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ssociation Between Childhood Trauma andatecholamine Response to Psychological Stress inolice Academy Recruits

hristian Otte, Thomas C. Neylan, Nnamdi Pole, Thomas Metzler, Suzanne Best, Clare Henn-Haase,achel Yehuda, and Charles R. Marmar

ackground: Childhood trauma is a risk factor for anxiety disorders in adulthood. One possible mechanism for this association isn increased neuroendocrine response to stress in adults with a history of childhood trauma.ethods: In a cross-sectional study, 76 police academy recruits (mean [�SD] age 28 � 5 years, 10 female) were exposed to a video

epicting real-life officers exposed to highly stressful incidents. Salivary cortisol and 3-methoxy-4-hydroxy-phenylglycol (MHPG, theajor metabolite of norepinephrine) were collected at baseline, immediately after the video, and 20 min after the video. Childhood

rauma before age 14 was assessed with an interview (Life Stressor Checklist–Revised).esults: Exposure to the video elicited significant MHPG and cortisol responses in both groups. Recruits with childhood traumaistories (n � 16) had a significantly greater MHPG response, as evidenced by a group effect (F � 8.0, p � .01), and a group � timenteraction (F � 4.1, p � .05). The cortisol response did not differ between groups.onclusions: Police academy recruits with childhood trauma histories have an increased catecholamine response to psychological

tress. This might serve as a risk factor for anxiety disorders in recruits, and these findings might generalize to other groups with a

istory of childhood trauma.

ey Words: Childhood trauma, stress, cortisol, catecholamines,TSD, depression

n the United States, more than 2.5 million cases of childabuse and neglect are reported each year (American Acad-emy of Pediatrics 2004). Childhood abuse and neglect, as

ell as other childhood trauma (e.g., parental loss), increase theisk for the development of anxiety disorders in adulthoodBremner et al 1993; Kendler et al 1992; Kessler et al 1997;ehuda 2004). A possible mechanism accounting for the associ-tion between childhood trauma and adult anxiety disordersould be an increased stress response of the hypothalamus–ituitary–adrenal axis and the sympathetic nervous system as aesult of early trauma (Nemeroff 2004). This hypothesis followsrom animal studies showing increased concentrations of corti-otropin-releasing-factor (CRF) and catecholamines in the cere-rospinal fluid and increased neuroendocrine and sympatheticervous system responses to stress in adult animals that hadversive experiences early in life (Coplan et al 1996, 1998; Liu etl 1997; Plotsky and Meaney 1993; Rosenblum et al 1994).

In humans, women with a history of childhood abuse andurrent depression (and comorbid posttraumatic stress disorderPTSD] in almost all cases) showed a greater plasma cortisolesponse to a psychological stress test than women with child-ood abuse but no current depression, women with currentepression but no childhood abuse, or women with neither of

rom the Department of Psychiatry (CO, TCN, TM, SB), University of California;Veterans Affairs Medical Center (CO, TCN, TM, SB, CH-H, CRM), San Fran-cisco, California; Department of Psychiatry (CO), University HospitalHamburg-Eppendorf, Hamburg, Germany; Department of Psychology(NP), University of Michigan, Ann Arbor, Michigan; and Department ofPsychiatry (RY), Mount Sinai School of Medicine, New York, New York.

ddress reprint requests to Christian Otte, M.D., University HospitalHamburg-Eppendorf, Department of Psychiatry and Psychotherapy,Martinistrasse 52, Hamburg 20246, Germany; E-mail: otte@uke.uni-hamburg.de.

eceived June 23, 2004; revised September 30, 2004; accepted October 5,

2004.

006-3223/05/$30.00oi:10.1016/j.biopsych.2004.10.009

these conditions (Heim et al 2000). Interestingly, the adrenocor-ticotropic hormone (ACTH) response was elevated in the groupof childhood abuse–exposed women with and without currentdepression, suggesting that a history of childhood abuse was amore important factor in ACTH responsiveness than the presenceof depression. In a multiple regression analysis, however, bothchildhood abuse and current psychopathology contributed to theincreased ACTH and cortisol responses to the psychologicalstress test (Heim et al 2002).

Another study examined women with a history of childhoodsexual and/or physical abuse, all of whom met criteria forlifetime PTSD (Elzinga et al 2003). Compared with abusedwomen without current PTSD, abused women with current PTSDhad similar baseline cortisol levels but an elevated cortisolresponse to personalized scripts of childhood abuse, with thegreatest magnitude of elevations during and shortly after expo-sure to the trauma scripts. Furthermore, psychophysiologic stud-ies demonstrated that in a group of women with childhoodabuse, women with current PTSD showed greater heart rateresponses to trauma-related stimuli (Orr et al 1998) and auditorystartle stimuli (Metzger et al 1999) than women without currentPTSD. These findings would suggest that current posttraumaticstress symptoms rather than childhood abuse exposure explainan enhanced cortisol and sympathetic response to stress.

Because all subjects in these previous studies had a history ofchildhood abuse, the aim of these studies was to determinewhether subjects with current mood and anxiety disorders and ahistory of childhood abuse show an increased response to stresscompared with subjects with a history of childhood abuse only.These studies were not designed to determine whether child-hood trauma per se in subjects without current psychopathologyis associated with an increased stress response compared withsubjects with neither childhood trauma nor current psychopa-thology. There is only one earlier study reporting that a history ofparental loss in the absence of current psychiatric symptoms wasassociated with an increased cortisol response to a psychosocialstressor in college students (Luecken 1998).

If childhood trauma in and of itself is associated with an

increased neuroendocrine and sympathetic nervous system re-

BIOL PSYCHIATRY 2005;57:27–32© 2005 Society of Biological Psychiatry

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ponse to stress, this might be a mechanism by which childhoodrauma could increase the risk for anxiety disorders in adulthood.herefore, in a cross-sectional study, we examined the salivaryortisol and 3-methoxy-4-hydroxy-phenylglycol (MHPG, the majoretabolite of norepinephrine) response to a laboratory stress

hallenge in police academy recruits without current psychopathol-gy during academy training before actual critical incident expo-ure. We hypothesized that recruits with a history of childhoodrauma would show a greater cortisol and MHPG response to atress challenge task compared with those without childhoodrauma.

ethods and Materials

articipantsThis sample is a baseline cross-sectional component of an

ngoing prospective study of traumatic stress in police officers,ho are still recruited into the study. For this baseline study, we

ecruited 76 participants (mean [�SD] age 28 � 5 years, 10emale) from the academies of the following police departments:an Francisco, Oakland, San Jose, Fremont, Palo Alto, Alameda,ichmond, and Vallejo, California. All members of each class invery police academy were asked to participate. The populatione studied includes 30% of all academy recruits enrolled inolice training and represents a convenience sample of thoseecruits who agreed to participate in the study. The institutionaleview board of the University of California, San Franciscopproved the study. After a complete description of the study tohe participants, written informed consent was obtained.

aseline Assessment During Academy TrainingWe evaluated all participants with the Structured Clinical

nterview for DSM-IV (SCID-IV; First et al 1996). General psy-hopathology was also determined by the Symptom Checklist0–Revised (Derogatis and Lazarus 1994). We measured alcoholse with the Michigan Alcoholism Screening Test (MAST; Selzert al 1975) and sleep with the Pittsburgh Sleep Quality IndexBuysse et al 1989). We determined trait dissociation with theissociative Experiences Scale (DES; Bernstein and Putnam986) and dissociation during the stress video with a modifiedersion of the Peritraumatic Dissociative Experiences Question-aire (PDEQ; Marmar et al 2004).

We used an interview version of the Life Stressor Checklist–evised (LSC-R; Wolfe et al 1996) to determine childhood traumaefore the age of 14 years. The LSC-R assesses 21 stressful life eventse.g., experiencing or witnessing serious accidents, illnesses, sud-en death, physical and sexual assault). For each event, theespondent indicated 1) whether the event occurred; 2) whether athe time of exposure the event triggered intense emotions consistentith DSM-IV criterion A2 for PTSD; 3) whether the event occurrednce or multiple times; and 4) the ages at which the event first andast occurred. We administered the LSC-R in an interview formatonducted by Ph.D.-level clinical psychologists, who calibratedheir assessments biweekly. We considered those participants ashildhood trauma–exposed who experienced traumatic life eventsith serious personal life threat or physical harm to the self, toaintain consistency with earlier studies of childhood sexual andhysical abuse (Bremner et al 2003; Elzinga et al 2003; Heim et al000, 2002). In the following, we refer to those events that involvederious personal life threat or physical harm to the self as childhood

rauma.

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ProceduresAll participants were individually tested at different times of

day, depending on their availability. Participants observed aninnocuous travelogue video for 10 min, followed by a 20-mincritical incident depiction video, then a 20-min travelogue videoagain during recovery. The critical incident video containedreal-life footage of 14 incidents that were edited into onecontinuous 20-min segment depicting police-related scenes,such as a suicide, a homicide, an officer being hit by a car, anautopsy, and an officer being killed by a detonated bomb.Participants rated their subjective distress on a visual analoguescale after watching the video. Subjects participated in otherparts of the study during the test day for several hours beforethey saw the stress video. There was no food intake, exercise, orsmoking for a minimum of 2 hours before the stress challenge,and we systematically assessed use of prescription and over-the-counter medication.

Hormone AssessmentThe saliva collections for cortisol and MHPG followed the

methods described by (Yang et al 1997). Saliva was collectedin two Salivette nylon swabs (Sarstedt, Newton, North Caro-lina) at each of three time points: time 1: immediately beforethe baseline travelogue video; time 2: immediately after the20-min critical incidents video; and time 3: 20 min after theend of the critical incident video and after the recoverytravelogue video. A recent meta-analysis showed that thecortisol response to a laboratory stressor peaks between 20and 40 min after stress onset (Dickerson and Kemeny 2004).Immediately after the collection, the swabs were placed in theSalivette tube and stored at 4°C until centrifugation. The tubeswere centrifuged at 1000 g for 2 min, and the filtrate wastransferred to separate polypropylene tubes for cortisol andMHPG and stored at �70°C until assayed. Salivary cortisol andMHPG tubes were shipped on dry ice to the neuroendocrinol-ogy laboratory at the Bronx Veterans Affairs Medical Center.Salivary cortisol was measured with a commercially availableradioimmunoassay kit (Abbot Laboratories, Abbott Park, Illi-nois). The MHPG was assayed by high-pressure liquid chro-matography, as described in greater detail by Yang et al(1997).

Data AnalysisDifferences in characteristics between participants with and

without childhood trauma were compared with t tests or analysisof covariance for continuous variables and �2 tests (or Fisher’sexact test for fewer than five observations per cell) for dichoto-mous variables.

Raw values of MHPG and cortisol at baseline, immediatelyafter the video, and 20 min after the video were analyzed bya linear mixed model fitting trauma exposure during child-hood as a between-groups fixed effect and time as a within-subjects repeated effect. Baseline values of the variable ofinterest were entered as a fixed covariate. We also includedgroup � time interactions in each model. Mixed-effect modelshave several advantages for the analysis of repeated-measuresdata: they can use all available data, can account for correla-tion between repeated measurements on the same subjects,do not assume homogeneity of variance across groups andtime points, and can handle missing data appropriately (Gue-

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esults

rauma CharacteristicsThere were 16 participants with childhood trauma. Age of

hildhood trauma onset ranged from 5 to 13 years, but theverage was 10 years (SD � 2.2). Traumatic events includedife-threatening disaster, being robbed, mugged, or physicallyttacked, being physically abused or physically attacked byomeone known to the participant, having a serious physical orental illness, being in a serious accident, and being seriouslyeglected. Most (87.5%) of the personal threat childhood traumaroup reported single exposure to their traumatic event. Twoecruits reported having one personally life-threatening eventccur repeatedly. Participants with and without childhood trau-a exposure were not different in the number of traumatic

vents that they experienced as adults (mean number of eventsuring adulthood for those with childhood trauma .67 � .61 vs.83 � .93 for those without childhood trauma, p � .50).

emographic Variables and Baseline PsychopathologyCharacteristics of the study participants are listed in Table 1.

articipants with and without childhood trauma did not differ inge or gender distribution. No subject had a current Axis Isychiatric disorder, as determined by the SCID-IV; however, 4f 16 recruits (25%) with childhood trauma exposure had aifetime diagnosis of a depressive episode, as opposed to 1 of 61ecruits (1.6%) without childhood trauma exposure (Fisher’sxact test, p � .01). There was no diagnosis of lifetime PTSD inhe sample because lifetime PTSD was an exclusion factor forarticipation in this study. The other lifetime diagnoses were pastanic disorder (n � 1), past social phobia (n � 2), and pastpecific phobia (n � 2). The two groups did not differ withegard to frequency of these lifetime diagnoses according to theCID-IV. Also, the groups with and without childhood traumaid not differ in terms of self-reported general current psycho-athology (SCL-90), alcohol use (MAST), sleep (Pittsburgh Sleep

able 1. Characteristics of 76 Police Academy Recruits, Divided by theresence of Childhood Trauma (age �14 years)

Recruits WithTrauma(n � 16)

Officers WithoutTrauma(n � 61) pa

ge (y) 27 (4) 28 (5) .41emales, n (%) 1/16 (6) 9/61 (15) .45CID-IV Current

Axis 1 Diagnosis 0 0CID-IV Lifetime

Depression, n (%) 4/16 (25) 1/61 (1.6) .005CL-90 GSI Score .1 (.1) .1 (.1) .89AST Score 2.0 (3.1) 2.2 (2.9) .84ES Score 8.3 (8.2) 5 (4.9) .10DEQ Score 1.4 (.4) 1.3 (.4) .16SQI 5.7 (2) 5.2 (2.7) .46

All variables are expressed as means (SD), unless otherwise indicated.rauma is defined as experience of an event that involved serious personal

ife threat or physical harm to the self, according to the Life-Stressor-Check-ist–revised. SCID-IV, Structured Clinical Interview for DSM IV; SCL-9 GSI,ymptom Checklist-90 Global Severity Index; MAST, Michigan Alcoholismcreening Test; DES, Dissociative Experiences Scale; PDEQ, Peritraumaticistress Inventory; PSQI, Pittsburgh Sleep Quality Index.

a�2 or t test.

uality Index), or trait dissociation (DES).

Neuroendocrine MeasuresWe had 1 missing value for baseline MHPG, 2 missing values

for MHPG after 40 min, and 2 missing values for cortisol after 40min. Given three time points for each subject and 76 subjects, wehad 5 missing values out of 228 total values (i.e. 2% of all valueswere missing). The low rate of missing values can be explainedby study procedures in which research assistants collected salivaimmediately during the procedure.

The range of time of day when the participants were testedwas 9:25 AM to 8:15 PM (mean 1:14 PM, SD 2.9 hours). Subjectswith a history of childhood trauma did the task on average 2.2hours later in the day (p � .006). Although time of day wasnegatively correlated with both baseline cortisol and cortisolresponse to the video, it was not related to MHPG or MHPGresponse. We included time of day as a covariate in the mixedmodels analyses.

Additionally, four subjects in the nontraumatized group tookmedication (doxylamine, ephedrine, estrogen/progesterone combi-nation, candesartan), which potentially could interfere with cortisoland MHPG responses. Therefore, we repeated the analyses withoutthose subjects.

Salivary MHPGThere were no differences in baseline MHPG values between

groups (7.3 � 5 ng/dL vs. 6.3 � 1.7 ng/dL, p � .52) (Figure 1).We found a significant effect of time, indicating that for thesample as a whole the video increased MHPG levels [F (1,61.8) �4.37, p � .03]. Furthermore, there was a significant effect ofgroup, reflecting the overall higher MHPG levels in the recruitswith childhood trauma histories [F (1,61.1) � 8.03, p � .01].Finally, there was a significant group � time interaction, indicat-ing that academy recruits with childhood trauma historiesshowed a greater increase in MHPG compared with those whodid not report childhood trauma [F (1,61.7) � 4.10, p � .047]. Theeffect of group [F (1,63.9) � 6.4, p � .01] and the time � groupinteraction [F (1,61.6) � 4.1, p � .047] remained when we

Figure 1. MHPG (3-methoxy-4-hydroxyphenylglycol) response (mean andSEM) to stress video in 76 police academy recruits, divided by the presenceof childhood trauma (age �14 years), defined as experience of an event thatinvolved serious personal life threat or physical harm to the self, according

to the Life-Stressor-Checklist–revised.

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epeated the analyses entering lifetime depression as a covariate.significant group effect [F (1,53) � 6.7, p � .01] and group �

ime interaction [F � 4.9(1,53), p � .03] also remained when wexamined men only to control for possible gender effects.urthermore, entering time of day as a covariate still resulted insignificant group effect [F (1,59) � 9.1, p � .01] and time �

roup interaction [F (1,59.7) � 4.6, p � .03].When we repeated the analyses excluding those four subjects

n the nontrauma group who were taking medication that mightnterfere with MHPG responses, the group effect remainedF (1,57.1) � 7.5, p � .01] and the group � time interaction wasearly significant [F (1,57.8) � 3.7, p � .059].

Consistent with our mixed-model analysis, 13 of 16 recruitsith childhood trauma exposure had a maximal MHPG increasebove the median of the maximal MHPG increase in thoseithout childhood trauma exposure (�2 � 5.3, p � .03).

alivary CortisolWe did not find baseline differences in cortisol levels between

oth groups (459 � 168 ng/dL vs. 468 � 163 ng/dL, p � .84)Figure 2). There was a significant effect of time, indicating thator the sample as a whole the video challenge elicited a cortisolesponse [F (1,72.9) � 11.2, p � .01]; however, no significantffect of group [F (1,74.1) � .41, p � .52] or group � timenteraction [F (1,72.9) � .52, p � .47] emerged. Entering lifetimeepression or time of day of testing as a covariate, excludinghose four subjects taking medication, or examining men onlyid not change the results; that is, for cortisol we again found aignificant effect of time but neither a significant group effect norroup � time interaction.

Consistent with our nonsignificant between-group differencesor cortisol, only 8 of 16 childhood trauma–exposed recruits had

maximal cortisol increase above the median of the cortisolncrease for those not exposed to a traumatic event in childhood�2 � .01, p � .99)

ubjective Distress and Dissociation During the VideoCompared with those without childhood trauma histories,

igure 2. Cortisol response (mean and SEM) to stress video in 76 policecademy recruits, divided by the presence of childhood trauma (age �14ears), defined as experience of an event that involved serious personal lifehreat or physical harm to the self, according to the Life-Stressor-Checklist–evised.

ecruits with childhood trauma histories showed significantly

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greater subjective distress during the stress video, as assessed bya 0–10 range visual analogue scale [5.8 � 2.3 vs. 3.9 � 2.6;t (1,74) � 2.0, p � .01]. There were no between-group differ-ences in dissociative reactions during the video, as measuredwith the modified PDEQ (Table 1).

Neither in the group as a whole nor in the traumatized ornontraumatized groups separately was there a correlation be-tween dissociative experiences during the video, as measuredwith the modified PDEQ, and MHPG or cortisol responses;however, subjective distress correlated with both the area underthe curve for the MHPG (r � .21, p � .09) and cortisol (r � .25,p � .03) response in the group as a whole.

Discussion

In a cross-sectional study, we found that a history of child-hood trauma in police academy recruits without current psycho-pathology is associated with an increased catecholamine re-sponse to simulated police-related stress. Although the videochallenge did elicit a significant cortisol response for the sampleas a whole, there was no effect of childhood trauma exposure onresponse magnitude.

Our findings are consistent with previous studies in whichpatients with childhood trauma and adult anxiety disordersshowed an increased sympathetic nervous system response topsychological stress during adulthood (Bremner et al 2003; Heimet al 2000; Metzger et al 1999; Orr et al 1998). Our study extendsthose earlier findings and suggests that childhood trauma expo-sure per se is associated with a larger catecholamine response tonovel stressors in adulthood, even in subjects without currentpsychopathology. It has been consistently shown that childhoodtrauma exposure increases the risk for the development ofanxiety disorders (Bremner et al 1993; Kendler et al 1992; Kessleret al 1997; Yehuda 2004). An increased catecholamine responsecould be a mechanism by which childhood trauma exposureincreases the risk for these disorders.

A possible mechanism by which childhood trauma exposurecould increase the catecholamine response to adult stressorsinvolves the amygdala, a central brain structure for disseminationof information that coordinates autonomic, neuroendocrine, andbehavioral responses to stressors (Davis 1992). There is evidencefrom functional neuroimaging studies that fear conditioningleads to an increase in amygdala activity (LeDoux 2003). It hasbeen hypothesized that prior trauma-induced activation of theamygdala enhances neuroendocrine and sympathetic nervoussystem responses to subsequent novel stressors through CRFpathways to the hypothalamus and locus ceruleus (Sanchez et al2001). In animals, previous exposure to stress increases cerebro-spinal fluid levels of CRF and the catecholamine release to novelstressors (Coplan et al 1996; Nisenbaum et al 1991). Furthermore,a catecholamine response was elicited by previously neutralenvironmental stimuli that had been paired with the stressor(Cassens et al 1980). Thus, one possible explanation for ourresults is that trauma exposure during childhood, a period ofheightened plasticity of corticolimbic neuronal systems, in-creases amygdala reactivity in adulthood to novel stressful oreven neutral situations, so that subsequent responses are af-fected. Koob (1999) proposed a model in which CRF from theamygdala activates brainstem locus ceruleus noradrenergic ac-tivity, which in turn activates forebrain CRF, effectively closing afeed-forward loop. Such a hypothesized mechanism might ex-plain the potentiation of stress responses with repeated exposure

that could lead to psychopathology.

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C. Otte et al BIOL PSYCHIATRY 2005;57:27–32 31

The increased catecholamine response after childhood traumaould also be explained by the formation of fear networks thatontain information about stimuli, responses, and meaningselated to emotional events (Foa et al 1989). Such networks areharacterized by mental representations that are readily activatedy many internal and external cues. Childhood trauma mightead to a lower threshold for interpreting stimuli as threateningnd to a selective attention bias toward searching for anddentifying threatening information, leading to a higher catechol-mine response (Foa et al 1989). This model would be consistentith our findings of significantly greater subjective distressuring the video in those participants with childhood traumaxposure.

Possible mechanisms for the association between exagger-ted catecholamine response to stressors and the development ofsychopathology include enhanced fear conditioning and over-onsolidation of traumatic memories (Pitman 1989). It has beenhown that norepinephrine in the amygdala increases contextualear conditioning (LaLumiere et al 2003). Furthermore, consoli-ation of emotional memory is increased by exogenous cat-cholamines and impaired after blockade of adrenergic � recep-ors (Cahill and Alkire 2003; Cahill et al 1994). Greater salivaryHPG during memory consolidation was associated with greater

ecall for an emotionally arousing story 1 week later (Southwickt al 2002). Importantly, it has been shown that salivary MHPGtrongly correlates with MHPG in the cerebrospinal fluid (Reustert al 2002), suggesting that salivary MHPG is a reliable proxy ofrain MHPG activity.

We did not find a greater increase in cortisol to the videohallenge in participants with childhood trauma exposure com-ared with those without childhood trauma history. This mightuggest that a greater increase in cortisol to adult stressors inhose with childhood trauma is associated with levels of currentsychopathology rather than childhood trauma exposure per se.nimal research has indicated that after stress only maladapted,ehaviorally “symptomatic” animals, but not well-adapted orontrol rats, show an increased cortisol response to stress (Cohent al 2003). These findings are also supported by earlier humantudies that found an increased cortisol response to stress and anncreased cortisol suppression after dexamethasone in childhoodrauma–exposed women with current PTSD or depression com-ared with childhood trauma–exposed women who did notevelop PTSD or depression (Elzinga et al 2003; Heim et al 2000;ewport et al 2004). Luecken (1998), however, found an in-reased cortisol response during a public speech task in univer-ity students with parental loss before the age of 16 yearsompared with subjects without parental loss. Differences in typef laboratory stressor, age at traumatization, study population,nd gender distribution might in part account for these varyingindings.

Several limitations of our study should be considered. Wessessed childhood trauma retrospectively, and no external sourcesere contacted to verify the trauma history. Furthermore, our

ample included only 13% women, thus limiting our ability to detectossible gender effects. We examined a highly selected population,olice academy recruits, and used a police-specific stressor. Thus, it

s unclear whether our results are generalizable to other populationsith histories of childhood trauma. Although the time points we

hose to measure the cortisol and MHPG response to stress enableds to detect the peak response of cortisol (Dickerson and Kemeny004), we did not capture the complete recovery period. Thus, weight have missed differences in cortisol feedback sensitivity be-

ween groups. Also, we found only a modest effect size of the

cortisol increase to the stress challenge, which might have damp-ened group differences. Furthermore, we did not measure ACTHand cannot exclude the possibility that there were differences inpituitary responsiveness between groups. Because we measuredsalivary free cortisol, other factors, such as differences in corticoste-roid-binding globulin, might have contributed to our failure to findgroup or group � time effects for cortisol. Finally, our small samplesize might have reduced our power to detect differences in thecortisol response.

Our findings have interesting implications for the treatmentand prevention of anxiety disorders associated with childhoodtrauma exposure. Two recent studies showed that �-adrenergicblockade with propranolol immediately after a traumatic eventmight mitigate the development of psychopathology (Pitman etal 2002; Vaiva et al 2003). It would be of interest to examine theeffects of propranolol in a population with childhood traumahistories to treat or prevent PTSD at the time of adult retrauma-tization. Furthermore, those police academy recruits with child-hood trauma and/or an increased catecholamine response tostress might be at increased risk to develop PTSD after actualcritical incident exposure during active-duty police service. Wewill follow these officers longitudinally after they enter policeservice to determine whether a history of childhood traumaexposure and/or an increased stress response to the video isassociated with greater PTSD symptoms at follow-up.

In summary, we found a greater increase in catecholaminebut not cortisol response to psychological stress in healthy youngpolice academy recruits who reported a history of childhoodtrauma exposure. This might be a possible mechanism by whichchildhood trauma exposure increases the risk for the develop-ment of anxiety disorders in adulthood.

This work was supported by the National Institute of MentalHealth (5R01MH056350/06). CO was supported by a postdoc-toral fellowship from the Deutsche Forschungsgemeinschaft(grant Ot 209/2-1).

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