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Cite this article as: Danka Savic, Goran Knezevic, Gordana Matic, Svetozar
Damjanovic, Zeljko Spiric, Posttraumatic and depressive symptoms in β-
endorphin dynamics, Journal of Affective Disorders, http://dx.doi.org/10.1016/j.
jad.2015.03.063
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Posttraumatic and depressive symptoms in β-endorphin dynamics
Danka Savic ∗, PhD.1, Goran Knezevic, PhD.2, Gordana Matic, PhD.3, Svetozar
1
University of Belgrade, Vinca Institute, Belgrade, Serbia
2
University of Belgrade, School of Psychology, Belgrade, Serbia
3
University of Belgrade, Institute for Biological Research “Sinisa Stankovic”, Belgrade,
Serbia
4
Institute of Endocrinology, Diabetes and Metabolic Disease, University of Belgrade,
Belgrade, Serbia
5
Clinic for Psychiatry, Faculty of Medicine of the Military Medical Academy, University of
∗
Corresponding author: Danka Savic, Vinca Institute, PO Box 522, Belgrade, Serbia, danka.s@sbb.rs
Beta-endorphin, posttraumatic and depressive symptoms
2
Abstract
(PTSD) and depression allostasis. Study subjects (N=392) included those with PTSD
and/or (stress-induced) depression, and healthy controls with and without traumas. The
aim of the study was to examine the network of relations centered around plasma beta-
endorphin. The network included anxiety (as a personality trait), traumatic events, pain,
time points (BEmean), reflecting the total amount of the peripherally secreted hormone,
and the coefficient of variation (BEvar), calculated as the ratio of standard deviation to the
mean, reflecting the hormone's dynamics. BEvar correlated with all other variables,
BEmean had no correlations. Structural equation modeling (SEM) was used to examine all
interrelations (including their directions) of BEvar and the state/trait variables in the context
of their entirety. The model revealed that hyperarousal and anxiety were the only direct
Traumatic events and intrusions act on BEvar via hyperarousal, while depressive
symptoms, avoidance, and pain act via anxiety. Hyperarousal should be emphasized as
the main agent not only because its effect on BEvar is larger than that of anxiety, but also
because it increases anxiety itself (via avoidance and pain). All influences on BEvar are
positive and they indicate long-term (sensitizing) effects (as opposed to direct stimulation,
for example, by acute pain, anger, etc.). Relations apart from beta-endorphin are also
discussed.
Introduction
opiomelanocortin, along with ACTH and other derivatives, mostly in the pituitary, but also
in the brain (mainly in the hypothalamic arcuate nucleus). It is best known for its analgesic,
euphoric, and sedative effects, achieving them via µ-opioid (predominantly) and δ-opioid
respiration, to name just a few systems in which the role of β-endorphin is still being
such as anxiety (Colasanti et al., 2011), anger control (Bruehl, 2009) and aggression
(Roubertoux et al., 2005), depression (Hegadoren et al., 2009), addictions (Barry, 2012),
etc.
Beta-endorphin achieves its actions via the two hormonal systems (central and
peripheral) that do not necessarily work in parallel. Although β-endorphin poorly crosses
the blood-brain barrier, there is indirect evidence of its hypothalamic actions, found in
human (Inder et al., 1996; Catlin et al., 1980) and animal studies (Hargreaves et al., 1990;
Selmanoff & Gregerson, 1986). Van der Kolk et al. (1985) cite evidence that there is a rise
requirements in surgical patients and which parallels rise of other CNS opioids. De Kloet et
al. (1981) report severe behavioral deficit in mice following the removal of the pituitary.
The same authors, as well as Meisenberg and Simmons (1983), Veening et al. (2012), and
Amir et al. (1980), suggest mechanisms of communication between the central and
Beta-endorphin is overly secreted during stress, to suppress the pain and help the
organism react. It also has a role in HPA axis regulation (Amir et al., 1980). For these
reasons, the relations of beta-endorphin with traumas and related disorders are also
2009). Hoffman et al. (1989) propose plasma β-endorphin as a marker for PTSD after
finding the hormone diurnal levels to be significantly lower than in controls. Although
traumas are not explicitly included in the diagnosis of any type of depression as they are in
PTSD, trauma history is a factor in etiology of depression. In patients with trauma history, it
is often difficult to disentangle between these two disorders having extremely high
comorbidity rate (for example, Brown et al. (2001) report 80% with respect to PTSD) as
their symptomatologies largely overlap. Kotov et al. (2011) suggest that unipolar
depression would fit better with anxiety disorders than with bipolar disorders. The common
symptoms encompass sleep and dream abnormalities, pain, aggression (in the context of
defensive behavior and pain), disturbed memory, heightened anxiety, low mood and
anhedonia, loss of interests, social malfunctioning, etc. The listed phenomena are
accompanied by endogenous opioid system dysregulation (Hamner and Hitri, 1992; Lutz,
2013). This is confirmed in research with opioid receptor antagonists (Pitman et al., 1990;
Glover, 1993). Besides, Risch (1982) and Goodwin et al. (1993) found hightened plasma
correlations of plasma β-endorphin levels with anxiety and phobia in a mixed sample of
According to DSM-IV, both PTSD and depression belong to Axis I disorders, for which
it was shown to be connected to personality traits (Malouff et al., 2005). Traits are basic
Beta-endorphin, posttraumatic and depressive symptoms
5
(Zuckerman, 2005). Beside psychiatric aspect of anxiety as a syndrome forming the base
of personality. The difference between the two aspects is only quantitative (Iwata et al.,
2000). In the Big Five model (Costa & McCrae, 1992), it is operationalized as a
and fearful, and in its core lies anticipation of negative events. As beta-endorphin is a
When excessive, anxiety leads to illness (Hensley & Varela, 2008; Weems et al.,
2007). We thus supposed that the connections between beta-endorphin and this trait
symptomatology. On the other hand, there is a finding (Savic et al., 2012a; de Kloet et al.,
2007) that the sole number of traumatic events (without taking into account the intensity of
manifested as personality traits. This finding led us to suppose that traumatic events might
pituitary) as well.
The main task of this study was to examine the network of connections between
all measures on the same individuals and application of Structural equation modeling
(SEM) enabled us to investigate each relation (whose existence is known from the
literature) within the context of all mutual influences among the variables of interest and to
Beta-endorphin, posttraumatic and depressive symptoms
6
perceive the entirety of this network. The starting hypothesis was that anxiety (as a
personality disposition) and traumatic events lie in the root of the relations of beta-
endorphin with posttraumatic/depressive symptoms. The work was done within a larger
psychology and biology of PTSD (only the data relevant to the title are presented here).
Although PTSD itself is not in the main focus of this article, we used the advantage of the
Methods
subjects, recruitment procedure and sources, hospital protocol, and the instruments NEO-
Subjects
For the original project, four hundred male subjects (mean age 43.0±9.1) were recruited
and classified into four groups: current PTSD (N=133), lifetime PTSD (N=66), trauma
controls (N=102) and healthy controls (N=99), matched by age and education level. Eight
of them did not have beta-endorphin measures and were excluded from this study, leaving
392 subjects. Ethical approval was obtained from the Ethical Review Board of the
University Medical School, Belgrade, Serbia. All participants signed written consent,
Procedure
The participants were hospitalized for 2.5 days for the purpose of this study, following a
standardized protocol, within which they filled out self-report questionnaires and underwent
Beta-endorphin, posttraumatic and depressive symptoms
7
hourly blood sampling (via an iv line) during the first night, from 2200h to 0900h (plus at
The analyses for this report were done on the whole sample using continuous variables.
estimated by scores on The Clinician Administered PTSD Scale CAPS-DX (Blake et al.,
1996), clusters B, C, and D, respectively. The range of scores was 0-8 per item, obtained
by summing the intensity and frequency levels. When administering the CAPS-DX to
healthy subjects, the instruction was to relate the questions to the most distressing event
in their life. All other used instruments are self-reporting questionnaires with 5-point Likert-
type scale response format. Depression symptoms were assessed by Beck Depression
Pain was estimated as a sum of scores on four items (1,12, 27, 42) from The Symptom
back, and Soreness of muscles. SCL-90-R (Derogatis, 1983) is an instrument with 90 items
for assessing the current complex of psychological symptoms, acute stress and global
psychopathological status, according to the axis I DSM IV for mental disorder classification.
Anxiety was evaluated as a sum of scores on eight items intended to measure this
Aggression was assessed by the Aggression Questionnaire, AQ (Buss & Perry, 1992),
an instrument with 29 items encompassing physical and verbal aggression, anger and
hostility.
Traumatic events were calculated by summing the experienced war and civilian (life)
Beta-endorphin, posttraumatic and depressive symptoms
8
WSAQ–R (Jovic et al., 2002) with 67 items, and civilian stressors were assessed by self-
reporting instrument Life Event Check List LS-17 (Wolfe & Kimerling, 1997). It is a list of 16
possible traumatic life events plus an open item offering a possibility to add a distressing
method (Euro Diagnostica, Malmo, Sweden) after extraction using sep-pak C18 cartridges.
In this assay, antibodies against synthetic human beta endorphin were used. Intra-assay
and inter-assay variations were less than 8%. The lowest detection limit of the assay was
representation of the resting state (reduced external stimuli) than the day values. For beta-
endorphin particularly, we wanted to see whether its rise would accompany nightmares,
Statistical analysis
Data were analyzed using SPSS version 11.5 (SPSS Inc., USA) and LISREL 8.53
deviation. Groups were compared by ANOVA and post hoc Tukey HSD (honest significant
measures and other chosen variables, Pearson's correlations were calculated (after
modeling (SEM) - path analysis - was used to test the directions of these relations
(causality) in the context of the entirety of all postulated interrelations. In other words, a
is beta weight from multiple regressions, predicting a variable from all other variables
having a direct effect on it). Path analysis also enables decomposing the total effect of a
group of predictors into direct and indirect (through mediators) influences. For an adequate
fit, Hu and Bentler’s (1999) combinational rule was followed. Root Mean Square Error of
Approximation (RMSEA) should be less than .06, Comparative Fit Index (CFI) above .95,
and Standardized Root Mean Square Residual (SRMR) less than .08. Models’χ2 statistics
and associated df, confidence intervals for RMSEA are also presented. The model is fit
Results
To illustrate the structure of the sample, the means and standard deviations of the studied
There are no group differences on BEmean, while BEvar differs between current
PTSD and both controls, lifetime PTSD differs only from the healthy, trauma controls only
from the current PTSD group, and healthy from both PTSD groups. All groups, except
lifetime PTSD and trauma controls that are statistically the same, differ in the number of
traumatic events, and all groups, except both controls (statistically the same), differ in
All further analyses were performed on the whole sample as it provides broad ranges
The first step was to examine whether beta-endorphin was related to the chosen
BEmean had no correlations (the range of sigma (2-tailed): 0.333-0.972), while BEvar was
significantly correlated with all other variables (the range of sigma (2-tailed): 0.000-0.001),
satisfying the Bonferroni correction at the .003125 level (Table 2). Therefore, only BEvar
entered SEM.
The suggested model of the directions, context (direct and indirect effects), and the
strengths of influences on beta-endorphin fluctuations (Figure 1) were found to fit the data
adequately χ2=26.35, df=18, p=0.09, RMSEA (90% CI) =0.034 (0.000; 0.061), CFI=1.00,
SRMR=0.026. All variables (except Aggressiveness) had total effects on BEvar, but most
of them only indirect (except Hyperarousal and Anxiety that had the direct effect). All paths
shown are significant. None of the paths going from BEvar had a satisfactory fit.
Discussion
Although we have supposed that Anxiety (capital A signifies the NEO-PI R measure) and
traumatic events would influence both measures of plasma beta-endorphin, BEmean did
not have correlations with any of the observed variables (Table 2). This is in line with
between healthy controls and groups with PTSD (Baker et al. 1997; Hamner and Hitri,
1992) or depression (studies cited in the review of Hegadoren et al., 2009). In the same
vein, no significant correlations of resting beta-endorphin levels with BDI scores (Darko et
al., 1992) or with severity of pain perception (Bernstein et al., 1995) were reported.
. Contrary to BEmean, BEvar correlates with all the symptom variables (Table 2).
BEvar represents night fluctuations of the hormone which can be interpreted in part as
would act as internal stressors and directly induce beta-endorphin fluctuations. However,
none of the subjects reported having nightmares which we ascribed to their perception of
Structural Equation Modeling (SEM) inserted further accuracy into our understanding
of the relations by taking into account all of them, together with the postulated directions
(paths). An important fact for interpretation of the results is that beta-endorphin was
measured overnight directly, while all other variables were assessed by psychiatric
interview (CAPS) or self-questionnaires, not as direct stimuli (e. g., not during a state of
acute pain, aggressive outburst, or in the midst of a depressive episode). Therefore, the
peripheral beta-endorphin system. Seeing that all paths to BEvar are positive (Figure 1),
these contributions would mean sensitization of the system. It is very likely that for the
same reason (no direct stimuli), none of the paths goes from β-endorphin.
Figure 1 shows that hyperarousal and Anxiety have notable mediating effect, i.e. other
However, comparison of these two shows that hyperarousal is the key agent of peripheral
with falling and staying asleep (this last component is probably most directly responsible
for increase in BEvar). Although these symptoms are strongly related to traumatic events,
the traumas are not a necessary condition for their appearance, as shown by the part (one
third) of variance not explained by the events. However, all the measured variables are
interrelated via stress response mechanism, thus some degree of stress (chronic or past)
result of the locus coeruleus-norepinephrine (LC/NE) system and it has reciprocal relations
with the opioid system (Van der Kolk et al., 1985). The regulatory role of beta-endorhin in
the LC would correspond to a negative path from BEvar to hyperarousal, but the
introduction of such a path resulted in an unsatisfactory model fit. As said above, the
differences in assessment between the hormone and all other variables should be borne in
mind.
Along with its other functions (Aston-Jones & Cohen, 2005), LC/NE system is a part of
the complex fear/anxiety network. When overly persistent, the LC tonic activity becomes
maladaptive and leads to anxiety disorders, together with impairments of gabaergic and
serotonergic systems. Finan and Smith (2013) argue that the mesolimbic dopamine
system is involved in the "comorbidity triad" insomnia, pain, and depression, emphasizing
the connection between opioids and arousal. This triad is included in the network of
insomnia).
It is well known that anxiety and trauma-induced disorders have reciprocal links (for
example, Marshall et al., 2010). Anxious individuals are more prone to develop a disorder
that, once developed, further increases the level of anxiety. In our data, it seems that
Beta-endorphin, posttraumatic and depressive symptoms
13
Anxiety (assessed as a current self-report) is more a reflection of the disorders than of the
risk factor, because the paths from depressive and PTSD symptoms to Anxiety render a
better fit than the ones with opposite direction that were also examined.
Bruehl et al. (2009) started their review on anger expression and endogenous opioids
with the sentence: "For more than 60 years, the experience of pain has been reported to
be associated with various negative emotional states, including depression, anxiety, fear,
and anger". Our result that Anxiety, depression, and pain influence aggression fits well
with these reports which include acute and chronic pain, as well as diverse assessments
of anger/aggression. Aggression does not always stem from anger, but these notions
studies on both phenomena in their review. Actually, the type of aggression linked to anger
2004). In our model, the former type enters the mentioned circuits (with Anxiety,
depression, and pain), while the latter (encompassed by the Buss and Perry's AQ used
here) is probably responsible for the part of variance not explained by the model. Buss and
Perry (1992) found that the AQ components Anger and Hostility correlate with a
Opioids seem to relieve chronic (assessed here) and dull pain more than acute one
(Ribeiro 2005). There was a suggestion that they act only on affective component of pain
that increases as a function of time, but newer evidence speaks in favor of opioid actions
(Schwartz et al, 2006), as well as in depression and insomnia (Finan & Smith, 2013). Chiu
(2005) found that poor sleep and depression independently contribute to the reduction of
pain threshold. Our model shows the same: paths from hyperarousal (sleep problems) and
The path from traumatic events to depression symptoms confirms our earlier
conclusion that the depression in our subjects is trauma-induced (Savic et al, 2012b), as
its influence on dexamethasone suppression test is the same as that of PTSD (increased
suppression). The path from PTSD to depressive symptoms probably means that the
comorbid depression diagnosed in a number of subjects with PTSD is developed later than
PTSD which is in line with Kessler et al. (1996) and Regier et al. (1998).
as a defense mechanism and it is to a great extent the result of hyperarousal and intrusion
The strenghts of some paths (effect sizes) are small. However, Møller and Jennions (2002,
p.497) state that "even a minute effect size may be biologically important” because
organisms "are affected by innumerable biotic and abiotic factors”. The path from Anxiety
to BEvar is 0.13, but taking into account that personality trait is a distant aspect of the
Only a few subjects were positive on the CAPS measures of dissociation, so it could
not have been included. Knowing that this phenomenon is tightly related to opioids, its
detailed assessment would enable enriching the model. The study would have also
Conclusion
To resume, the fact that BEmean is not affected by the same variables that do affect
the examined variables while the overall quantity of the secreted hormone is not.
Traumatic events, intrusion, avoidance, depression, pain, and in the first place,
hyperarousal and Anxiety sensitize the peripheral beta-endorphin system, i.e., stimulate its
Beta-endorphin, posttraumatic and depressive symptoms
15
readiness to react. All these variables, together with aggression, form a network of
References
Amir, S., Brown, Z.W., and Amit, Z., 1980. The Role of Endorphins in Stress: Evidence
norepinephrine function: adaptive gain and optimal performance. Annu Rev Neurosci. 28,
403-450.
Baker, D.G., West S.A., Orth, D.N., Hill, K.K., Nicholson, W.E., Ekhator, N.N., Bruce, A.B.,
Wortman, M.D., Keck, P.E., Jr, Geracioti, T.D., Jr., 1997. Cerebrospinal fluid and plasma
Barry, S.M., Grisel, J.E., 2012. β-Endorphin and Alcoholism. In: Contreras, C.M. (Ed.)
http://www.intechopen.com/books/neuroscience-dealing-with-frontiers/beta-endorphin-and-
alcoholism.
Beck, A.T., Brown, G.K., Steer. R.A. (1996). Beck Depression Inventory Second Edition,
Bernstein, L., Garzone, P.D., Rudy, T., Kramer, B., Stiff, D., Peitzman, A., 1995. Pain
284.
Blake, D.D., Weathers, F.W., Nagy, L.M., et al. (1996). Clinician Administered PTSD Scale
for DSM-IV: Current and Lifetime Diagnostic Version. National Centre for Posttraumatic
Brown, T.A., Campbell, L.A., Lehman, C.L., Grisham, J.R., Mancill, R.B., 2001. Current
and lifetime comorbidity of the DSM-IV anxiety and mood disorders in a large clinical
Bruehl, S., Burns, J.W., Chung, O.Y., Chont, M., 2009. Pain-related effects of trait anger
Buss, A.H., Perry, M., 1992. The aggression questionnaire. J Pers Soc Psychol 63, 452-
459.
Catlin, D.H., Poland, R.E., Gorelick, D.A., Gerner, R.H., Hui, K.K., Rubin, R.T., Li, C.H.
1980. Intravenous infusion of beta-endorphin increases serum prolactin, but not growth
Colasanti, A., Rabiner, E.A., Lingford-Hughes, A., Nutt, D.J., 2011. Opioids and anxiety.
Darko, D.F., Risch, S.C., Gillin, J.C., Golshan, S., 1992. Association of β-endorphin with
de Kloet, C.S., Vermetten, E., Heijnen, C.J., Geuze, E., Lentjes, E.G.W.M., Westenberg,
Derogatis, L.R., 1983. SCL-90R: Administration, scoring and procedures manual II.
Finan, P.H., Smith, M.T., 2013. The comorbidity of insomnia, chronic pain, and depression:
Glover, H., 1993. A preliminary trial of nalmefene for the treatment of emotional numbing in
combat veterans with post-traumatic stress disorder. Isr J Psychiatry Relat Sci 30, 255–
263.
Goodwin, G.M., Austin, M-P., Curran, S.M., Ross, M., Murray, C., Prentice, N., Ebmeier,
Beta-endorphin, posttraumatic and depressive symptoms
18
K.P., Bennie, J. , Carroll, S., Dick, H., and Fink, G., 1993. The elevation of plasma β-
Hamner, M.B., Hitri, A., 1992. Plasma Beta-Endorphin Levels in Post-Traumatic Stress
Hargreaves, K.M., Flores, C.M., Dionne, R.A., Mueller, G.P., 1990. The role of pituitary
Hegadoren, K.M., O'Donnell, T., Lanius, R., Coupland, N.J., Lacaze-Masmonteil, N., 2009.
43(5):341-353.
Hensley, L. & Varela, R.E., 2008. PTSD Symptoms and Somatic Complaints Following
Hurricane Katrina: The Roles of Trait Anxiety and Anxiety Sensitivity. J Clin Child Adolesc
Hoffman, L., Watson, P.B., Wilson, G., Montgomery, J., 1989. Low Plasma β-Endorphin in
Hu, L., Bentler, P. M., 1999. Cutoff criteria for fit indexes in covariance structure analysis:
Inder, W.J., Livesey, J.H., Ellis, M.J., Evans, M.J., Donald, R.A., 1996.The effect of beta-
adrenal axis hormones in normal human subjects. Clin Endocrinol (Oxf). 44(1), 7-13.
Iwata, N., & Higuchi, H. R., 2000. Responses of Japanese and American university
students to the STAI items that assess the presence or absence of anxiety. J Pers Assess
74(1), 48-62.
Joreskog, K.G., Sorbom, D., 2002. LISREL8: Structural Equation Modeling with the
Likncolnwood, IL.
Jovic, V., Opacic, G., Knezevic, G., Tenjovic, L., Lecic-Tosevski, D., 2002. War Stressors
Kessler, R.C., Nelson, C.B., McGonagle, K.A., Liu, J., Swartz, M., Blazer, D.G. 1996.
Comorbidity of DSM-III-R major depressive disorder in the general population: results from
Kotov, R., Ruggero, C.J., Krueger, R.F., Watson, D., Yuan, Q., Zimmerman, M., 2011.
New Dimensions in the Quantitative Classification of Mental Illness. Arch Gen Psychiatry,
68(10), 1003-1011.
Kubryak, O.V., Umriukhin, A.E., Emeljanova, I.N., Antipova, O.S., Guseva, A.L., Pertsov,
S.S., Sudakov, S.K., 2012. Increased β-endorphin level in blood plasma as an indicator of
Beta-endorphin, posttraumatic and depressive symptoms
20
positive response to depression treatment. Bulletin exp biol med 153(5), 758-760.
Lutz, P. and Kieffer, B. L., 2013. Opioid receptors: distinct roles in mood disorders. Trends
Malouff, J. M., Einar, B. T., Schutte, N. S., 2005. The Relationship Between the Five-
Marshall, G.N., Miles, J.N.V., Stewart, S.H., 2010. Anxiety Sensitivity and PTSD Symptom
Severity Are Reciprocally Related: Evidence from a Longitudinal Study of Physical Trauma
McEllistrem, J.E., 2004. Affective and predatory violence: A bimodal classification system
of human aggression and violence. Aggression and Violent Behaviour 10, 1-30.
Meisenberg, G., Simmons, W.H., 1983. Peptides and the blood-brain barrier, Life Sci
32(23), 2611–2623.
Merenlender-Wagner, A., Dikshtein, Y., Yadid, G., 2009. The beta-endorphin role in stress-
Møller, A., Jennions, M. D., 2002. How much variance can be explained by ecologists and
Pitman, R.K., van der Kolk, B.A., Orr, S.P., Greenberg, M.S., 1990. Naloxone-reversible
Regier, D.A., Rae, D.S., Narrow, W.E., Kaelber, C.T., Schatzberg, A.F., 1998. Prevalence
of anxiety disorders and their comorbidity with mood and addictive disorders. Br J Psych
Roubertoux, P.L., Guillot, P.-V., Mortaud, S., Pratte, M., Jamon, M., Cohen-Salmon, C.,
Tordjman, S., 2005. Attack behaviors in mice: From factorial structure to quantitative trait
Savic, D., Knezevic, G., Damjanovic, S., Spiric, Z., Matic, G., 2012a. The role of
personality and traumatic events in cortisol levels — Where does PTSD fit in?.
Savic, D., Knezevic, G., Damjanovic, S., Spiric, Z., Matic, G., 2012b. Is there a biological
Van der Kolk, B., Greenberg, M., Boyd, H., Krystal, J.,1985. Inescapable Shock,
Veening, J.G., Gerrits, P.O., Barendregt, H.P., 2012. Volume transmission of beta-
endorphin via the cerebrospinal fluid; a review. Fluids and Barriers of the CNS 9:16.
Weems, C.F., Pina, A.A., Costa, N.M., Watts, S.E., Taylor, L.K., Cannon, M.F., 2007.
Predisaster Trait Anxiety and Negative Affect Predict Posttraumatic Stress in Youths After
Wolfe, J., Kimerling, R., 1997. Gender issues in the assessment of PTSD. In: Wilson, J.P.
& Keane, T.M. (Eds.), Assessing Psychological Trauma and PTSD, Guilford Press, New
Zuckerman, M., 2005. Psychobiology of Personality, 2nd ed. Cambridge University Press,
New York.
Figure caption
fluctuations. The arrowed lines between boxes denote significant paths; the arrows show
Beta-endorphin, posttraumatic and depressive symptoms
23
the directions of influences; the associated numbers denote path coefficients; small arrows
Table 1. Mean values of the examined variables in the whole sample and by groups. The
meanings of variables given in the text.
Y S N E AL N N N
-
BEmea -.041 -.033 -.005 -.025 -.003 .002 -.049
.027
n
.419 .516 .929 .617 .955 .972 .601 .333
.219
** ** ** ** ** ** **
.252 .205 .218 .273 .275 .171 .218
**
BEvar
This work was financed by European Commission, via Sixth Framework Programme
Projects Nos 179018 and 41009. The funders had no role in: the study design; collection,
analyses and interpretation of the data; writing of the report; submitting of the paper.
Contributors
All authors designed and wrote the protocol of the study whose part is this manuscript.
Also, all authors have participated in the interpretation of results and approved the final
manuscript. Danka Savic wrote the manuscript and together with Goran Knezevic
performed statistical analyses.
This work was financed by European Commission, via Sixth Framework Programme
Projects Nos 179018 and 41009. The funders had no role in: the study design; collection,
analyses and interpretation of the data; writing of the report; submitting of the paper.
Figure(s)
.39 0.27
.27
.22
.41
.56 DEPRESSIVE
ANXIETY
SYMPTOMS .32
.47
.35
.18
.13
.25
1.00 TRAUMATIC
EVENTS
β-ENDORPHIN
.26
.56 fluctuations
.91
INTRUSIONS
.69 .18 .20
.39
.71
AVOIDANCE HYPERAROUSAL
.23 .53 .32