. They were asked not to drink alcohol during the hours before or during days when saliva samples were collected.
Samples were stored at –70°C before laboratory centrifugation and duplicate assays for salivary cortisol using luminescence immunoassay (LIA) reagents provided by Immuno-Biological Laboratories, Inc. Hamburg, Germany (40). Assay sensitivity was 0.015 µg/dL. Intraassay variation on low, medium, and high controls averaged 2.78%, 10.45%, and 4.79%, respectively. The mean values of the low, medium, and high controls were 0.054 µg/dL, 0.228 µg/dL, and 0.863 µg/dL, respectively. The interassay coefficients of variation for the low, medium, and high controls were 10.9%, 10.5%, and 5.5%, respectively.
Cardiovascular and Respiratory Physiology
Placement of electrodes/sensors, data recording, and data reduction followed conventions and published guidelines (e.g., (25,41)). Physiological channels were sampled at 400 Hz. A standard lead II ECG was obtained. An impedance cardiograph (HIC-2000; Instrumentation for Medicine, Inc., Old Greenwich, CT) measured electrical impedance changes using four spot electrodes attached to the neck and thorax. A Finapres 2300 BP monitor (Ohmeda, Inc., Madison, WI) was used to obtain the continuous arterial pressure waveform at the second digit of the nondominant hand. Respiratory pattern data were measured using thoracic and abdominal bellows (Lafayette Instrument, Inc., Lafayette, IN) connected to pneumographic transducers (James Long Co., Inc., Caroga Lake, NY). Expiratory partial pressure of carbon dioxide (pCO2) was measured continuously through a cannula at the nostrils by a calibrated infrared capnograph (N-1000; Nellcor, Hayward, CA). An automatic blood pressure (BP) monitor (Dinamap 1846SX) measured BP with a cuff around the upper right arm. Inflation was triggered 2 minutes after onset of each test segment.
Physiological signals were analyzed and averaged for each 5-minute period using an integrated suite of biosignal analysis programs written in MATLAB (Mathworks, Inc., Natick, MA) that has been described elsewhere (42). Heart rate (HR) was measured from the ECG. PEP was calculated as the interval from the ECG Q-point to the impedance cardiogram (ICG) B-point. Stroke volume was calculated using the Kubicek formula and multiplied with HR to obtain cardiac output (CO). Systemic vascular resistance was calculated as [1/3 SBP + 2/3 DBP]/CO. Aortic characteristic impedance and arterial compliance were measured using Wesseling's pulse-contour analysis method (43,44). Rate-pressure product was calculated as HR x SBP. Calibrated thoracic and abdominal respiration channels were used to calculate tidal volumes and respiratory rate.
High-frequency (lnHF), low-frequency (lnLF), and very-low-frequency (lnVLF) power of heart period variability were computed as the natural logarithms of the summed power spectral density of time between two consecutive R waves of the ECG (RR interval) between 0.15 to 0.5 Hz, 0.07 to 0.15 Hz, and 0.0033 to 0.07 Hz, respectively. A respiration-controlled transfer function, adjusting the lnHF estimate of RSA for respiratory rate and depth alteration confounds (RSATF), was quantified by fast Fourier transform and the averaged periodogram method as the magnitude of the transfer function relating RR interval to lung volume oscillations at the prominent respiratory frequency (45). Baroreflex control of heart rate (BRC), a vagally mediated measure of the sensitivity of the baroreflex loop, was estimated as the magnitude of the transfer function relating the RR interval to systolic pressure oscillations at the prominent SBP frequency in the 0.07 to 0.15 Hz band (46). Spectral coherence for RSATF and BRC was at least 0.5. The lnLF power of SBP variability (Mayer-wave) was computed as the summed power spectral density of SBP between 0.07 to 0.15 Hz. BRC and Mayer-wave were estimated for baseline periods only, because these measures were unstable during stress periods.
Physiological data were reviewed by a senior psychophysiologist (F.H.W.) blind to patient information. Improbable or inconsistent values prompted reanalysis. Outliers more than 2 standard deviations from the group mean that appeared improbable for that individual or measure were eliminated. Less than 1% of data were excluded.
Data Analysis
In the TSST, psychophysiological signals were averaged for baseline, anticipation, speech, math, and the first two 5-minute segments of recovery. Cortisol data were log-transformed to stabilize the variance. Baseline cortisol slope was calculated by regressing cortisol values on time from awakening on all points for 2 days. Waking cortisol was the average of waking levels for 2 days. Waking rise was the 2-day average of the difference between the cortisol levels at waking and 30 minutes postwaking. Recovery at 9:00 PM on the day of the TSST was the difference score between the average log cortisol level at 9:00 PM during the 2-day baseline and the 9:00 PM cortisol level after the TSST. Recovery at wake and waking rise the next day were computed similarly.
A hierarchical linear model with group (depressed or nondepressed), time, and their interaction was used, assuming autoregressive covariance structure to examine differences in TSST response trajectories among groups (47). Baseline values were subtracted for each response in the trajectory. Baseline differences in psychosocial measures, demographic and medical variables, cortisol, and baseline TSST were examined with Mann-Whitney-Wilcoxon or 
2 tests. Based on the literature and hypotheses, a small number of primary variables were tested (positive and negative affect, log cortisol level, PEP, lnHF). These primary measures were relatively independent with only a moderate correlation between positive and negative affect and negligible correlations among the other variables; thus, we used a p < .05 criterion. We present an effect size for group comparisons (48).
For hypothesis generation, we also explored a comprehensive set of autonomic measures using p < .01 as the screening criterion. These exploratory measures included lnLF, lnVLF, RSATF, RR interval, SBP, DBP, rate-pressure product, CO, systemic vascular resistance, aortic characteristic impedance, arterial compliance, baroreflex control, Mayer-wave, respiratory rate, tidal volume, and pCO2. We report p values, but readers should be warned that with repeated testing there will be many false-positives.
We examined differences between depressed and nondepressed groups on smoking, alcohol consumption, and exercise. We found no significant differences at baseline or during the days of the TSST.
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RESULTS |
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In addition, the depressed group had significantly shorter disease-free intervals and fewer ethnic minorities. We could not detect differences on other demographics (age at baseline, initial diagnosis, and recurrence, education, income, marital status, employment status), prognostic medical variables (time from initial diagnosis and from metastasis to study entry, estrogen and progesterone receptor status, site of metastasis, treatment with surgery, reconstruction, chemotherapy, radiation, and hormone therapy, and treatment within 2 months of TSST), or any cardiovascular risk factors (Table 1).
Baseline Trier Social Stress Test: Primary Measures
At TSST baseline, depressed patients reported significantly lower positive affect (PANAS) and exhibited lower levels of basal RSA (lnHF) than nondepressed (Table 2, Fig. 1).
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Baseline Trier Social Stress Test: Secondary Autonomic Nervous System Measures
In exploratory analyses, lnLF and lnVLF (Table 2, Fig. 1) were significantly lower in depressed patients, but we could not detect differences in basal RSATF, a measure adjusting RSA for respiratory confounds, indicating that sources of autonomic oscillatory activity other than respiration were compromised in this group and pointing to a more general autonomic inflexibility. No group differences were found for respiratory rate and tidal volume that could account for the observed between-individual variations in RSA.
Trier Social Stress Test Reactivity: Primary Measures
During the TSST, depressed patients reported significantly lower positive and higher negative affect than the nondepressed group (PANAS) (main effects for group, Table 3, Fig. 1). Analysis of RSA (lnHF) indicated that baseline differences, with depressed patients exhibiting significantly lower levels than nondepressed, were maintained during the TSST (group main effect: Table 3, Fig. 1). For all measures, significant effects for time (Table 3) indicated that participants responded to the speech and math stressors with affective, ANS, and cortisol increases.
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Trier Social Stress Test Reactivity: Secondary Autonomic Nervous System Measures
In exploratory analyses, the significantly lower baseline level of lnVLF for depressed patients was maintained throughout the stressor (main effect for group, Table 3, Fig. 1). Hemodynamic stress reactivity in aortic characteristic impedance was significantly blunted in the depressed group (group x time interaction: Table 3, Fig. 1). The nondepressed group reacted with greater aortic characteristic impedance (arterial "stiffness") during the time of the stressor despite starting at the same level.
Hypothalamic–Pituitary–Adrenal Axis Activity
Depressed compared with nondepressed women had a lower 2-day average baseline waking rise in log cortisol level (Table 1, Fig. 2). However, no other differences in cortisol measures could be detected between groups at baseline, during the TSST, or during recovery. A significant effect for time (Table 3) indicated that log cortisol levels increased in response to the speech and math stressors for both groups with the typical delayed peak at approximately 20 minutes poststress (Fig. 2).
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We conducted this TSST in collaboration with another study in our program project examining depression in men and women at risk for cardiovascular disease (CVD) (49) sharing exact protocols. For visual comparison, we present a figure in which depressed and nondepressed MBC and CVD females' cortisol responses to the TSST can be seen (Fig. 2).
Each of the results described remained significant after removing the nine women who were taking antidepressants but did not qualify for a current or lifetime diagnosis of depression.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMETHODRESULTSDISCUSSIONCONCLUSIONSNOTESREFERENCES |
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The depressed patients with MBC exhibited significantly attenuated baseline and TSST RSA (lnHF), a measure of parasympathetic functioning attenuated in other depressed samples (22,54,55). Although these women showed overall HPA blunting, their ANS appeared responsive to stress. RSA is related to ability to regulate emotions (56). Because emotion regulation skills can be successfully learned (57), RSA might be a good measure of the biologic impact of psychotherapy for depression (58–60).
In exploratory analyses, we found reductions for the depressed group in other heart rate variability (HRV) parameters at baseline (lnLF, lnVLF) and throughout the TSST (lnVLF). LnLF reflects both sympathetic and parasympathetic influences on the cardiovascular system and is strongly associated with blood pressure regulation. LnVLF, in addition to sympathetic and parasympathetic inputs, may be influenced by the thermoregulatory, peripheral vasomotor, and renin–angiotensin systems (61). HRV measures across all three frequency bands have been found to be reduced in depressed patients with CVD (17). In addition, depressed patients showed lower aortic impedance reactivity pointing to blunted sympathetic stress reactivity.
The principal suggestion from this study is the strong effect of depression on vagal attenuation in MBC survivors. Studies in healthy participants have related compromised parasympathetic functioning to greater stress vulnerability and lowered emotion regulatory capacity. The parasympathetic system is important for restoring homeostasis after stress and thus may be important in allostatic regulation. Vagal attenuation has been proposed as a pathophysiological link between depression and CVD risk (62). The current study indicates that depression is also associated with this ANS inflexibility in patients with MBC.
Depressed patients may have greater impairment across multiple physiological systems because of alterations in central nervous system regulation, e.g., in the central serotonergic system (63,64). Through descending pathways, this may alter subjective, immune, and autonomic function. This linkage may be the result of reduced flexibility in physiological responses as indexed by lower baseline RSA, less increase in RSA over the course of the TSST, or the pervasiveness of their negative affect.
Limitations
We assigned women to our depressed group based on meeting criteria for SCID diagnosis or their use of antidepressants. This method of assignment does not select for an extremely depressed (MDD) sample to compare with nondepressed as is the case in previous research in the general population. However, this sample more closely mirrors general levels of depression in patients with MBC who are actively coping with a threat to life. Levels of MBC depression that reach a diagnostic level are relatively rare, and yet the physiological impact of depression may still exist.
The significantly shorter disease-free intervals in the depressed group were statistically unrelated to outcomes. Additionally, there were fewer depressed nonwhites; however, there were too few nonwhites to examine statistical differences on outcomes reliably. Future studies may want to examine ethnic differences in these outcomes more thoroughly.
This was an observational study of depressed versus nondepressed patients with MBC. We cannot be certain what caused reduction in parasympathetic activity in the depressed group and so caution is warranted. Antidepressants are often given to women with MBC as they cope with the threat of death. Studies have found that some antidepressants may improve HRV (65), but our study found that the depressed group was significantly lower despite antidepressant use. Although it is known that older tricyclic antidepressants with pronounced anticholinergic side effects (66) may reduce parasympathetic activity, only three women in the HRV analyses were taking such medication.
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CONCLUSIONS |
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We thank Dirk Hellhammer, PhD, Seymour Levine, PhD, Rachel Yehuda, PhD, and Robert Sapolsky, PhD, for consultation regarding the interpretation of our cortisol results for this article; and Ben Varasteh and the General Clinical Research Center at Stanford for conducting cortisol assays. In addition, we thank project director Bita Nouriani, MS; research assistants Manijeh Parineh, Nausheen Ali, Allyson DeLorenzo, Julie Hall, and Suzanne Twirbutt; panel members for the TSST; and the women who participated.
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NOTES |
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Received for publication December 29, 2005; revision received May 4, 2006.
DOI:10.1097/01.psy.0000238216.88515.e5
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