Allen 2013, Revisión TSST

ARTICLE IN PRESS
G Model
NBR 1866 1–31
Neuroscience and Biobehavioral Reviews xxx (2013) xxx–xxx
Contents lists available at ScienceDirect
Neuroscience and Biobehavioral Reviews

journal homepage: www.elsevier.com/locate/neubiorev
1 Review
2 Biological and psychological markers of stress in humans:

3 Focus on the Trier Social Stress Test
4 Q1 Andrew P. Allen a,b , Paul J. Kennedy a,b , John F. Cryan a,c , Timothy G. Dinan a,b ,
5 Gerard Clarke a,b,∗
a
6 Alimentary Pharmabiotic Centre, University College Cork, Cork, Ireland
b
7 Department of Psychiatry, University College Cork, Cork, Ireland
c
8 Department of Anatomy and Neuroscience, University College Cork, Cork, Ireland
9
10 a r t i c l e i n f o a b s t r a c t
11
12 Article history: Validated biological and psychological markers of acute stress in humans are an important tool in trans-
13 Received 1 August 2013 lational research. The Trier Social Stress Test (TSST), involving public interview and mental arithmetic
14 Received in revised form 1 November 2013 performance, is among the most popular methods of inducing acute stress in experimental settings,
15 Accepted 6 November 2013
and reliably increases hypothalamic-pituitary-adrenal axis activation. However, although much research
16 has focused on HPA axis activity, the TSST also affects the sympathetic-adrenal-medullary system, the
17 Keywords:
immune system, cardiovascular outputs, gastric function and cognition. We critically assess the utility
18 Stress
of different biological and psychological markers, with guidance for future research, and discuss fac-
19 Cortisol
20 ACTH
tors which can moderate TSST effects. We outline the effects of the TSST in stress-related disorders, and
21 Serotonin if these responses can be abrogated by pharmacological and psychological treatments. Modified TSST
22 HPA axis protocols are discussed, and the TSST is compared to alternative methods of inducing acute stress. Our
23 Sympathetic-adrenal-medullary system analysis suggests that multiple readouts are necessary to derive maximum information; this strategy
24 Brain–gut axis will enhance our understanding of the psychobiology of stress and provide the means to assess novel
25 Heart rate therapeutic agents.
26 Immune system © 2013 Published by Elsevier Ltd.
27 Genetics
28 Contents
29 1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
30 1.1. General introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
31 1.2. The Trier Social Stress Test . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
32 2. Biomarkers and psychological effects of the TSST . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
33 2.1. Biomarkers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
34 2.1.1. Hypothalamic-pituitary-adrenal (HPA) axis effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
35 2.1.2. Immune system effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
36 2.1.3. Sympathetic-adrenal-medullary system effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
37 2.1.4. Cardiovascular effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
38 2.1.5. Brain–gut axis effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
39 2.1.6. Biomarkers: summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
40 2.2. Psychological effects. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
41 2.2.1. Subjective effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
42 2.2.2. Cognitive effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
43 2.2.3. Neurobiological effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
44 2.2.4. Psychological effects: summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
45 3. Procedural considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
46 3.1. Biomarkers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
47 3.1.1. HPA axis measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
∗ Corresponding author at: Department of Psychiatry, 1.15 Biosciences Institute, University College Cork, Cork, Ireland. Tel.: +353 21 4901408.
E-mail address: G.Clarke@ucc.ie (G. Clarke).
0149-7634/$ – see front matter © 2013 Published by Elsevier Ltd.

http://dx.doi.org/10.1016/j.neubiorev.2013.11.005
Please cite this article in press as: Allen, A.P., et al., Biological and psychological markers of stress in humans: Focus on the Trier Social Stress
Test. Neurosci. Biobehav. Rev. (2013), http://dx.doi.org/10.1016/j.neubiorev.2013.11.005
ARTICLE IN PRESS
G Model
NBR 1866 1–31
2 A.P. Allen et al. / Neuroscience and Biobehavioral Reviews xxx (2013) xxx–xxx
3.1.2. Immune system measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00

3.1.3. Sympathetic-adrenal-medullary system measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
3.1.4. Cardiovascular measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
3.1.5. Brain–gut axis measures. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
3.1.6. Procedural considerations in biomarkers: summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
3.2. Psychological effects. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
3.2.1. Subjective measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
3.2.2. Cognitive measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
3.2.3. Procedural considerations in psychological effects: summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4. Factors moderating the effects of the TSST . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.1. Gender and age . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.1.1. Age and gender differences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.1.2. Sex hormones and menstrual cycle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.2. Genetics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.3. Personality and individual differences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.3.1. Personality factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.3.2. Stressor appraisal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.4. Social factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.4.1. The interview panel . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.4.2. Social support and social status . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.4.3. Cultural factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.5. Factors moderating the effects of the TSST: summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
5. TSST response and stress-related psychiatric disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
5.1. Depression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
5.2. Anxiety . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
5.3. Other stress-related psychiatric disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
5.4. Factors moderating TSST response in stress-related disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
5.5. Treatment for stress-related psychiatric disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
5.5.1. Psychological treatment for stress-related psychiatric disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
5.5.2. Pharmacological treatment for stress-related psychiatric disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
5.5.3. Dietary interventions for stress . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
5.6. TSST and stress-related psychiatric disorders: summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
6. Modified versions of the TSST . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
6.1. Repeated measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
6.2. Control TSST . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
6.3. Group assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
6.4. Children and adolescents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
6.5. Virtual/imagined TSST committee . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
6.6. Hybrid versions of the TSST . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
6.7. Modified versions of the TSST: summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
7. Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
7.1. Comparison with other methods of inducing stress and measuring HPA axis activity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
7.1.1. Pharmacological stimulation of the HPA axis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
7.1.2. The cold pressor task . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
7.1.3. The CO2 challenge test . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
7.1.4. The cortisol awakening response . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
7.1.5. Cognitive tasks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
7.1.6. Noise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
7.1.7. Comparison with other methods of inducing stress and measuring HPA axis activity: summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
7.2. Future research . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
7.3. Summary and conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
48 1. Introduction et al., 2007; Starcke and Brand, 2012). Although acute stress is 60
important for responding to threatening situations, chronic stress is 61
49 1.1. General introduction damaging to health (McEwen, 2007). Over time, stressful life events 62
can induce chronic stimulation of the HPA axis, leading to depres- 63
50 Exposure to a situation perceived as threatening or excessively sion (Checkley, 1992; Juruena et al., 2011), and poorer prognosis 64
51 demanding (a stressor) leads to the release of chemicals which can for cancer and heart disease (Maddock and Pariante, 2001). Early- 65
52 help cope with the stressor (e.g. Joels and Baram, 2009; Schwabe life stress is associated with disorders such as depression (Batten 66
53 et al., 2012). Acute stress can alter numerous biological functions, et al., 2004; Dinan, 2005), post-traumatic stress disorder (Koenen 67
54 such as the hypothalamic-pituitary-adrenal (HPA) axis (Foley and et al., 2007), and irritable bowel syndrome (Mayer et al., 2001), 68
55 Kirschbaum, 2010), the immune system (Steptoe et al., 2007), the and chronic work stress can exacerbate anxiety and depression 69
56 autonomic nervous system (Xhyheri et al., 2012), and the enteric (Smith, 2000). Moreover, chronic stress will result in changes in 70
57 nervous system (Ziegler, 2012). Psychologically, acute stress is a subsequent reactivity to an acute stressor (e.g. Chatkoff et al., 2010; 71
58 subjectively negative experience (but see Jamieson et al., 2013), and Low et al., 2009; Roth et al., 2012). Given the contrast between 72
59 can have positive as well as negative effects on cognition (Lupien acute and chronic stress, it is of interest to examine the effects 73
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74 of acute stress in the context of disorders associated with chronic research contexts. Finally, the TSST is compared to different meth- 138
75 stress. ods of studying acute stress, and suggestions for future research are 139
76 Preclinical methods for inducing stress are well established offered (Section 7). 140
77 (Buynitsky and Mostofsky, 2009) and preclinical research has pro-

78 vided insight into the effects of stress, the possible role of factors 2. Biomarkers and psychological effects of the TSST 141
79 such as neurotransmitters (e.g. Browne et al., 2011; Cryan et al.,

80 2004; Julio-Pieper et al., 2012) and the interaction between the 2.1. Biomarkers 142
81 central and enteric nervous systems (Cryan and Dinan, 2012). There
82 is now growing recognition that preclinical efforts to gain greater 2.1.1. Hypothalamic-pituitary-adrenal (HPA) axis effects 143
83 insight into the effects of stress and stress mechanisms need to be In response to stress, the release of corticotropin-releasing fac- 144
84 bolstered by translationally relevant studies in human populations. tor from the paraventricular nucleus of the hypothalamus leads to 145
85 Accordingly, a stressor which can reliably produce a psychophysi- the release of ACTH from the pituitary gland, which in turn leads 146
86 ological stress response in humans under controlled conditions is to the secretion of cortisol from the adrenal gland (see Fig. 2). 147
87 of immense value to this field. Glucocorticoids such as cortisol can affect the activity of miner- 148
alocorticoid receptors as well as glucocorticoid receptors, and the 149
88 1.2. The Trier Social Stress Test interaction between the two types of receptor may play a key 150
role in mediating glucocorticoid feedback inhibition (Pariante and 151
89 Social stressors are amongst the most reliable forms of stress Lightman, 2008). A significant increase in HPA axis activity follow- 152
90 in humans and other species (Dickerson and Kemeny, 2004; ing exposure to the TSST is well established. 153
91 Tamashiro et al., 2005). The Trier Social Stress Test (TSST) is an acute
92 stress protocol used to experimentally study the stress response 2.1.1.1. ACTH and cortisol. Numerous studies have indicated 154
93 in human subjects. It was designed by researchers at the Univer- increases in ACTH and cortisol (e.g. Buske-Kirschbaum et al., 2007; 155
94 sity of Trier and first outlined in the early nineties (Kirschbaum Gerra et al., 2001; Kirschbaum et al., 1994; Munro et al., 2005), with 156
95 et al., 1992, 1993). The procedure runs as follows (Kudielka et al., studies observing an increase in salivary, plasma and serum corti- 157
96 2007): after a rest period on entering the laboratory, which helps sol (e.g. Gaab et al., 2002, 2005a; Jezova et al., 2004; Kirschbaum 158
97 to establish a clear baseline (Balodis et al., 2010), participants et al., 1993, 1999). Peaks in salivary cortisol levels commonly occur 159
98 are introduced to a role-playing scenario. They have to prepare a 10 min after cessation of stress exposure (e.g. Gaab et al., 2002; Het 160
99 speech to convince a panel that they are the perfect candidate for et al., 2009; Petrowski et al., 2010; Rimmele et al., 2007, 2009), 161
100 a job, which they must then present to a panel of assessors, fol- although peaks have also been observed 5 min (Childs et al., 2006), 162
101 lowed by a mental arithmetic task (serial subtraction). Following and 20 min (Rohleder et al., 2001) post-stress. Cortisol has also been 163
102 these tasks participants rest and post-stressor measures are taken; found to increase 14–20 min after the onset of stress anticipation 164
103 ideally, multiple time points should be used to chart changes in (Engert et al., 2013) and cortisol levels recovered more steeply in 165
104 biological and psychological effects (see Fig. 1 for a detailed out- participants who had experienced higher anticipatory stress (Juster 166
105 line of the typical procedure). Whereas public speaking and mental et al., 2012). Taken together, these findings suggest that multiple 167
106 arithmetic tasks in isolation induce small or inconsistent effects, time point sampling is necessary to fully capture the stress-induced 168
107 the TSST employs a combination of elements (public speaking, cortisol response. 169
108 mental arithmetic, anticipation, social evaluation) to produce mod- A minority of participants have a HPA axis response that does 170
109 erate stress in a majority of participants (Kirschbaum et al., 1993) not fall over repeated exposure (Kirschbaum et al., 1995b) and a 171
110 and reliable responses in the hypothalamic-pituitary-adrenal axis minority may even experience sensitisation (Wüst et al., 2005). In 172
111 (HPA axis) in particular (Kudielka et al., 2007), with cortisol and the majority of participants who experience increased cortisol, this 173
112 adrenocorticotropic hormone (ACTH) being most frequently stud- response habituates to repeated TSST administration over repeated 174
113 ied. Characteristics of the TSST which may explain its effectiveness sessions (Gerra et al., 2001; Mischler et al., 2005; Schommer et al., 175
114 come from a meta-analysis which has indicated that stressor tasks 2003; von Känel et al., 2006) (see Section 6.1 for further discussion 176
115 associated with social-evaluative threat and are uncontrollable (i.e. of repeated exposure to the TSST). 177
116 the participants’ behaviour does not have a clear effect on the out-
117 come of the task) are particularly effective in inducing a HPA axis 2.1.1.2. Vasopressin. Vasopressin is involved in the regulation of 178
118 response (Dickerson and Kemeny, 2004). Het et al. (2009) have the HPA axis and may also be altered in stress-related disor- 179
119 highlighted that there are two types of research in which the test is ders such as depression (Scott and Dinan, 1998). For example, 180
120 used; research investigating the effects of stress on outcomes rel- the response of the pituitary gland’s vasopressin V3 receptors to 181
121 evant to the stress process (e.g. neuroendocrine or psychological arginine vasopressin stimulation is increased in depression (Dinan 182
122 variables), as well as research on how certain factors (e.g. gender and Scott, 2005). Exogenous vasopressin enhanced the cortisol 183
123 or psychiatric disorders) may moderate the stress response. response to the TSST, although vasopressin did not have this effect 184
124 Stress is associated with a number of physiological effects (see for a low-stress control or bike ergometry (Shalev et al., 2011). How- 185
125 Fig. 2). The following review discusses the effects of the TSST on key ever, the TSST did not affect plasma vasopressin in lactating women 186
126 biomarkers of stress (e.g. HPA axis activity, immune activation), as (Heinrichs et al., 2001). 187
127 well as its psychological effects (cognitive performance and subjec-

128 tive effects) (Section 2). Procedural considerations for biomarkers 2.1.1.3. DHEA and DHEA-S. The androgen precur- 188
129 and psychological effects are than discussed (Section 3), followed sors dehydroepiandrosterone/DHEA and its metabolite 189
130 by factors which can moderate TSST effects (Section 4). The effects dehydroepiandrosterone-sulphate/DHEA-S increase in response 190
131 of the TSST in participants with stress-related psychiatric disor- to the TSST in healthy participants, and this response is positively 191
132 ders (e.g. anxiety disorders, major depressive) are then discussed related to that of cortisol (Izawa et al., 2008; Lennartsson et al., 192
133 (Section 5). Modifications of the TSST are outlined, as well as how 2012b). Higher levels of work stress have been associated with a 193
134 these modified versions may impact on biological and psychologi- lower DHEA-S response to the TSST, although this effect was not 194
135 cal outcomes (Section 6). Minor modifications to the TSST have been evident for DHEA (Lennartsson et al., 2013). Participants with low 195
136 made to investigate specific research questions; this review focuses baseline DHEA-S have shown a stronger cognitive response to a 196
137 on modifications which may be useful for a number of different social rejection version of the TSST (Akinola and Mendes, 2008). 197
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Fig. 1. Typical Trier Social Stress Test procedure. (A). Key procedural stages: The baseline rest and stress procedures are carried out in separate rooms (depicted as Room A and
Room B). The baseline rest phase takes place in Room A. Following task instructions, participants then complete the stress procedure in Room B. The content of the speech
varies between laboratories but most commonly involves participants imagining they have applied for their ideal or dream job, and have to convince a committee why they
are the best candidates for the job. Importantly, for the stress procedure to be successful, committee members are pre-trained to be completely impartial and provide no
encouragement verbally or non-verbally. They are also typically introduced as experts in behavioural analysis and at identifying non-verbal signs of stress. Participants are
told to continue speaking if they stop early. If the participant stops for 20 s before the 5 min is up, they are told to continue, and if another pause occurs the panel ask a series of
prepared questions. Following the speech task participants are then given a surprise mental arithmetic task; they must serially subtract a two-digit number from a four-digit
number (e.g. 17 from 2023), speaking aloud. If they make an error they are required to start again. Following the stress procedure, participants return to Room A for the
recovery period. (B). Example sampling schedule: The baseline rest period varies depending on the type of samples which will be collected. If salivary cortisol is the key measure
then a 30 min period is required to allow hypothalamic-pituitary-adrenal axis activity to normalise, as the process of attending the laboratory session itself will likely cause an
increase in HPA-axis activity in many participants. If blood is to be collected via an indwelling catheter, a baseline rest period of 45–60 min is recommended (Kudielka et al.,
2007). Samples/measures are collected immediately pre- and post-stress. Following the stress procedure, repeated samples are collected at 10–15 min intervals. The length
of the recovery period will depend upon the nature and number of measures being taken, although a period of 60 min is frequently used. Typical time points for sampling
are indicated by numbers in red. (C). Measures: A number of physiological and psychological parameters may be measured throughout the procedure via saliva (e.g. cortisol,
␣-amylase), blood (e.g. plasma/serum cortisol, cytokines, noradrenaline), psychophysiological tests (galvanic skin response, heart rate, blood pressure), cognitive measures
(e.g. attention, memory, executive function) and psychometric tests (e.g. stress, anxiety, perceived control).
198 Although DHEA and cortisol are both secreted by the adrenal influence cytokine production (Sapolsky et al., 2000). Indeed, the 218
199 cortex, cortisol is secreted from the zona fasciculata, while DHEA TSST response of the transcription factor nuclear factor kappa B, 219
200 is secreted from the zona reticularis (Nguyen and Conley, 2008). which induces inflammatory genes, has been associated with cor- 220
201 DHEA and cortisol responses can diverge – for example, DHEA tisol responses (Wolf et al., 2009). 221
202 does not show the post-awakening increase evident in cortisol Following the TSST, increases have been observed in lym- 222
203 (Hucklebridge et al., 2005). However, the findings from TSST phocytes, monocytes (Buske-Kirschbaum et al., 2002b, 2007), 223
204 research suggest that DHEA and cortisol responses do not diverge neurophil, basophil (Buske-Kirschbaum et al., 2002b) granulocytes, 224
205 in response to psychosocial stress (Lennartsson et al., 2012b). T cells, T helper cells and natural killer cells, but not B cells (Buske- 225
Kirschbaum et al., 2007) and higher monocytes have been observed 226
206 2.1.2. Immune system effects 1 h post-TSST (Rohleder et al., 2002). The effect on monocytes was 227
207 Cell types involved in the immune system include lymphocytes not replicated in a later study, although the TSST did increase leuko- 228
208 (the principal effector cells of the immune system; comprising T cytes (Gaab et al., 2005a). Changes in cortisol and ACTH in response 229
209 cells and B cells), cytokines, neurophils, basophils granulocytes to the TSST correlated positively with changes in granulocyte and 230
210 and T helper cells. These cells can be mobilised to fight infection natural killer cells and correlated negatively with changes in B cells 231
211 or modulate inflammation (e.g. Guo et al., 2002; Salazar-Mather (Buske-Kirschbaum et al., 2007). Although the TSST increased sali- 232
212 et al., 1996) but in addition to these functions the immune systems vary cortisol in healthy undergraduates, there was no effect on 233
213 are sensitive to stress (for reviews, see Kemeny and Schedlowski, C-reactive protein, and a non-significant increase in salivary lev- 234
214 2007; Pruett, 2003). Furthermore, HPA activity and the immune els of secretory immunoglobulin-A (Campisi et al., 2012), although 235
215 systems are linked; pro-inflammatory cytokines can activate the an increase in light chain immunoglobulin-A has been observed 236
216 HPA axis (Turnbull and Rivier, 1999) and alter glucocorticoid recep- elsewhere (Trueba et al., 2012). Levels of the pro-inflammatory 237
217 tor translocation (Miller et al., 1999), and glucocorticoids can cytokine interleukin-6 (IL-6) increase in response to the TSST in 238
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Fig. 2. Psychophysiological reaction to stress. The hypothalamus and other regions of the central nervous system interact in response to stress and anxiety. Strong anticipatory
anxiety increases activation in the pregenual ACC, but moderate anxiety reduces activation (Straube et al., 2009). Recent life stress is associated with reduced mPFC size
(Ansell et al., 2012), and acute stress can alter reward processing in the OFC (Porcelli et al., 2012). The amygdala, which contains corticotropin-releasing factor receptors
(Jochman et al., 2005), is sensitised by stress (van Marle et al., 2009), and is involved in the formation of stress-related memories in the hippocampus (Kim et al., 2001). The
hippocampus itself is involved in inhibitory regulation of the HPA axis (Herman et al., 2005). Stress precipitates a chain of events in the HPA axis and immune systems: (A).
The hypothalamus activates the pituitary gland through the secretion of corticotropin-releasing factor. (B). The pituitary gland activates the adrenal gland through secretion
of ACTH. (C). The adrenal gland secretes cortisol. The negative feedback mechanism of cortisol (Gibbison et al., 2013; Posener et al., 1997) is reduced by chronic exposure to
stress, maintaining excessive secretion of cortisol. (D). Glucocorticoid receptors are activated by cortisol from the adrenal glands. The structures involved in the function of
neurotransmitters such as noradrenaline, dopamine and serotonin contain GC receptors (Czyrak and Chocyk, 2001; Laaris et al., 1995; Li et al., 2011). Excessive stimulation
of GC receptors impairs the function of these neurotransmitters. (E). Altered neurotransmitter function affects the CNS, visible in cognitive function (see Section 2.2.2 for
a discussion of cognitive effects of the TSST). (F). Heightened cortisol secretion leads to a disrupted response in the immune system (Corwin et al., 2013; Sapolsky et al.,
2000). (G). Immune responses lead to immunotransmitter activation in the CNS (Shanahan, 1999); pro-inflammatory cytokines can enter the CNS, where they interact with a
cytokine network, and in cases of chronic stress this can enhance the risk of neuropsychiatric disorder (Capuron and Miller, 2011). CNS, central nervous system; ACC, anterior
cingulate cortex; MPFC, medial prefrontal cortex; OFC, orbitofrontal cortex; GC, glucocorticoid; 5-HT, serotonin; NA, noradrenaline; DA, dopamine
239 healthy adults (Slavich et al., 2010); salivary IL-6 can increase by with higher heart rate during the mental arithmetic task and lower 254
240 50% in response to the TSST and remain elevated 20 min post- cortisol response (Izawa et al., 2013b). 255
241 stressor (Izawa et al., 2013b). Lipopolysaccharide (LPS)-stimulated

242 IL-6 production has also been found to increase immediately post- 2.1.3. Sympathetic-adrenal-medullary system effects 256
243 TSST, returning to baseline levels 1 h later (Bellingrath et al., 2013). The sympathetic-adrenal-medullary system releases the cate- 257
244 Although the cortisol response habituated to repeated TSST admin- cholamines adrenaline and noradrenaline, activating a “fight or 258
245 istration over three weekly sessions in healthy men, IL-6 did not flight” response (Wetherell et al., 2006). Adrenaline increases fol- 259
246 (von Känel et al., 2006). IL-2 has been found to be higher post- lowing the TSST (Gold et al., 2004; Jezova et al., 2004). Furthermore, 260
247 TSST for teachers with poor coping strategies (Bellingrath et al., the sympathetic-adrenal-medullary system shows less habituation 261
248 2010). Compared to a control condition (reading a newspaper), than the HPA axis to repeated exposure to the TSST (three sessions 262
249 plasma IL-1␤ has been raised by the TSST, although TNF-␣, IL-2, with four week intervals between them) (Schommer et al., 2003). 263
250 IL-12, interferon-␥ (IFN-␥) and IL-6 did not change significantly Adrenaline response did not change across sessions; noradrenaline 264
251 (Yamakawa et al., 2009). The interaction between the immune sys- showed less of an increase for the third session, although this may 265
252 tem, sympathetic nervous system and the HPA axis is evident in have been due to elevated levels at the beginning. Sympathetic- 266
253 findings that higher IL-6 elevation following the TSST is associated adrenal-medullary activity can also be tracked using the enzyme 267
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268 ␣-amylase (for a review, see Nater and Rohleder, 2009) and gal- et al., 2012). Increases in leptin (a protein which regulates sati- 332
269 vanic skin response, a measure of activity of sweat glands which ety) post-TSST have been associated with reduced intake of foods 333
270 are innervated by the sympathetic nervous system (GSR; El-Sheikh high in sugar and fat for healthy women (Tomiyama et al., 2012), 334
271 et al., 2008; Graeff et al., 2003). The TSST induces increased salivary although the TSST did not induce a significant change in leptin. 335
272 ␣-amylase (sAA), with peaks observed immediately post-stress Stress response to the TSST can also affect feeding behaviour in 336
273 (Gordis et al., 2006; Het et al., 2009) and increased GSR (Jezova et al., those suffering from an eating disorder (see Section 5.3). Given 337
274 2004; Rohrmann et al., 1999). Although the TSST increases sAA as the reliable increase in HPA axis activity by the TSST, it is ideal for 338
275 well as plasma adrenaline and noradrenaline, these responses are investigating the impact of stress on brain–gut axis functioning, in 339
276 not correlated, suggesting that although sAA and catecholamines relation to both stress related functional gastrointestinal disorders 340
277 can both be used to assess sympathetic-adrenal-medullary system such as IBS, and with regard to modulating hunger and satiety. 341
278 activity, these measures are not redundant (Nater et al., 2006).
2.1.6. Biomarkers: summary 342
279 2.1.4. Cardiovascular effects The TSST reliably induces increased HPA axis activity (with 343
280 In contrast with the peak in cortisol which occurs post- extensive evidence for heightened ACTH and cortisol secretion 344
281 stress, the TSST raises heart rate throughout stress exposure, and post-stress, as well as recent evidence for an associated increase 345
282 heart rate returns to pre-stress levels within approximately 5 min in DHEA and DHEA-S) as well as sympathetic-adrenal-medullary 346
283 (Buske-Kirschbaum et al., 2002a; Childs et al., 2006). Peaks in activity (evident in enhanced adrenaline and sAA). There is also evi- 347
284 heart rate have been observed at the beginning of the stressor dence that the TSST can alter cardiovascular activity (e.g. increased 348
285 (Rimmele et al., 2007), as well as 1 min (Rimmele et al., 2009), heart rate and systolic blood pressure) and immune system activ- 349
286 15 min (Yamakawa et al., 2009) and 30 min (Jezova et al., 2004) ity (e.g. by increasing activation of the pro-inflammatory cytokine 350
287 into the stressor. Heart rate variability can also provide insight into IL-6). Effects of the TSST on the brain–gut axis are an interesting 351
288 the activity of the sympathetic and parasympathetic nervous sys- avenue for TSST research, with emerging evidence for altered feed- 352
289 tems. Heart rate variability measures include power in the high ing behaviour, although there is a lack of research using the TSST 353
290 frequency range (HF; 0.15–0.4 Hz), which is indicative of parasym- to examine the effects of acute stress on factors such as abdominal 354
291 pathetic tone, power in the low frequency range (LF; 0.04–0.15 Hz) discomfort and urgency. 355
292 which has been suggested as a marker of sympathetic tone, and the
293 ratio of HF to LF, which is indicative of an interaction between sym- 2.2. Psychological effects 356
294 pathetic and vagal activity (for a review, see Xhyheri et al., 2012).
295 Although the TSST consistently increases heart rate, heart rate vari- 2.2.1. Subjective effects 357
296 ability (high frequency band variance) did not differ between a Although exposure to stress can lead to different subjective 358
297 TSST and a control condition (reading a newspaper aloud) (Rohleder effects depending upon appraisal of the stressor (see Section 4.3), 359
298 et al., 2006), nor did the TSST affect cardiac vagal tone, as assessed stress is generally a subjectively negative experience. The TSST 360
299 via respiratory sinus arrhythmia (Altemus et al., 2001). In contrast, increases reported stress (Buske-Kirschbaum et al., 2002b; Sugaya 361
300 another study indicated that a number of heart variability measures et al., 2012), and anxiety (Jezova et al., 2004; Rimmele et al., 362
301 changed significantly between baseline and post-TSST, including 2007, 2009; Rohrmann et al., 1999; von Dawans et al., 2011), and 363
302 HF, LF and HF/LF (Lackschewitz et al., 2008). The TSST has increased reduces reported calmness (Childs et al., 2006; Kirschbaum et al., 364
303 both systolic blood pressure (SBP; i.e. highest reading) and diastolic 1999). Administration of the TSST also leads to higher wakeful- 365
304 blood pressure (DBP; i.e. lowest reading) (Jezova et al., 2004). Other ness (Kirschbaum et al., 1999), although the TSST did not increase 366
305 studies have indicated that SBP, but not DBP, increased in response reported alertness elsewhere (Gray et al., 2012; Sketchley-Kaye 367
306 to the TSST (Campisi et al., 2012; Gerra et al., 2001). A measure of et al., 2011). Broader measures of mood have also been used; the 368
307 mean arterial blood pressure which combines SBP and DBP recov- TSST worsened negative mood as assessed by the positive and neg- 369
308 ered more steeply in participants experiencing higher anticipatory ative affect scale (PANAS) (Firk and Markus, 2009; Yim et al., 2010) 370
309 stress (Juster et al., 2012). as well as on the multidimensional mood questionnaire (Rimmele 371
et al., 2007, 2009) and on a visual analogue scale (Childs et al., 2006). 372
310 2.1.5. Brain–gut axis effects

311 In addition to modulating activity in the central and auto- 2.2.2. Cognitive effects 373
312 nomic nervous systems, stress and associated HPA axis activity can The endocrine, immune and central nervous systems are closely 374
313 affect the enteric nervous system; corticotropin-releasing factor connected (Leonard and Song, 1999); stress hormones can easily 375
314 signalling pathways in the gut alter gastrointestinal motility (Liu cross the blood–brain barrier, and can affect learning and memory 376
315 and Wood, 2012). The gastrointestinal tract may in turn modu- (Buchanan and Lovallo, 2001; Lupien et al., 2007; Takahashi et al., 377
316 late affect and even higher cognitive function (Mayer, 2011). Acute 2004), and TSST exposure can increase plasma lactate (Kubera et al., 378
317 psychological stress induced by dichotomous listening increases 2012), which can be used as an alternative to glucose as a source of 379
318 gut-specific autonomic innervation, assessed using rectal mucosal energy for the brain (it should be noted that sodium lactate can be 380
319 blood flow (Murray et al., 2004). Similarly, stress induced by men- used as a pharmacological means of panic induction, e.g. Plag et al., 381
320 tal arithmetic and a Stroop task increases rectal sensitivity in both 2012). The endocrine effects of the TSST can lead to changes in cog- 382
321 irritable bowel syndrome patients and healthy controls (Posserud nition; participants with a higher cortisol increase from the TSST 383
322 et al., 2004). It is thus plausible that the TSST can exacerbate symp- performed better at a declarative memory task requiring free recall 384
323 toms associated with irritable bowel syndrome, such as abdominal of words (Domes et al., 2002; Nater et al., 2007). In contrast to this 385
324 pain and urgency, although gastrointestinal effects have not rou- enhancing effect, other research has indicated no effect on declar- 386
325 tinely been assessed in research employing the TSST. ative memory (Hidalgo et al., 2012), impaired delayed memory of 387
326 The TSST can also affect eating behaviour; in children, a higher cards in children (Quesada et al., 2012), and impaired declarative 388
327 cortisol response to stress was associated with greater caloric memory for a word list in response to the TSST and oral adminis- 389
328 intake in the absence of hunger (Francis et al., 2013). In contrast, tration of hydrocortisone (Kirschbaum et al., 1996). The TSST led to 390
329 lower cortisol reactivity to the TSST has been associated with higher greater false recognition of semantically related distracter words 391
330 calorie consumption post-stress, with this effect more evident in on a recall task (Payne et al., 2002) although such an effect was 392
331 those with high scores on a scale of emotional eating (van Strien not found elsewhere (Beato et al., 2013). High cortisol responders 393
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394 to the TSST have shown worse delayed recall for emotional and if the positive and negative feedback conditions are regarded as a 460
395 emotionally neutral pictures, whereas those who did not show a challenge and a threat respectively; this can allow for differentia- 461
396 cortisol response had improved memory for emotionally negative tion between “positive stress” and “negative stress”. 462
397 pictures (Buchanan and Tranel, 2008). TSST-induced stress led to

398 reduced memory for emotionally neutral words, but to unimpaired 2.2.3. Neurobiological effects 463
399 or even enhanced recall of emotional words (Jelici et al., 2004; Cortisol responders to the Montreal Imaging Stress Test (MIST; 464
400 Smeets et al., 2006), although the TSST reduced recall of positive Dedovic et al., 2005) which involves a mathematical challenge with 465
401 words in particular (Domes et al., 2004). Participants exposed to feedback, based on the Trier Mental Challenge Test (Pruessner et al., 466
402 the TSST have shown enhanced memory of stressor-relevant mate- 1999), have higher hippocampal deactivation during stress, as well 467
403 rial (Smeets et al., 2009; Wiemers et al., 2013a), and TSST stress led as more errors on a visual recognition task (Khalili-Mahani et al., 468
404 to better recognition of central over peripheral event information 2010). Furthermore, the cortisol responders showed hippocam- 469
405 (Echterhoff and Wolf, 2012). The evidence thus suggests that the pal deactivation prior to the onset of the stressor, suggesting that 470
406 cognitive effects of the TSST may be moderated by the emotional the anticipation of the stressor may have similar effects on this 471
407 valence and relevance of the stimuli used. brain area. In cortisol responders, the MIST has led to broader 472
408 The TSST has also impaired working memory for neutral stimuli deactivation in limbic system structures including the hypothala- 473
409 in high cortisol responders (using a digit span task, requiring par- mus and medio-orbitofrontal cortex as well as the hippocampus 474
410 ticipants to recall a series of digits either in the order presented (Lederbogen et al., 2011; Pruessner et al., 2008) and Pruessner 475
411 or in reverse order) (Elzinga and Roelofs, 2005), although only et al. suggested that differing brain activities may be related to 476
412 when adrenergic activity was not normalised post-stressor. Work- fear response, such as increased amygdala activity rather than 477
413 ing memory (assessed using an n-back task) was impaired by the decreased hippocampus activity; using a task like the TSST or MIST 478
414 TSST following administration of the mineralocorticoid antagonist in conjunction with fear induction may shed further light on this. 479
415 spironolactone, which increased cortisol availability (Cornelisse Adolescents with higher cortisol response to the TSST-C (see Sec- 480
416 et al., 2011a). The TSST led to slower reaction time and fewer cor- tion 6.3) have also shown reduced response in the left hippocampus 481
417 rect responses for n-back tasks completed 10 min after exposure to to fearful faces (Liu et al., 2012). An event-related MRI has also been 482
418 the stressor (Schoofs et al., 2008), and larger cortisol increases were developed to examine specific effects of social evaluative threat 483
419 associated with slower response times. The n-back tasks required separately from challenging arithmetic; cortisol responders to the 484
420 participants to attend to a series of single digits and state if the MIST showed deactivation in the limbic system to negative social 485
421 currently presented stimulus was the same as the stimulus pre- evaluation specifically, with increased bilateral activation in the 486
422 sented two or three trials earlier, requiring participants to hold prefrontal cortex for the maths challenge (Dedovic et al., 2009a). 487
423 and continuously update information in working memory. Schoofs Structural imaging is also of interest; greater hippocampal volume 488
424 et al. (2008) also found that the stress-induced impairment was has been found to be associated with a stronger cortisol increase in 489
425 attenuated towards the end of the task. Performance on a reading response to the TSST, as well as impaired declarative memory per- 490
426 span task was also impaired by the TSST (Luethi et al., 2008). In formance, but only pre-TSST (Pruessner et al., 2007). Future studies 491
427 contrast to this impairing effect on reading span, a positive correla- utilising brain imaging-based psychosocial stress tasks such as the 492
428 tion was evident between TSST-induced cortisol levels and both MIST will be of great importance in understanding the interactions 493
429 encoding and maintenance for a change-detection task (Stauble between psychosocial stress, cognition and emotion at the neuro- 494
430 et al., 2013). Stauble et al. argued that such a positive effect may be biological level (see King and Liberzon, 2009, for further discussion 495
431 obscured by tests which do not examine different stages of memory of neuroendocrine measurement in the context of imaging). Func- 496
432 processing. The TSST has been found to improve spatial memory tional connectivity analysis could also be of interest; processing of 497
433 for map routes (Luethi et al., 2008), but did not improve spatial emotional faces has been shown to be differentially modulated by 498
434 memory on a virtual water Morris maze (Klopp et al., 2012). The the TSST according to the visual hemifield in which face stimuli are 499
435 TSST slowed reaction time for a go/no-go task using neutral stimuli presented, indicating functional asymmetry and suggesting possi- 500
436 (Scholz et al., 2009); it would be of interest to see if such an effect ble interhemispheric transfer of information (Brüne et al., 2012), 501
437 may be moderated by emotional valence in verbal stimuli, similar although functional imaging was not used in this study. 502
438 to the effects shown in verbal recall. Indeed, the TSST may affect
439 processing of emotional stimuli at an early, automatic stage; corti- 2.2.4. Psychological effects: summary 503
440 sol response has been associated with attentional shifting on trials The TSST heightens self-reported stress and anxiety, as well 504
441 with masked angry faces (Ellenbogen et al., 2010). Another manner as negative mood broadly. Attention and memory responses to 505
442 in which cognition and emotion can interact in producing a given the TSST may depend upon the emotional valence of the stim- 506
443 response to the TSST is that rumination about the stressor may lead uli used. TSST exposure has been found to modulate numerous 507
444 to enhanced mood effects, which can manifest on a physiological forms of complex cognition. The TSST and adaptations for brain 508
445 level (Brosschot, 2010). imaging have implicated a number of brain regions involved in the 509
446 The TSST can also moderate more complex cognition, includ- acute stress response, particularly the hippocampus. Further inves- 510
447 ing task switching (Plessow et al., 2012a), dual task performance tigation into the specific roles of these regions should be a focus 511
448 (Plessow et al., 2012b), cognitive flexibility (Plessow et al., 2011), of future research. However, the complexity of the relationship 512
449 creativity (Akinola and Mendes, 2008), choice between present and between stress, associated biomarkers and cognition will neces- 513
450 future rewards (Kimura et al., 2013), answering questions requir- sitate extensive research on the subject. 514
451 ing estimation (Kassam et al., 2009), strategising (Leder et al., 2013)
452 and decision making involving risk (Pabst et al., 2013a,b; Van den 3. Procedural considerations 515
453 Bos et al., 2009), as well as a measure of risk-taking behaviour in

454 adolescents (Reynolds et al., 2013). Two of these studies (Akinola 3.1. Biomarkers 516
455 and Mendes, 2008; Kassam et al., 2009) used a modification of

456 the TSST whereby participants either received positive or nega- 3.1.1. HPA axis measures 517
457 tive feedback from the panel, rather than a cold, unencouraging TSST responses in ACTH, salivary and total plasma cortisol were 518
458 response. A measure of stress appraisal such as the transactional comparable for when testing occurred at different times of day 519
459 stress questionnaire (see Section 4.3.2) can be used to ascertain between 0900 and 1900 h, although basal levels were higher in the 520
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521 morning (Kudielka et al., 2004c). However, the authors also point salivary glands may control the secretion of proteins differently 586
522 out that they could not control for chronotype, i.e. the waking hours (Bishop and Gleeson, 2009; Brandtzaeg, 2007). When comparing 587
523 preferred by an individual. If the TSST is conducted early in the day, studies by different authors, it should be noted that the assays used 588
524 waking times should be taken into account to control for the cortisol to assess cytokines have not been standardised across laboratories 589
525 awakening response (Pruessner et al., 1997b). The time window for (Kennedy et al., 2012). Furthermore, research assessing saliva and 590
526 conducting the TSST in the late afternoon is broader than during the plasma samples has indicated a lack of correspondence in results: 591
527 morning (Kudielka et al., 2007). Thus, although past research has although 16 out of 27 assessed cytokines were correlated for saliva 592
528 tested in the morning (e.g. von Känel et al., 2006) or both the morn- collected by passive drool and saliva collected by filter paper placed 593
529 ing and the evening (e.g. Het et al., 2009; Kirschbaum et al., 1993), a under the tongue, cytokines assessed in plasma from venipuncture 594
530 large number of studies have restricted testing to afternoon hours blood samples showed only 3 correlations with passive drool saliva 595
531 (e.g. Bellingrath et al., 2010; Kirschbaum et al., 1996, 1999; Pace (IL-6, IFN-␥ and macrophage inflammatory protein-1␣) and none 596
532 et al., 2006; Petrowski et al., 2012; Young et al., 2000). In general, with filter paper (Williamson et al., 2012). High-sensitivity assays of 597
533 whatever the method of stimulation it is easier to elevate cortisol C-reactive protein have also indicated a moderate-to-strong corre- 598
534 when it is relatively low in the afternoon than when it is high in the lation between salivary and serum measures (Ouellet-Morin et al., 599
535 morning. 2011). The association between salivary and blood measures may 600
536 Foley and Kirschbaum (2010) argue that the acute stress effects thus not be as reliable for many cytokines as it is for cortisol. IL-6 has 601
537 of the TSST have been best characterised using salivary cortisol. been activated by the TSST in a number of studies, although there is 602
538 Although plasma, serum and salivary cortisol can be increased currently no commercially available kit for assessing salivary IL-6, 603
539 by the TSST, it has been argued that the assessment of salivary so measures between laboratories will vary considerably, whereas 604
540 instead of plasma cortisol may account for the difference in findings commercial kits are available for salivary C-reactive protein. Pas- 605
541 between studies, such as conflicting evidence regarding moderat- sive drool is recommended as a method of collection, given that 606
542 ing effects of the menstrual cycle (Kelly et al., 2008; Kirschbaum cotton salivettes may interfere with assays for IL-6 (Minetto et al., 607
543 et al., 1999). However, there is a high correlation between salivary 2007). An alternative to saliva sampling is to measure cytokines 608
544 cortisol and unbound cortisol in plasma and serum, which persists via fluid derived from serum transport into the mouth via oral 609
545 in response to a number of challenges that alter HPA axis activ- mucosa, known as gingivial crevicular fluid or oral mucosal transu- 610
546 ity, such as ACTH stimulation and dexamethasone suppression test date (Nishanian et al., 1998); this method has indicated heightened 611
547 (DST; see Section 7.1) (Hellhammer et al., 2009). Salivary cortisol IL-6 responses to the TSST in men (Moons et al., 2010). However, 612
548 should thus be an adequate measure of bioavailable cortisol. oral mucosal transudate has its own shortcomings; IL-6 measured 613
549 It is also important to bear in mind that, due to factors such as in oral mucosal transudate has been found to correlate only mod- 614
550 cortisol pulsatility, which leads to variation in cortisol levels over estly with IL-6 levels in plasma (Fernandez-Botran et al., 2011). 615
551 shorter periods of time than the broader, diurnal pattern (Young With regard to time of day, IL-6 levels peaked at awakening and 616
552 et al., 2004a), single time point cortisol measurements can be highly declined over the morning, but then rose again at night, while CRP 617
553 variable. Furthermore, researchers cannot chart the progress of the levels were elevated at awakening but did not change substantially 618
554 cortisol response with only a single post-stress measure (Ramsay between 10.00 and 1.00 (Izawa et al., 2013a). 619
555 and Lewis, 2003). Consequently, every effort must be made to

556 ensure that samples are taken at multiple time points and with
3.1.3. Sympathetic-adrenal-medullary system measures 620
557 due regard for the factors which can adversely influence results (see
sAA is useful as a less invasive means of testing activity of the 621
558 Inder et al., 2012, for a review of practical issues related to collec-
sympathetic-adrenal-medullary system than adrenaline or nora- 622
559 tion and analysis of salivary cortisol). Nevertheless, salivary cortisol
drenaline (Rohleder et al., 2004); this is also the case for GSR, which 623
560 is a reliable index of HPA axis reactivity during the TSST once the
can be measured continuously throughout the TSST speech task. 624
561 appropriate controls are in place. Moreover, this measure has been
Research has indicated that sAA is not confounded with flow rate 625
562 shown to be responsive to anxiolytic agents (Fries et al., 2006), sug-
of saliva (Rohleder et al., 2006) and that SAA response to the TSST 626
563 gesting it is of use in assessing pharmaceutical interventions that
predicts plasma noradrenaline response (Thoma et al., 2012). How- 627
564 can modulate the acute stress response.
ever, whereas the HPA axis is particularly activated in response to 628
stressful situations associated with factors such as unpredictabil- 629

565 3.1.2. Immune system measures
ity and social-evaluative threat (Dickerson and Kemeny, 2004), the 630
566 The lack of the use of control groups in studies on stress
sympathetic-adrenal-medullary system responds to pleasurable 631
567 and inflammatory factors such as cytokines has been criticised,
stimuli as well as those involved in stress (Clow, 2001). Conse- 632
568 particularly since not only the experimental stressor but also diur-
quently, care must be taken in interpreting results. It has been 633
569 nal variation and blood sampling processes may have effects on
shown that the TSST’s effect on a ratio of sAA to cortisol has a 634
570 cytokines (Izawa et al., 2013a; Steptoe et al., 2007). Given that a
stronger association with measures of chronic stress and depres- 635
571 control version of the TSST is available (see Section 6.2), this could
sion than for cortisol or sAA alone (Ali and Pruessner, 2012); this 636
572 be remedied in future research. The timing of post-stressor mea-
may offer a measure that tracks the effects of long-term stress more 637
573 surement is also relevant; as the effect of mental stress on cytokines
reliably. 638
574 may occur indirectly, through mechanisms such as lymphocytes or
575 endothelial cells, the effect may not actually be manifest until hours
576 after the occurrence of stress (Steptoe et al., 2001); the typical time 3.1.4. Cardiovascular measures 639
577 course of the TSST may thus not detect all effects. It is thus advisable Similar to GSR, heart rate and heart rate variability can be contin- 640
578 to extend the length of the post-stress sampling period when mea- uously measured throughout testing, including during the stressor. 641
579 suring these factors (Steptoe et al. measured cytokines at 45 min This confers these measures with an advantage over measures 642
580 and 2 h post-stress). which are less practical to take during the speech and arithmetic 643
581 Although saliva samples are non-invasive, blood measures of task (e.g. blood and saliva samples). However, care should be taken 644
582 cytokines are a more accepted method than salivary measures. in interpreting heart rate changes, as heart rate may be less specific 645
583 There are a number of other methodological issues to consider in to stressful stimuli than HPA axis activity (Gordis et al., 2006). To 646
584 using salivary measures of cytokines. The assessment of salivary this end, it is important to also assess subjective mood effects in 647
585 cytokines may require assessment of salivary flow rate, as different response to the TSST.
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Table 1
Advantages of different biomarkers of TSST response.
Biomarker Non-invasive Can be measured Specifically Similar results Consistently

continuously during responsive to for blood/saliva responsive to
speech task stress repeated TSST
√ √
Plasma cortisol X X X
√ √ √
Salivary cortisol X X
Blood cytokines X X X IL-6, IFN-␥, CRP IL-6
ACTH X X X n/a X
√
Salivary cytokines X X IL-6, IFN-␥, CRP n/a
√ √ √
Heart rate X n/a
√ √
Galvanic skin response X n/a n/a
√
Adrenaline X X X n/a
√
Noradrenaline X X X n/a
√
sAA X X X n/a
648 3.1.5. Brain–gut axis measures findings that a response to the TSST characterised by anger, com- 696
649 The lack of assessment of gastrointestinal responses to the TSST pared to a response characterised by fear, can lead to a greater 697
650 is unfortunate, as questionnaires assessing symptoms of irritable increase in cortisol, but not proinflammatory cytokines (Moons 698
651 bowel syndrome have been developed which can be used to assess et al., 2010). In contrast, an anger response to a version of the MIST 699
652 gastrointestinal problems (see Bijkerk et al., 2003, for a discussion). (which was modified to induce anger) was associated with reduced 700
653 For example, visual analogue scales from the irritable bowel sever- cortisol response (Kazén et al., 2012). Biomarker responses to the 701
654 ity scoring system (IBS-SSS; Francis et al., 1997) can be used to TSST can thus be moderated by what type of mood the participant 702
655 quickly assess current levels of bloating, urgency and abdominal experiences during the stressor. In terms of what type of scale to 703
656 pain. use in measuring subjective responses to the TSST, although visual 704
analogue scales and Likert scales have comparable reliability (van 705
657 3.1.6. Procedural considerations in biomarkers: summary Laerhoven et al., 2004) and validity (Davey et al., 2007), visual ana- 706
658 In protocol design one needs to consider factors such as ease of logue scales may be more sensitive to subtle effects, given their 707
659 sampling (whether sampling is invasive and/or can be performed continuous nature. 708
660 without interrupting the psychosocial stressor), although other fac-

661 tors may also influence ease of sampling (e.g. with heart rate/GSR
662 participants may have to avoid moving their hands to avoid move- 3.2.2. Cognitive measures 709
663 ment artefacts). One also needs to consider medium of sample (e.g. The relationship between acute stress and cognition may not 710
664 blood or saliva), whether the biomarker is specifically responsive always be simply linear; both high and low levels of circulating glu- 711
665 to psychosocial stress, and level of habituation following repeated cocorticoids can impair memory performance compared to more 712
666 exposures. Given the extensive literature indicating that salivary moderate levels (Lupien et al., 2002). It may thus be of interest to 713
667 cortisol is increased by the TSST, combined with the advantages of compare cortisol non-responders to the TSST, those with a moder- 714
668 this biomarker outlined in Table 1, salivary cortisol will be the most ate response and those with a high response. It should be noted that 715
669 useful stress biomarker for much research employing the TSST. the linearity of the cognitive effects of arousal states such as stress 716
may depend on factors such as difficulty of the cognitive tasks (e.g. 717
670 3.2. Psychological effects Hanoch and Vitouch, 2004) or strategies employed during cognitive 718
tasks in response to increasing stress (e.g. Fisher, 1986; Matthews 719
671 3.2.1. Subjective measures et al., 2010), indeed, there is evidence that spatial learning strate- 720
672 Subjective and physiological measures are frequently included gies are altered in response to stress increases following the TSST 721
673 in TSST research; a re-analysis of previous studies indicated a pos- (Schwabe et al., 2007). In employing repeated measures of cognitive 722
674 itive relationship between sAA and negative affect, but a negative performance care should be taken to avoid practice effects. 723
675 correlation between cortisol and negative affect; the latter finding As well as the TSST affecting cognitive performance, cogni- 724
676 suggests cortisol may have a protective effect on subjective effects tive ability seems to be associated with the endocrine response 725
677 of stress (Het et al., 2012). However, another analysis of previous to the TSST: participants with higher executive functioning (as 726
678 research which assessed both psychological and physiological TSST measured with a letter fluency task) measured before the TSST 727
679 responses found that only 25% of the analysed studies indicated a have been shown to have a lower cortisol and reported anxiety 728
680 significant correlation between cortisol and perceived emotional response to the TSST (Hendrawan et al., 2012), although lower 729
681 stress (Campbell and Ehlert, 2012). This may be due to HPA axis performance on a nonverbal memory task predicted lower corti- 730
682 responses to the TSST lagging behind the subjective psychological sol reactivity to the TSST in adolescents (Slattery et al., 2013); this 731
683 response (Schlotz et al., 2008). An analysis of data from nine differ- difference in findings may be due to the longer time lag between 732
684 ent studies indicated that subjective mood rated during the TSST TSST stress and cognitive assessment in the latter study. The tim- 733
685 (between the public speech and the mental arithmetic task) is more ings of recall and stress exposure should also be considered; two 734
686 highly correlated with cortisol and heart rate responses, although studies indicated that immediate retrieval of emotional stimuli 735
687 the magnitude of the covariation was still small (Hellhammer and studied post-TSST reduced a positive effect of the TSST on long- 736
688 Schubert, 2012). It will thus be useful to collect mood data between term emotional memory consolidation (Wolf, 2012). Wolf has thus 737
689 the public speaking and mental arithmetic task where this is prac- suggested that although post-learning stress may be associated 738
690 tical. with enhanced consolidation, post-stress learning may interfere 739
691 It is worthwhile collecting subjective data in addition to phys- with consolidation of emotional memory. If using fMRI methods, 740
692 iological measures, as a given level of arousal may be interpreted it should be borne in mind that undergoing scanning can be stress- 741
693 differently by different participants (e.g. one participant may feel ful in itself; fMRI scanning has been shown to increase subjective 742
694 a positive excitement during the procedure whereas another may nervousness as well as sAA, with cortisol rising in a minority of 743
695 feel upset). The relevance of collecting mood data is underlined by participants (Muehlhan et al., 2011).
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744 3.2.3. Procedural considerations in psychological effects: the TSST may be attenuated (Dedovic et al., 2009b). Potential gen- 806
745 summary erational differences will need to be monitored in future research 807
746 Subjective psychological data should be collected in addition using the TSST, and modifications may need to be made to account 808
747 to biomarkers to aid in interpretation of the physiological stress for such generational differences. A difference in perception of the 809
748 response, and ideally should be collected between the interview psychosocial stressor is likely also true of participants who are 810
749 and mental arithmetic task as well as pre- and post-stressor. Indi- generally less used to a university environment or interview per- 811
750 vidual differences in cognitive ability and practice effects should formance than students. For example, in a middle-aged sample, 812
751 be considered in investigating the interaction between acute stress lower educational attainment was associated with a higher cortisol 813
752 and cognition, as well as the possibility that effects may be non- response to the TSST (Fiocco et al., 2007). It may thus be desirable to 814
753 linear. have an acclimatisation period to the testing environment, before 815
exposing participants to the stressful speech task. 816
754 4. Factors moderating the effects of the TSST 4.1.2. Sex hormones and menstrual cycle 817
One explanation for gender moderating either cortisol effects 818
755 4.1. Gender and age or subjective effects but not both is that female sex steroids are 819
interacting with TSST effects (Kudielka et al., 2007). Women in 820
756 4.1.1. Age and gender differences the follicular stage and those taking oral contraceptives showed 821
757 Researchers have conducted TSST research on a broad age range a smaller response in salivary cortisol to the TSST than women in 822
758 of participants. Children (mean age = 12.1 years) and younger adults luteal phase or men (Kirschbaum et al., 1999), and women taking 823
759 (mean age = 23.5) show greater heart increases in response to the oral contraceptives compared to women in the luteal phase have 824
760 TSST than older adults (mean age = 67.3) (Kudielka et al., 2004b). indicated greater glucocorticoid sensitivity of pro-inflammatory 825
761 Younger men have shown a greater ACTH response than older men, cytokine production (Rohleder et al., 2003). Women but not men 826
762 and older men a higher salivary cortisol response than older women displayed a negative declarative memory effect of a TSST-induced 827
763 (Kudielka et al., 2004a). Men had a higher cortisol response to the rise in cortisol (Almela et al., 2011a), but a negative relationship 828
764 TSST than women in samples of young to middle-aged participants between peak cortisol and declarative memory has more specifi- 829
765 (e.g. Eisenberger et al., 2007; Uhart et al., 2006). Kelly et al. (2008) cally been observed in the luteal phase only in women (Espin et al., 830
766 found that women reported a greater increase in irritability and fear 2013). The effects of the TSST on sex hormones may be moderated 831
767 immediately following the TSST, although gender did not moder- by age: in men and women aged 30–50, levels of sex steroids (estra- 832
768 ate any changes in heart rate or plasma cortisol. There is evidence diol, testosterone, androstenedione, as well as sex hormone binding 833
769 that glucocorticoid sensitivity to IL-6 production may be moder- globulin) were increased by the TSST, and across sexes there were 834
770 ated by gender (Rohleder et al., 2001) although a gender effect was contrasting associations between changes in sex hormones and 835
771 not shown for IL-6 in oral mucosal transudate (Slavich et al., 2010). changes in HPA axis and sympathetic-adrenal-medullary axis activ- 836
772 Young men have increased glucocorticoid sensitivity to IL-6 pro- ity (e.g. changes in testosterone were associated with changes in 837
773 duction post-TSST than older men (Rohleder et al., 2002). Gender cortisol, ACTH and heart rate in women but with changes in heart 838
774 has not moderated sAA response to the TSST, although there is evi- rate only in men) (Lennartsson et al., 2012a). However, in a younger 839
775 dence for higher sAA in older participants (Almela et al., 2011b; mixed-sex sample (mean age in the mid-twenties), testosterone 840
776 Strahler et al., 2010). Medial prefrontal cortex damage has been and estradiol were not affected by the TSST (Schoofs and Wolf, 841
777 associated with heightened TSST cortisol response in women but an 2011). When employing the TSST in a sample of older women, 842
778 attenuated response in men (Buchanan et al., 2010). The TSST has estradiol can lead to higher increases in negative mood (Dumas 843
779 enhanced working memory and memory for emotionally arous- et al., 2012) as well as reduction in attention and psychomotor 844
780 ing over neutral pictures in males only (Cornelisse et al., 2011b). performance speed (Newhouse et al., 2010). 845
781 There is evidence that the TSST can enhance classical conditioning Given the broad moderating effect of gender, many studies eval- 846
782 for negative stimuli in males (Luethi et al., 2008); TSST exposure uating the effects of the TSST have recruited only male or female 847
783 has also enhanced fear conditioning in males, but inhibited such participants. In the case of the recruiting females only, the stage of 848
784 conditioning in females (Jackson et al., 2006). the menstrual cycle should be controlled which presents its own 849
785 Lupien et al. (2007) make the point that, for older participants, logistical challenges, especially where multiple assessments are 850
786 the testing environment itself may impose some of the character- required. 851
787 istics associated with Trier stress (e.g. novelty, unpredictability) to

788 a greater extent than younger populations. Indeed, younger people 4.2. Genetics 852
789 are more likely to be more familiar with being filmed (e.g. through
790 their use of social media); consequently the filming of the partici- The examination of genetic factors involved in acute stress has 853
791 pant may not induce as much stress in younger people. At the same been an exciting development in TSST research. FK506 binding 854
792 time, although they may be more familiar with interview perfor- protein 5 and G-protein coupled type-1 CRH receptor, which are 855
793 mance and with being filmed, young participants who are earlier encoded by the genes FKBP506 and CRHR1 respectively, have been 856
794 in their career paths may have a greater emotional investment in implicated in the HPA axis response (e.g. Lee et al., 2011; Tyrka 857
795 performing well in an interview scenario, as their future success et al., 2009). The CRHR1 polymorphisms rs7209436, rs110402, and 858
796 will hinge on their ability to perform well in interviews. The inter- rs242924 were associated with the cortisol response, while the 859
797 action between perceived performance and stress is thus likely FKBP506 polymorphism rs3800372 was associated with cortisol 860
798 to be stronger in such participants. Furthermore, younger partic- response in males only (Mahon et al., 2013). Gender interactions 861
799 ipants may find the mental arithmetic task more stressful than have also been shown for the Val66Met polymorphism of the BDNF 862
800 older participants, due to generational differences in reliance upon gene, with males val/val homozygotes showing a greater cortisol 863
801 technology for performing calculations. The point has also been response than val/met heterozygotes, with the opposite trend in 864
802 raised that gender socialisation may play a major role in gender females (Shalev et al., 2009). Polymorphisms of the glucocorticoid 865
803 differences in the psychosocial stress response; if the socialisation receptor gene (NR3C1) have been associated with HPA axis response 866
804 of children is becoming less pronounced in its gender differenti- to the TSST in males, with carriers of the A to G transition in the 867
805 ation over time, the moderating effect of gender on responses to 3 untranslated region at exon 9␤ showing a higher HPA response 868
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869 (Kumsta et al., 2007) and BclI (a polymorphism located in intron B) not indicated elsewhere (Schommer et al., 1999). Moderation of 933
870 GG carriers showing an attenuated response (Kumsta et al., 2007; HPA axis effects by trait anxiety has also been equivocal (Jezova 934
871 Wüst et al., 2004). Participants homozygous for the mineralocor- et al., 2004; Takahashi et al., 2005a). Perfectionism has been asso- 935
872 ticoid receptor haplotype MR-2C/MRI180 showed higher cortisol, ciated with a greater increase in salivary cortisol (but not adrenaline 936
873 ACTH and heart rate responses to the TSST (van Leeuwen et al., or noradrenaline) in response to the TSST (Wirtz et al., 2007a). 937
874 2011). Although personality factors may offer limited explanatory power 938
875 A polymorphism of the 5-HT transporter gene predicted cor- for responses to a single TSST, associations between personality and 939
876 tisol responses to the TSST; those with the short/short genotype cortisol responses may be evident after repeated exposure to the 940
877 showed the strongest response to the stressor (Way and Taylor, TSST (Kudielka et al., 2009). 941
878 2010). Research using the mental arithmetic component of the

879 TSST in adolescent girls has shown a similar trend (Gotlib et al., 4.3.2. Stressor appraisal 942
880 2008), and children with both secure attachment and long/long As different people interpret psychosocial stressors in differ- 943
881 alleles showed lower galvanic skin response in response to the TSST ent ways, it is plausible that appraisal might account for why 944
882 (Gilissen et al., 2008). However, an effect of 5-HT transporter geno- some people are less stressed by the TSST. The transactional 945
883 type was not observed elsewhere for the TSST (Wüst et al., 2009) stress questionnaire, also known as primary appraisal secondary 946
884 or a modified social stress test (Bouma et al., 2010); this lack of an appraisal scale or PASA, assesses items based on the theoreti- 947
885 effect may be due to a moderating role of the dopamine D4 recep- cal constructs of primary appraisal (threat and challenge) and 948
886 tor gene (Armbruster et al., 2009; Foley and Kirschbaum, 2010). secondary appraisal (control expectancy and perception of one’s 949
887 Research with children has shown that carriers of the Met allele ability) (Lazarus and Folkman, 1984). Perception of one’s ability is 950
888 of the catechol-O-methyltransferase (COMT) Val158Met polymor- re-formulation of the concept of efficacy expectations, taken from 951
889 phism have a higher cortisol response (Armbruster et al., 2012), Bandura (1977). The PASA has been found to explain 22% of the 952
890 while heart rate response is moderated by the COMT polymor- variance in baseline-corrected cortisol following TSST (Gaab et al., 953
891 phism and sAA response is moderated by the 5-HT transporter gene 2005b). This suggests that these factors concerning the appraisal 954
892 (Mueller et al., 2012). In response to the TSST for groups (see Section of the situation may be more useful than measures of personal- 955
893 6.3), T-allele carriers on the neuropeptide S receptor gene poly- ity traits in predicting cortisol responses. Associations between the 956
894 morphism rs324981, which increases neuropeptide potency at the transactional stress questionnaire and cortisol response to the TSST 957
895 neuropeptide S receptor, showed greater increases in cortisol and have been shown elsewhere (Het et al., 2009) as well as associa- 958
896 subjective stress (Kumsta et al., 2013). tions between the transactional stress questionnaire and immune 959
897 Genetics can also moderate the cognitive effects of the TSST: biomarker responses to the TSST; higher control expectancy pre- 960
898 Met homozygotes on the COMT Val158Met polymorphism per- dicted lower tumour necrosis factor-␣ (TNF-␣) and IL-6 expression 961
899 formed worse on an n-back task (Buckert et al., 2012). The COMT in response to the TSST, while lower challenge predicted lower IL- 962
900 Val158Met polymorphism affects dopamine availability in the pre- 6 expression (Wirtz et al., 2007b). It is worth noting that the PASA 963
901 frontal cortex (Sesack et al., 1998; Weinshilboum et al., 1999); assesses appraisal of the stressor before it occurs, as opposed to 964
902 genetic factors may thus underscore the effects of serotonin, retrospectively reporting on the effects of a stressor. 965
903 dopamine and the interaction between the two on acute physi-
904 ological stress responses. Similar mechanisms also seem evident 4.4. Social factors 966
905 for noradrenaline: carriers of a functional deletion variant of the

906 ADRAA2B gene encoding the ␣2B-adrenergic receptor showed 4.4.1. The interview panel 967
907 impaired performance on a face recognition task; this was evident Panel behaviour may moderate the response to the TSST; criti- 968
908 for neutral faces under stress and for negatively emotional faces in cal versus supportive committees have shown differing effects on 969
909 the control condition (Li et al., 2013). cognitive performance (Akinola and Mendes, 2008; Kassam et al., 970
910 Given findings indicating gene–environment interactions in 2009), although a critical committee did not induce a larger cor- 971
911 response to the TSST (Gilissen et al., 2008), an increasing amount of tisol response than a supportive one (Taylor et al., 2010; Way 972
912 research is examining how epigenetic processes moderate the psy- and Taylor, 2010). However, performing the TSST speech task 973
913 chophysiology of the stress response (e.g. Lam et al., 2012; Mathews in the presence of an inattentive audience led to lower cortisol 974
914 et al., 2011) as well as stress-related disorders such as irritable and reported self-consciousness than presenting to an evaluative 975
915 bowel syndrome (Dinan et al., 2010). Epigenetic processes in acute audience (Dickerson et al., 2008). Compared to participants who 976
916 psychosocial stress have been shown using the TSST; DNA methy- performed in front of a panel, those who completed the TSST tasks 977
917 lation of the OXTR1 target sequence of the oxytocin receptor gene alone had lower heart rate during the tasks and lower salivary corti- 978
918 (located in the region of OXTR exon 3) increased between pre- and sol at post-stress and recovery (Gruenewald et al., 2004). A measure 979
919 post-stress, but decreased at a 90-min follow-up. However, the tar- of stress appraisal such as the transactional stress questionnaire 980
920 get region of the brain-derived neurotrophic factor gene (located (Gaab et al., 2005b) can be used to ascertain if the positive feed- 981
921 around the 3 end of brain-derived neurotrophic factor exon 6) back, negative feedback and no feedback conditions are regarded 982
922 did not change (Unternaehrer et al., 2012). Epigenetic factors may as a challenge and a threat respectively; this can allow for differen- 983
923 also be predictive of HPA axis response to the TSST: glucocorticoid tiation between “positive stress” and “negative stress”. The gender 984
924 receptor exon 1F methylation is predictive of total cortisol output of the panel is also relevant; young men and women only showed a 985
925 in females (Edelman et al., 2012). cortisol increase when the panel member were of the opposite sex, 986
and this effect was only observed in women in the follicular phase 987
926 4.3. Personality and individual differences of the menstrual cycle (Duchesne et al., 2012). 988
927 4.3.1. Personality factors 4.4.2. Social support and social status 989
928 Participants vary in their stress response to the TSST. However, The social nature of the TSST is further indicated by findings 990
929 “classic” measures of personality have shown equivocal results: of a moderating effect of social support (Foley and Kirschbaum, 991
930 lower extraversion in men and higher neuroticism in women, as 2010). Social support attenuates the cortisol response to the TSST 992
931 well as lower openness regardless of sex, led to a blunted cor- (Ditzen et al., 2008; Eisenberger et al., 2007), although the effects of 993
932 tisol response (Oswald et al., 2006), although such effects were social support from a stranger, boy/girlfriend and no social support 994
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995 are moderated by the gender of the participant (Kirschbaum et al., with depression (Dockray et al., 2009). Consistent with this find- 1055
996 1995a). In children, social support by a friendly dog was found to ing, cortisol responses to the TSST have been found to be larger in 1056
997 be more effective in attenuating the cortisol response to the TSST- size and longer in duration for adolescents with major depressive 1057
998 C than a toy dog or support from a friendly human (Beetz et al., disorder compared to healthy controls (Rao et al., 2008). A pos- 1058
999 2012). Oxytocin has been found to enhance the attenuation of HPA sible explanatory factor is trait rumination, which was associated 1059
1000 axis response by social support, suggesting a possible mechanism with slower cortisol recovery in depressed adolescents (Stewart 1060
1001 for the positive effect of social support (Heinrichs et al., 2003). A et al., 2013). In young adult females, those with a current major 1061
1002 higher degree of dispositional social trust is also associated with an depressive episode showed slower recovery in both salivary cor- 1062
1003 attenuated cortisol increase in men (Takahashi et al., 2005b). tisol and negative affect than participants who were at risk for 1063
1004 Lower levels of subjective social status were associated with depression (Dienes et al., 2013). Older patients with depression 1064
1005 higher IL-6 responses at 45 min and 2 h post-baseline, and predicted (mean age = 62.3) have shown reduced cortisol response to the 1065
1006 perception of the TSST as more threatening and less manageable TSST (Taylor et al., 2006), and young adults with major depression 1066
1007 (Derry et al., 2013). Despite this perception of the TSST as more (mean age = 33) did not differ from age-matched controls in corti- 1067
1008 threatening for those of lower subjective social status, such partic- sol response, though they had lower ␤-endorphin response (Young 1068
1009 ipants have shown a lower cortisol response to the TSST in another et al., 2000). Pro-inflammatory cytokines are increased in chronic 1069
1010 study (Gruenewald et al., 2006). stress and depression (Leonard and Song, 2007) and inflammatory 1070
responses may have a role in the pathophysiology of depression 1071
1011 4.4.3. Cultural factors (Raison et al., 2006); in response to the TSST, IL-6 activation is 1072
1012 The TSST has been used to induce a stress response in various increased in participants with higher levels of depressive symp- 1073
1013 regions; for example, a HPA axis response has been induced by the toms (Fagundes et al., 2013) and in male patients with current 1074
1014 TSST in research conducted in Germany (e.g. Rimmele et al., 2007), major depression and early-life stress (Pace et al., 2006). Partici- 1075
1015 the USA (e.g. Childs et al., 2006), the UK (e.g. Gray et al., 2012), Japan pants who were remitted from depression for at least six months 1076
1016 (e.g. Yamakawa et al., 2009), and other countries. Nonetheless, it is did not show a difference in TSST response compared to healthy 1077
1017 possible that a public speech task may have differing psychological controls with no history of depression (Lange et al., 2013). 1078
1018 effects in different cultures. Unfortunately, there has been a rela- Research should report the nature of participants’ depressive 1079
1019 tive lack of cross-cultural research examining if culture moderates state; melancholic depression is associated with higher basal HPA 1080
1020 the effects of the TSST on psychological and biological markers of axis activity and less immune activation than depression without 1081
1021 the acute stress response. An exception is a study which found that melancholic features (Kaestner et al., 2005), and atypical depres- 1082
1022 stress has been attenuated more by implicit than explicit social sup- sion is associated with suppressed activity in the sympathetic 1083
1023 port in Asian Americans compared to European Americans (Taylor nervous system (Carney et al., 2005; Veith et al., 1994) and HPA 1084
1024 et al., 2007). axis (O’Keane et al., 2012). Furthermore, it has been suggested 1085
that the manifestation of HPA axis dysfunction in depression may 1086
1025 4.5. Factors moderating the effects of the TSST: summary alter as the symptoms associated with depression change over time 1087
(O’Keane et al., 2012). Participants at risk for suicide (those with a 1088
1026 Age and gender are perhaps the most widely investigated mod- first degree relative who completed suicide, but without current 1089
1027 erating factors of TSST response. Women have a lower cortisol psychopathology themselves) did not show improvement on mea- 1090
1028 response to the TSST, but this response can be altered by the men- sures of cognitive inhibition following the TSST (McGirr et al., 2010). 1091
1029 strual cycle, which should be controlled for in research employing Indeed, changes in the HPA axis and immune system induced by 1092
1030 the TSST. sAA response to the TSST is higher in older participants, chronic stress lead to damage in the prefrontal cortex, hippocam- 1093
1031 although heart rate response may be lower. The effects of cortisol pus and amygdala, critical brain regions associated with learning 1094
1032 on learning and memory may be more positive in males than in and memory, as well as anxiety and depression (Leonard and Myint, 1095
1033 females. The age of participants may alter their perception of the 2009), and hippocampal damage has been shown to abolish the HPA 1096
1034 stressor, and adaptations are necessary for child participants (see axis response to the TSST (Buchanan et al., 2009). Future research 1097
1035 Section 6.3). should further examine cognition following acute stress in partici- 1098
1036 Other factors which can moderate the stress response to the pants with current depression. 1099
1037 TSST include genetic factors underpinning glucocorticoid and min-

1038 eralocorticoid receptor function (see DeRijk and de Kloet, 2008, for 5.2. Anxiety 1100
1039 a review of corticoid receptor genetics and stress), as well as the

1040 genetics underlying monoaminergic function, primary appraisal In adolescents with generalised anxiety disorder, but not in 1101
1041 and secondary appraisal of the TSST (which is more predictive of healthy controls, noradrenaline and growth hormone increased 1102
1042 stress response than more general measures of personality traits), and prolactin and ␤-endorphin levels decreased following test- 1103
1043 social support, social status, interview panel members’ gender and ing (using a Stoop task and a mental arithmetic task as well as 1104
1044 behaviour towards the participant. Cultural factors may also mod- TSST) (Gerra et al., 2000). Children with social phobia have been 1105
1045 erate the stress response to the TSST, although further research on shown to have a greater subjective response than controls to the 1106
1046 the topic is required. TSST for children, and higher heart rate throughout the experimen- 1107
tal session (Krämer et al., 2012). Social phobia is also associated 1108
1047 5. TSST response and stress-related psychiatric disorders with slower HR recovery and reduced respiratory sinus arrhyth- 1109
mia reactivity (Schmitz et al., 2011), although social phobia did not 1110
1048 5.1. Depression increase cortisol or sAA responses (Krämer et al., 2012). The TSST 1111
increased cortisol and sAA in adults with social phobia (van Veen 1112
1049 A meta-analysis of the effects of various stressors in clinical et al., 2009), although this study lacked a healthy control group. 1113
1050 depression has indicated that baseline cortisol levels are similar Adults with social phobia are also more likely to experience mod- 1114
1051 to healthy controls, but cortisol levels are generally elevated dur- erate to severe depersonalisation (a sense that the self is not real) 1115
1052 ing recovery (Burke et al., 2005), and research in healthy children and derealisation (a sense that the world is unreal) than healthy 1116
1053 and adolescents has indicated that cortisol reactivity is positively controls in response to the TSST, and this was related to subsequent 1117
1054 associated with behaviours and emotional problems associated post-event processing and safety behaviours (Hoyer et al., 2013). 1118
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1119 Patients with panic disorder have been shown to have an atten- participants with moderate to severe maltreatment in childhood 1181
1120 uated response to the TSST in cortisol but not heart rate (Petrowski experienced a greater IL-6 increase in response to the TSST than 1182
1121 et al., 2010, 2013). PTSD is associated with greater subjective controls (Carpenter et al., 2010). In contrast, maltreatment in child- 1183
1122 response to the TSST but in contrast to panic disorder it was not hood was associated with blunted ACTH and cortisol response to 1184
1123 associated with altered cortisol reactivity (Simeon et al., 2007a). the TSST in adult participants without current psychopathology 1185
1124 Comorbid lifetime major depression within the PTSD group was (Carpenter et al., 2007) and a blunted cortisol response in girls 1186
1125 not associated with greater TSST cortisol response. There is other aged 12–16 (MacMillan et al., 2009). Early life stress can also affect 1187
1126 evidence that comorbid anxiety and depression may have different cognition; both emotional abuse and physical neglect in childhood 1188
1127 effects than either disorder in isolation. Compared to participants were associated with impaired spatial working memory in healthy 1189
1128 with “pure” depression or anxiety disorders, those with comorbid adults (Majer et al., 2010). Severity of depression seems to play a 1190
1129 anxiety and depression had a heightened ACTH response to the role in the interaction between early life stress and depression; 1191
1130 TSST (Young et al., 2004b). A negative correlation between ACTH moderate/severe depression was associated with a blunted cor- 1192
1131 and noradrenergic activity has been observed in healthy controls tisol response to the TSST regardless of childhood maltreatment, 1193
1132 and participants with “pure” anxiety, whereas this relationship did whereas a history of maltreatment led to a more prolonged cor- 1194
1133 not hold for either those with “pure” depression or comorbid anx- tisol response in those with milder depression (Harkness et al., 1195
1134 iety and depression (Young et al., 2005). 2011). It has been suggested that a dampened HPA axis response 1196
could reflect resilience rather than risk for future psychopathol- 1197
1135 5.3. Other stress-related psychiatric disorders ogy (Carpenter et al., 2007). However, longitudinal research will 1198
be necessary to show if psychophysiological responses to acute 1199
1136 Stressful life events are associated with the onset and exacerba- psychosocial stress are predictive of resilience or susceptibility to 1200
1137 tion of chronic gastrointestinal disorders (Bradesi and Mayer, 2009; psychiatric disorders. Recent traumatic events can also affect TSST 1201
1138 Mayer, 2000) and participants with higher levels of stress were responses; cortisol reactivity to the TSST was lower in male par- 1202
1139 more likely to report functional gastrointestinal disorders (Suarez ticipants with exposure to violence as a victim or witness in the 1203
1140 et al., 2010). In line with findings that the TSST can alter gastroin- previous two years, but without a history of maltreatment (Peckins 1204
1141 testinal effects, adults with irritable bowel syndrome and without et al., 2012). 1205
1142 psychiatric comorbidity have shown an attenuated increase in Gender may moderate TSST effects within a depressed sample; 1206
1143 cortisol in response to the TSST compared to healthy controls females with chronic major depressive disorder exhibited a greater 1207
1144 (Suárez-Hitz et al., 2012). However, results from our laboratory cortisol response to the TSST than female controls, whereas in males 1208
1145 indicate that cortisol levels in irritable bowel syndrome remain depression was associated with reduced cortisol peak percentage 1209
1146 significantly elevated up to 1 h following exposure to the TSST in change (Chopra et al., 2009). In contrast, remitted depression (com- 1210
1147 comparison to healthy control participants (Kennedy et al., 2013). pared to no depressive history) attenuated the cortisol response in 1211
1148 Heart rate, cortisol and blood pressure responses to the TSST-C (see females, but did not affect cortisol response in males (Bagley et al., 1212
1149 Section 6.3) were higher for children with recurrent abdominal pain 2011). 1213
1150 than controls, although these effects were non-significant (Dorn

1151 et al., 2003).
1152 The gastric peptide and cortisol secretagogue ghrelin has an
1153 increased response to the TSST in participants with bulimia ner- 5.5. Treatment for stress-related psychiatric disorders 1214
1154 vosa (Monteleone et al., 2012), although stress-induced changes in

1155 ghrelin do not acutely moderate changes in desire to binge (Rouach 5.5.1. Psychological treatment for stress-related psychiatric 1215
1156 et al., 2007). HPA axis response to the TSST is correlated with disorders 1216
1157 increased desire to binge in participants with binge eating disorder, The TSST has been used to examine the effects of psychological 1217
1158 and participants with binge eating disorder have a blunted corti- interventions for stress-related disorders. A higher level of practice 1218
1159 sol response (Rosenberg et al., 2012). In obese participants, TSST of compassion meditation reduces IL-6 responses as well subjective 1219
1160 stress was associated with higher initial rate of eating (chocolate distress in the TSST, but not cortisol (Pace et al., 2009). Consis- 1220
1161 pudding) and reduced deceleration of eating towards the end of eat- tent with findings that trait mindfulness can attenuate cortisol and 1221
1162 ing, but only for those participants with binge eating disorder, even subjective anxiety response to the TSST (Brown et al., 2012), state 1222
1163 though those with binge eating disorder did not report greater sub- anxiety reaction to the TSST has been attenuated by mindfulness- 1223
1164 jective stress (Schulz and Laessle, 2012). Despite an altered ghrelin based stress reduction (MBSR) in participants with generalised 1224
1165 response, participants with bulimia nervosa did not have a higher anxiety disorder (Hoge et al., 2013), and by mindfulness-based cog- 1225
1166 cortisol response (Monteleone et al., 2012). nitive therapy in participants with partially remitted depression 1226
1167 Participants at high risk for psychosis showed an attenuated (Britton et al., 2012); this effect may be due in part to reduced 1227
1168 response to the TSST; this group also indicated higher levels of rumination (Van Vugt et al., 2012); trait rumination has also been 1228
1169 depression and chronic stress, which may explain the altered acute shown to predict the size and duration of the TSST cortisol response 1229
1170 stress response (Pruessner et al., 2013). (Zoccola et al., 2010). In a community sample, MBSR was compared 1230
to an active control group who received an intervention which 1231
1171 5.4. Factors moderating TSST response in stress-related disorders was similar to MBSR but avoided components which are specific 1232
to mindfulness – MBSR did not have differing effects on subjective 1233
1172 The effects of depression may interact with childhood mal- or cortisol response to TSST, but led to a reduction in inflammatory 1234
1173 treatment in how participants respond to the TSST. The TSST led effects (assessed with topical capsaican) (Rosenkranz et al., 2013). 1235
1174 to higher cortisol and heart rate levels in women with both a Contemplative/emotional training has been found to accelerate 1236
1175 major depressive disorder and sexual or physical abuse in child- autonomic recovery from the TSST, as well as reducing reactivity 1237
1176 hood (Heim et al., 2000). It also increased ACTH for those with for those who practiced more (Kemeny et al., 2012). Healthy partic- 1238
1177 both problems or just abuse, although ACTH was not higher than ipants have shown reduced cortisol response and stress appraisal 1239
1178 controls for those with major depressive disorder only. Early life on the TSST following cognitive-behavioural stress management 1240
1179 adversity and chronic stress predicted enhanced adrenal response training (Gaab et al., 2003), and a stress management and resilience 1241
1180 to the TSST in depressed adolescents (Rao et al., 2008), and adult programme reduced stress, heightened perceived control and 1242
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1243 ␣-amylase recovery in stressed participants without a psychiatric specific mechanisms underlying such effects should be elucidated 1305
1244 disorder (Rose et al., 2013). in future research and novel therapeutics should be tested for 1306
efficacy in normalising the stress response. There is also emerg- 1307
1245 5.5.2. Pharmacological treatment for stress-related psychiatric ing evidence that dietary interventions may alter TSST response, 1308
1246 disorders although there is a paucity of research in this area using clinical 1309
1247 Research using the TSST and similar paradigms has also inves- samples. 1310
1248 tigated the effects of pharmacological agents under conditions of

1249 acute stress. Research using simulated public speaking (Guimarães
1250 et al., 1987; McNair et al., 1982) has indicated that benzodiazepines 6. Modified versions of the TSST 1311
1251 can reduce anxiety at pre-stress (Graeff et al., 2003). Pre-treatment

1252 with the benzodiazepine alprazolam blunts the ACTH and cortisol 6.1. Repeated measures 1312
1253 response to the TSST in healthy participants, but not state anx-
1254 iety, heart rate, adrenaline or noradrenaline (Fries et al., 2006), Researchers may wish to expose participants to the TSST on 1313
1255 which suggests that HPA axis responses may be more sensitive more than one occasion; for example, pre- and post-treatment 1314
1256 to detecting the effects of anti-anxiety drugs. Fries et al. (2006) when examining the effects of treatment for depression. However, 1315
1257 suggest that GABA binding may be a plausible mechanism for this where psychophysiological responses habituate to repeated expo- 1316
1258 effect; the T1521C polymorphism in the GABAA ␣6 receptor sub- sure to the TSST, this makes it difficult to separate the effects of 1317
1259 unit gene has been shown to attenuate ACTH, cortisol and blood treatment from habituation. Previous studies have exposed partic- 1318
1260 pressure responses to the TSST (Uhart et al., 2004). Administration ipants repeatedly to the TSST. Pruessner et al. (1997a) aggregated 1319
1261 of lamotrigine, a glutamate antagonist used to treat bipolar disor- data from multiple visits; although it is also possible that data 1320
1262 der, reduced cortisol, growth hormone and diastolic blood pressure aggregation reduces the level of noise in the data created by cortisol 1321
1263 response to the TSST in healthy volunteers (Makatsori et al., 2004). pulsatility (Young et al., 2004a), Pruessner et al. suggest that exclu- 1322
1264 The SSRI (selective serotonin reuptake inhibitor) paroxetine has sion of the first day’s cortisol response should have greatly reduced 1323
1265 been found to significantly reduce blood pressure during a modified a masking effect of novelty on cortisol response to other stressful 1324
1266 version of the TSST (Golding et al., 2005), although heart rate was aspects of their study. Nonetheless, as novelty is arguably a use- 1325
1267 not affected. Dysfunctional serotonergic function is associated with ful factor in inducing stress, “masking” this aspect of a stressful 1326
1268 dysfunctional HPA axis function and immune activity in depression experience should alter the nature of the stressor, and under- 1327
1269 (Leonard, 2006), and treatment with interferon-␣ can alter sero- mine the extent to which it is stressful. In one study involving 1328
1270 tonin metabolism as well as neuroendocrine activity (Capuron and repeated TSST exposure, some degree of novelty was maintained 1329
1271 Miller, 2004). SSRI’s may thus be relevant in studying immune and by making changes to the job applied for in the verbal part of 1330
1272 HPA axis response to acute stress in people with depression. Nora- task and the numbers involved in the arithmetic task for each 1331
1273 drenaline reuptake inhibitors also alter changes in the immune and TSST session (Kirschbaum et al., 1995b). For about one third of 1332
1274 endocrine systems induced by chronic stress (Leonard, 2001); the the participants, cortisol was markedly increased for all five days 1333
1275 effects of such substances in the acute stress response is thus also of participation (a Monday–Thursday plus the following Monday), 1334
1276 of interest. suggesting that at least some people do not quickly habituate to 1335
this stressor. Conversely, a minority of participants (16%) show 1336
1277 5.5.3. Dietary interventions for stress sensitisation to the TSST (Wüst et al., 2005). Vital exhaustion (a psy- 1337
1278 Dietary interventions for stress may also be of interest; both chological state of exhaustion comprising fatigue, irritability and 1338
1279 omega 3 phosphatidylserine (Hellhammer et al., 2012) and fer- demoralisation) reduced habituation to repeated exposure to the 1339
1280 tilised egg powder (Schult et al., 2010) have been found to restore TSST (Kudielka et al., 2006). Mean cortisol response was low for 1340
1281 HPA axis responses to the TSST which had been blunted in partici- all TSST exposures in participants with high levels of vital exhaus- 1341
1282 pants with high levels of chronic stress. Phospholipids did not alter tion. 1342
1283 the HPA axis response to the TSST, although participants receiv- Others have similarly modified the speech and arithmetic com- 1343
1284 ing a higher dose showed better memory performance post-TSST ponents between repeated TSST assessments and utilised longer 1344
1285 in participants aged 41–51 (Schubert et al., 2011). It may thus be inter-session intervals, such as one week (Gerra et al., 2001; 1345
1286 of interest to evaluate if other dietary changes can normalise the Mischler et al., 2005; von Känel et al., 2006) and four weeks 1346
1287 stress response to the TSST in depressed or anxious participants. (Schommer et al., 2003). The results of these studies indicated 1347
that although HPA axis outcomes (ACTH, salivary and serum corti- 1348
1288 5.6. TSST and stress-related psychiatric disorders: summary sol) habituated over two to three sessions, heart rate responses 1349
remained relatively stable. The lack of habituation in heart rate 1350
1289 Responses to the TSST in cases of stress-related disorders are may be due to a consistent level of general arousal elicited by 1351
1290 summarised in Table 2. There is evidence that major depression can repeated performances of the speech task despite a decline in the 1352
1291 lead to lengthened cortisol response to the TSST, and the inflam- severity of stress. Neither adrenaline nor noradrenaline response 1353
1292 matory response has also been shown to be altered in depression. habituated (Gerra et al., 2001; Schommer et al., 2003), nor did IL-6 1354
1293 Although panic disorder and PTSD are both considered anxiety dis- response habituate (von Känel et al., 2006), although the evidence 1355
1294 orders, they did not indicate the same moderating effect on HPA on blood pressure is less clear (Gerra et al., 2001; von Känel et al., 1356
1295 axis activity. Comparability may be reduced by the significant age 2006). 1357
1296 differences in the samples of some studies; child- versus adult- It thus seems that although a number of psychophysiological 1358
1297 onset depression have been associated with differences in HPA axis factors do not rapidly habituate to the TSST, for a majority of partic- 1359
1298 and immune measures (Kaufman et al., 2001). Response to the TSST ipants HPA axis responses to the TSST are attenuated after the first 1360
1299 in stress-related disorders may be moderated by gender and early visit. Greater procedural differences, e.g. speech content, serial sub- 1361
1300 life stress; major stressors in early life should be assessed. Other traction, can reduce the level of habituation (Foley and Kirschbaum, 1362
1301 stress-related disorders such as binge eating and irritable bowel 2010). Longer periods between TSST exposure may also reduce 1363
1302 syndrome may lead to perturbed stress responses. habituation; salivary cortisol response was attenuated with a 24 h 1364
1303 Both pharmacological and psychotherapeutic interventions for period between TSST performances but not after a 10 week inter- 1365
1304 stress-related disorders can moderate the TSST response. The val (Petrowski et al., 2012). Animal models of stress habituation 1366
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G Model
Table 2
Responses to TSST in stress-related disorders.
Disorder Paper Sample Age Outcomes assessed Effect of TSST and psychiatric Substance
disorder use/pre-treatment
Anxiety disorders: Generalised Gerra et al. (2000) N = 40: (all male) 20 with Mean = 12.4, SD = 0.6 Plasma cort, adrenaline, Noradrenaline, testosterone, GH, No
anxiety disorder (GAD) GAD, 20 HC noradrenaline, ACTH, ␤-endorphin, HR, SBP, increase more in GAD.
GH, prolactin, testosterone, HR, BP Prolactin, ␤-endorphin, decrease
(pre- and post-stress) more in GAD. Non-significant
differences for cort & ACTH
Anxiety disorders: Social Hoyer et al. (2013) N = 89: 55 with SP SP: mean = 26.5, SD = 6, HC: Saliva and plasma cort (8 Higher No
phobia (male = 21, female = 24), 34 mean = 25.3, SD = 6.4 timepoints), HR, PASA (following depersonalisation/derealisation in
HC (male = 18, female = 16) speech preparation), SP, which was associated with
depersonalisation/derealisation, higher primary appraisal, safety
stress, safety behaviours behaviours and post-event
ARTICLE IN PRESS
(immediately post-stress), processing. Cort and HR not
A.P. Allen et al. / Neuroscience and Biobehavioral Reviews xxx (2013) xxx–xxx
post-event processing (one week reported
post-stress)
Krämer et al. N = 81: 41 with SP SP: mean = 10.1, SD = 1.4, Saliva cort, sAA (baseline, Heightened increase in anxiety in No
(2012) (male = 20, female = 21), 40 HC: mean = 10, SD = 1.1, immediately post-stress, response to TSST and higher HR
HC (male = 20, female = 20) range = 8–12 post-stress +10, 20, 30 min), HR, throughout experimental session
subjective anxiety (baseline, in SP
post-preparation, between TSST
tasks, immediately post-stress,
post-stress +10, 20, 30 min)
Schmitz et al. N = 56: 30 with SP SP: mean = 10.1, SD = 1.2, HR, GSR, respiratory sinus Reduced respiratory sinus No
(2011) (male = 15, female = 15), 26 HC: mean = 10, SD = 1.1, arrhythmia, subjective anxiety arrhythmia activity compared to
HC (male = 15, female = 11) range = 8–12 (timing same as Krämer et al., HC, slower HR recovery
2012)
van Veen et al. N = 18 (female = 8, Mean = 39.1 Saliva cort, sAA (stressor onset Higher saliva cort and Responders to
(2009) male = 10), SP, no lifetime −60, 10, +10, 20, 30, 40, 50, 90, alpha-amylase. No HC group 20–60 mg
comorbidity 120, 180, 240, 360, 420) citalopram. Use of
psychotropic
medication
stopped 2 weeks
pre-test.
Tryptophan
depletion or
control
administered
Anxiety disorders: Panic Petrowski et al. N = 34: 34 with PD PD: mean = 35, SD = 12, HC: Saliva cort (at stressor −10, +1, 10, PD leads to lower cort response, no PD participants
disorder (2010) (female = 23, male = 11), 34 mean = 35.3, SD = 12.2 20, 30, 40, 50), HR moderation for HR. Second TSST taking medication
HC (female = 23, male = 11), exposure = lower cort response for
HC, no habituation for HR
Petrowski et al. N = 64: 32 with PD PD: mean = 32.9, SD = 11.2, Saliva and plasma cort and ACTH PD leads to lower cort response, no No
(2013) (female = 20, male = 12), 32 HC: mean = 31.2, SD = 11.1 (stressor onset −15, 1 min, end of moderation for HR. Trend for
HC (female = 20, male = 12) stressor +1, 10, 20, 30, 45, 60 min), higher response in subjective
HR (3 min periods pre-stress, anxiety
speech task, arithmetic task,
post-stress) subjective anxiety
(pre- and post-stress)
Anxiety disorders: Simeon et al. N = 139: 35 PTSD PTSD: mean = 41.5, Plasma cort (post-anticipation, PTSD and DD led to higher TSST compared to
Post-traumatic stress disorder (2007a,b) (female = 19, male = 16), 46 SD = 11.5, DD: mean = 31.2, post-stressor, post-stress +30, subjective response, but did not DST
dissociative disorder SD = 10.3, HC: mean = 32.8, +60 min), urinary cort, subjective moderate plasma cort response
(female = 26, male = 20), 58 SD = 10.8 stress (post-stressor)
HC (female = 26, male = 32)
15
16
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G Model
Table 2 (Continued)
Depression Chopra et al. (2009) N = 54: 26 chronic MD MD: mean = 43.3, SD = 5.7, Saliva cort, subjective stress Females: greater cort response in 18 MD taking
(female = 12, male = 14), 28 HC: mean = 39.4, SD = 6 post-stressor (stressor onset -35, MD. Males: lower peak percent psychotropic
HC (female = 14, male = 14) 20, immediately prior to onset, cort change in MD. Trend for higher medication, 16
+20, 40, 60, 80 min) subjective stress in MD generally taking
antidepressants
ARTICLE IN PRESS
Dienes et al. (2013) N = 57 (all female) 15 MD, MD: mean = 18.4, SD = 0.9, Saliva cort, positive and negative MD group had higher net increase 2 MD participants
20 at risk, 22 HC At risk: mean = 18.7, affect (baseline, immediately, 10, in cort than at risk, slower recovery taking
SD = 0.8, HC: mean = 18.9, 25, 40 min post-stress) in negative affect fluoxetine/amphetamine
SD = 1.2
Harkness et al. N = 71: 30 no/mild No/mild depression: Saliva cort (baseline, Higher cort in mild/moderate 8 participants
(2011) depression (female = 20, mean = 14.7, SD = 2.3, post-preparation, immediately depression with childhood taking
male = 10), 16 moderate Moderate: mean = 15.7, post-stress, post-stress +1, 2 h) maltreatment. Moderate/severe anti-depressant
(female = 9, male = 7), 25 SD = 1.6, Severe: mean = 16, depression: blunted cort regardless medication
severe (female = 19, SD = 2 of child maltreatment
male = 6)
Heim et al. (2000) N = 49 (all female) 13 with MD + CA: mean = 32, No Plasma cort, ACTH, HR (stressor Higher ACTH for CA group (+15, No
both current MD and CA, MD, CA: mean = 30, MD, no onset −15, 0, +15, 30, 45, 60, 75, 30 min). Higher cort for MD + CA
14 CA and no MD, 10 MD CA: mean = 34.6, HC: 90 min) group (+30, 45, 60 min). Trend for
and no CA, 12 HC mean = 29 higher HR in MD + CA group
(+15 min)
Pace et al. (2006) N = 28 (all male) physically MD: mean = 29.9, SD = 9.6, Plasma IL-6, NF-␬B DNA-binding, Higher IL-6 (baseline and 90 min), No
healthy, 14 with MD and HC: mean = 29.4, SD = 8 natural killer (NK) cells (baseline at higher increase in NF-␬B
early-life stress, 14 HC stress onset −1 min, baseline +30, DNA-binding for MD group. No
60, 75, 90 min) group difference in NK cells
Rao et al. (2008) N = 55: 30 with MD MD: mean = 15.1, SD = 1.4, Saliva cort (baseline: 30 min Higher and more prolonged cort No
(female = 17, male = 13), 25 HC: mean = 15, SD = 1.5 intervals for 2 h, post-stress: response for MD group
HC (female = 13, male = 12) immediately post-stress plus
10 min intervals for 60 min)
Stewart et al. N = 64: 31 with current MD: M = 16, SD = 1.6, HC: Saliva cort (baseline, Lower cort response in depression 9 depressed
(2013) depression (female = 25, mean = 14.6, SD = 2 post-preparation, immediately participants taking
male = 6), 33 HC post-stress, 25, 65 min post-stress) psychotropic
(female = 22, male = 11) medicine
Taylor et al. (2006) N = 68 (high cardiovascular MD: mean = 62.3, SD = 6.4, Saliva cort, HR, BP, subjective MD had lower cortisol response Excluded if taking
disease risk) 48 with MD HC: mean = 62.5, SD = 6 emotions (PANAS), RSA, C-reactive and lower RSA during stress medications
(female = 32, male = 16), 20 protein (pre-baseline, pre- and affecting HPA axis
HC (female = 8, male = 12) post-anticipation, post-stressor,
10, 20, 30, 45, 60 min into recovery)
Young et al. (2000) N = 20: 10 with MD MD: mean = 33, SD = 11, Plasma cort, ␤-endorphin (stressor MD leads to lower ␤-endorphin Treatment
(female = 4, male = 6), 10 HC: mean = 33.9, SD = 11.5 onset −50, 20, 10, 0, +5, 10, 15, 20, response, higher negative mood postponed until
HC, Axis I comorbidity 25, 30, 35, 40, 55, 70) subjective post-stress, no moderation for cort end of study
excluded (female = 4, mood (end of TSST, 20 min later)
male = 6)
NBR 1866 1–31
G Model
Table 2 (Continued)
Anxiety and depression Young et al. N = 96: 15 pure MD Pure MD: mean = 28.7, Blood cort and ACTH (10 min Comorbid group showed greater MD and anxiety
(2004a,b) (female = 7, male = 8), 15 SD = 7.7, Pure anxiety: intervals from 30 min before stress ACTH response. All anxiety and untreated
pure anxiety (12 SP, 3 PD, 1 mean = 25.4, SD = 8.5, onset to 1 h post-stress) subjective depression group had higher
PTSD; female = 9, male = 7), Comorbid: M = 23.2, anxiety (immediately pre-stress, subjective anxiety at each
18 comorbid MD and SD = 5.5, HC: M = 26, post-stress, 20 min post-stress), measurement
anxiety (13 SP, 5 = PD, SD = 7.1 HR, BP (30 min and immediately
ARTICLE IN PRESS
2 = PTSD; female = 14, pre-stress, end of stress)
male = 4;, 48 HC
(female = 29, male = 19)
Young et al. (2005) N = 90: 13 pure MD Pure MD: mean = 28.2, Blood cort and ACTH (10 min Negative correlation between GH MD and anxiety
(female = 7, male = 6), 15 SD = 7.7, Pure anxiety: intervals from 30 min before stress and ACTH in HC and pure anxiety, untreated
pure anxiety (12 SP, 3 PD, 1 mean = 25.4, SD = 8.5, onset to 1 h post-stress). GH but not in pure MD and comorbid
PTSD; female = 8, male = 7), Comorbid: M = 23.2, (separate day to blood; clonidine anxiety and MD
17 comorbid MD and SD = 5.5, HC: M = 25.8, infusion −30, 15, 1 min, end of
anxiety (13 SP, 4 = PD, SD = 7.1 infusion 15, 30, 60, 90, 120 min)
2 = PTSD; female = 13,
male = 4), 45 HC
Eating disorders Monteleone et al. N = 20 (all female) 10 with BN: mean = 24.1, Salivary cort, ghrelin (baseline, Higher ghrelin response in BN No
(2012) BN, 10 HC range = 20–28, HC: immediately post-stress, end of
mean = 25.3, stress +15, 30, 50 min)
range = 21–29.5
Rosenberg et al. N = 24: 8 obese with BED BED: mean = 49.8, SD = 4.9, Serum cort (stress onset −30, 0, Blunted cort response in BED group No
(2012) (female = 6, male = 2), 8 Non-BED obese: +15, 35, 55, 75 min), HR, BP,
obese without BED mean = 50.3, SD = 5.7, HC: subjective stress, anxiety
(female = 5, male = 3), 8 mean = 32.6, SD = 3.55 (immediately pre- and post-TSST)
normal weight controls
Irritable bowel syndrome Suárez-Hitz et al. N = 77 (all female) 57 with IBS: mean = 29.3, Saliva cort, plasma ACTH (baseline, Blunted increase in cort and lower No
(2012) IBS (34 = no Axis I range = 20–51, HC: post-preparation, immediately ACTH at recovery for IBS without
comorbidity, 16 = major mean = 29, range = 23–43 post-stress, post-stress +20, 30, 40, psychiatric comorbidity compared
depression/dysthymia, 60 min) subjective stress (baseline, to HC. Higher PASA for IBS group
3 = generalised anxiety, post-preparation, immediately and higher subjective stress for IBS
5 = PD, 4 = social phobia, post-stress) PASA group with comorbidity
3 = specific phobia), 20 HC (post-preparation)
Ultra-high risk for psychosis Pruessner et al. N = 42: 21 with UHR UHR: mean = 20.8, Saliva cort, HR, BP (stress onset Lower cort, lower SBP for UHR 6 UHR patients
(2013) (female = 9, male = 12), 21 range = 16.4–27.2, HC: −45, 30, 15, 1, +1, 10, 20, 40, taking
HC (female = 9, male = 12) age = 20.8, range 15.9–27.4) 60 min), subjective stress antidepressant
(immediately post-stress) medication
Key: BED, binge eating disorder; BN, bulimia nervosa; BP, blood pressure; CA, childhood abuse; cort, cortisol; DD, dissociative disorder; GH, growth hormone; GSR, galvanic skin response; HC, healthy controls; HR, heart rate; IBS,
irritable bowel syndrome; MD, major depression; PD, panic disorder; PTSD, post-traumatic stress disorder; SBP, systolic blood pressure; SP, social phobia; UHR, ultra-high risk for psychosis.
17
ARTICLE IN PRESS
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NBR 1866 1–31
1367 support these suggestions; habituation in prolactin response can Researchers have designed a version of the TSST for use with 1428
1368 be attenuated by exposure to differing types of stressor (Jean Kant larger groups of participants (TSST-G; von Dawans et al., 2011), 1429
1369 et al., 1985), and habituation in adrenaline and corticosterone and tested it against a less stressful control condition for grouped 1430
1370 response can be attenuated by longer inter-stressor intervals (De participants. While standing in a line with five other participants, 1431
1371 Boer et al., 1990). participants speak for 2 min each on their suitability for a relevant 1432
job (mobile walls are used to restrict eye contact between partic- 1433
ipants). In a control condition, participants read a scientific text 1434

1372 6.2. Control TSST
rather than preparing and performing a speech. Unlike the con- 1435
trol condition in Het et al. (2009), control participants are required 1436
1373 A non-stress control condition is required for research using
to speak in front of the panel. However, they simply read aloud 1437
1374 the TSST aims to examine the effects of stress per se, rather than
the extract simultaneously in front of the panel, followed by serial 1438
1375 the difference between groups in terms of their response to stress.
addition of numbers. Video cameras are present in the testing room 1439
1376 Although some TSST studies have included a control group that
for the experimental condition but not the control condition. Sali- 1440
1377 simply involves sitting quietly, a control TSST has been designed
vary cortisol increased in response to the TSST-G, and not in the 1441
1378 which aims to be as similar as possible to the typical TSST with the
control group; heart rate increased under both conditions, but to 1442
1379 exception that it should not be stress-inducing (Het et al., 2009).
a greater extent in the stress condition. Participants in the TSST-G 1443
1380 Participants are required to talk about a film, novel or recent holiday
group reported higher post-test stress, strain, challenge and lower 1444
1381 trip (the topic is thus less relevant to self-presentation and self-
controllability than the control group. The serial position in which 1445
1382 esteem than in the experimental TSST). Social-evaluative threat is
the participants were called did not have a significant effect. The 1446
1383 reduced, as participants do not speak in front of a committee and
TSST-G lasts longer than the TSST overall, although the free speech 1447
1384 they are not led to believe that they are being recorded. Salivary
task for any given participant is shorter. Childs et al. (2006) used 1448
1385 cortisol concentrations were found to increase in the TSST condi-
a free speech task that was equally long for grouped and individ- 1449
1386 tion but fall in the control TSST, and participants in the control
ual participants, although this may be impractical in larger groups. 1450
1387 TSST reported less feelings of threat, challenge, as well as higher
Where group tests last longer there may be a greater component 1451
1388 control expectancy (suggesting lower amounts of uncontrollabil-
of anticipation compared to individual participants, particularly for 1452
1389 ity) and self-concept of own ability. A second experiment using
grouped participants who speak after the rest of the group. In com- 1453
1390 a crossover design and communication via intercom for the con-
parison, those participants who speak first in a group will have a 1454
1391 trol TSST also indicated higher cortisol, threat, challenge and lower
longer recovery period. 1455
1392 self-concept of self ability in the TSST condition than in the con-
1393 trol, regardless of condition order. Another control condition for the
1394 TSST has involved describing a favourite book or film to an assis- 6.4. Children and adolescents 1456
1395 tant followed by performing a Solitaire game without being taped
1396 or evaluated, and has been associated with lower anxiety, negative Researchers have also developed a TSST for children (the TSST- 1457
1397 mood, salivary cortisol, salivary ␣-amylase heart rate, blood pres- C) (Buske-Kirschbaum et al., 1997). The verbal component requires 1458
1398 sure than the TSST (Childs and de Wit, 2010; Childs et al., 2011; children to finish a story in as exciting a manner as possible, and 1459
1399 Hamidovic et al., 2010). to perform this task better than the other children taking part. The 1460
1400 More recently, a friendly TSST (f-TSST) has been designed arithmetic component is graded based on age group (e.g. subtract- 1461
1401 (Wiemers et al., 2013b); unlike the procedure by Het et al. (2009), ing 7 from 758 for children aged 9–11 years). The committee give 1462
1402 it involves speaking in front of a panel. The f-TSST requires partic- positive feedback, and the children are encouraged to continue if 1463
1403 ipants to write about their education, career aspirations, hobbies, they finish before the 5 min are up. The TSST-C has also been used 1464
1404 and favourite book or film before being interviewed without being with adolescents aged 10–14 years (Gordis et al., 2006). Salivary 1465
1405 filmed. The panel smile and nod to indicate encouragement, and cortisol was increased by the TSST-C, as was sAA. sAA has also been 1466
1406 avoid pauses in the interview by promptly asking follow-up ques- increased by a version of the TSST-C which used academic topics for 1467
1407 tions. The f-TSST did not increase HPA axis activity or negative the speech task (Stroud et al., 2005, as cited in Granger et al., 2006). 1468
1408 affect, although it did increase salivary ␣-amylase. However, more A modified version of the TSST which can be used with both chil- 1469
1409 encouraging panels have elsewhere shown comparable HPA axis dren and adults has been developed (TSST-M; Yim et al., 2010). It 1470
1410 effects to the classic, unencouraging TSST panels (Taylor et al., requires participants to give a presentation that they are to imagine 1471
1411 2010). Control conditions have also been designed for group assess- they are giving to a new class; they are to talk about their person- 1472
1412 ment (see Section 6.3). ality (including one positive and one negative aspect thereof) and 1473
why they would be liked by the class. The TSST-M increased sali- 1474
1413 6.3. Group assessment vary cortisol and led to higher negative affect and lower positive 1475
affect; the increase in cortisol applied to 9–10 year olds as well 1476
1414 Group assessment for the TSST is desirable, as it can reduce the as 11–12 year olds. However, the authors note that the test may 1477
1415 time commitment of confederates (Childs et al., 2006), although not be suitable for a wide age range of children. Greater cortisol 1478
1416 this may not always be practical where sample collection is slower response to the TSST-M was associated with enhanced recall of the 1479
1417 (e.g. if collecting blood samples). Childs et al. (2006) compared par- test two weeks later for children, adolescents and adults (Quas et al., 1480
1418 ticipants tested individually and those tested in groups of two to 2012). In a later study this effect was again evident for 7–8 year olds, 1481
1419 three, with grouped participants completing the verbal and mental although in those aged 12–14 higher arousal was associated with 1482
1420 arithmetic tasks one after the other. Similar to repeated measures both fewer correct and fewer incorrect responses, suggesting that 1483
1421 Trier designs, each participant was given a different starting num- stress might reduce willingness to respond in the adolescent group 1484
1422 ber for serial subtraction to avoid learning effects. Participants (Quas et al., 2013). An advantage of the TSST-M is that the person- 1485
1423 tested in groups did not experience a significantly different change ality speech may be more consistently stressful across participants 1486
1424 in salivary cortisol or reported anxiety compared to participants than the job speech from the original TSST, since the job application 1487
1425 tested one at a time. However, peak heart rate was higher for context allows participants to focus on the specifics of the qualifi- 1488
1426 grouped participants, with heart rate increasing more dramatically cations they hold, and thus avoid having to explicitly address their 1489
1427 for the first 5 min of the stressor. own personality and likability. 1490
ARTICLE IN PRESS
G Model
NBR 1866 1–31
1491 6.5. Virtual/imagined TSST committee negative affect, sAA and cortisol. Smeets et al. also developed a con- 1554
trol Maastricht Acute Stress Test which requires hand immersion in 1555
1492 Similar to grouped assessment, a virtual reality version of a lukewarm water and a simple counting task; this did not increase 1556
1493 committee could greatly reduce the labour required of the TSST sAA or salivary cortisol levels. 1557
1494 committee. However, such a methodology may be less stressful

1495 than performing for a panel “in the flesh”; neither a speech task
6.7. Modified versions of the TSST: summary 1558
1496 within an environment generated by a virtual reality helmet nor
1497 a math task outside the virtual reality environment induced sig-
Numerous adaptations have been made to the “classic” TSST 1559
1498 nificant changes in anxiety or cortisol, although both increased
to meet the requirements of researchers. Repeated versions of 1560
1499 heart rate (Kotlyar et al., 2008b). Performing for an imagined audi-
the TSST have generally led to habituation in HPA axis responses, 1561
1500 ence behind a one-way mirror or for a virtual reality audience
although longer periods between tests seem to attenuate this effect. 1562
1501 increased cortisol compared to a control group, although perform-
A control TSST without an interview committee has been shown 1563
1502 ing in front of a live panel led to a greater response than the virtual
not to increase HPA axis response, although control versions with 1564
1503 reality or imaginary panel (Kelly et al., 2007). A one-way mirror
a friendly or encouraging panel have shown mixed effects. The 1565
1504 has been used in social phobia research, perhaps from concern
TSST has been shown to be effective when administered to groups, 1566
1505 that the classic TSST would be too stressful to complete for many
and a control version for groups is also available. This may free up 1567
1506 participants with this condition. The Leiden Public Speaking Task
resources which could be used to perform a control Trier as well 1568
1507 involves speaking in front of a pre-recorded audience; it has been
as the stressful version. However, virtual committees may require 1569
1508 shown to induce a substantial cortisol response in 55% of partici-
further development and evaluation before they can be treated as 1570
1509 pants in an adolescent sample (Westenberg et al., 2009), with the
a reliable means of inducing psychosocial stress. The TSST for chil- 1571
1510 response being stronger in adolescents than in children (Sumter
dren provides an age-appropriate psychosocial stressor, although 1572
1511 et al., 2010). A virtual reality version of the TSST which uses immer-
the TSST-M has potential for use in both children and adults, allow- 1573
1512 sive computer-generated rooms (Jönsson et al., 2010) rather than
ing for more direct examination of the effects of maturation on the 1574
1513 the head-mounted displays has led to a cortisol response substan-
stress response. Combining the TSST with pharmacological chal- 1575
1514 tially greater than that observed in the virtual reality condition of
lenges and cold pressor tasks can potentially allow for a more 1576
1515 Kelly et al. (2007), although given the small sample size this should
detailed examination of psychosocial stress effects on human psy- 1577
1516 be interpreted with caution. Virtual reality methodology could have
chophysiology. 1578
1517 the added advantage of holding the responses of the panel more
1518 constant (Westenberg et al., 2009).
7. Discussion 1579
1519 6.6. Hybrid versions of the TSST

7.1. Comparison with other methods of inducing stress and 1580
1520 The DST (see Section 7.1) and the TSST have been combined, measuring HPA axis activity 1581
1521 with dexamethasone taken at bedtime and exposure to the TSST

1522 occurring the following morning. The participants who took dex- 7.1.1. Pharmacological stimulation of the HPA axis 1582
1523 amethasone showed typical suppression of cortisol compared to The correlation between salivary cortisol and unbound corti- 1583
1524 a placebo group, but also displayed increased heart rate through- sol in plasma and serum persists across the TSST, DST and ACTH 1584
1525 out the protocol, including during exposure to the TSST (sAA and stimulation (Hellhammer et al., 2009). The DST involves the admin- 1585
1526 blood pressure did not differ between dexamethasone conditions). istration of 1 mg of dexamethasone at 23.00 and examination of 1586
1527 The authors suggest that this methodology allows for the examina- HPA axis activity at 16.00 and 23.00 the following day; as healthy 1587
1528 tion of interactions between the sympathetic nervous system and controls will have suppressed HPA axis activity for at least 24 h after 1588
1529 the HPA axis (Andrews et al., 2012). Conversely, the TSST has been overnight administration, samples have also been taken at 08.00, 1589
1530 combined with the administration of propranolol, which reduces although this time point was not as efficient for detecting abnormal 1590
1531 sympathetic nervous system responses to stress; heightened cor- results in melancholic depression (Carroll, 1982). ACTH stimulation 1591
1532 tisol responses have been shown in participants who received can be performed through a short Synacthen test, which typically 1592
1533 propranolol instead of placebo, suggesting that one system may involves the administration of 0.25 mg ACTH1–24 , although a lower 1593
1534 compensate where the activity of the other is reduced (Andrews dose of 1 ␮g may be more useful in a clinical context (Abdu et al., 1594
1535 and Pruessner, 2013). However, propranolol does not alter IL-6 1999), and assessing HPA axis activity at similar time points to the 1595
1536 response to the TSST (von Känel et al., 2008). TSST (e.g. Blair et al., 2013; Clark et al., 1998). The TSST has an effect 1596
1537 The cold pressor task is a means of inducing stress by sub- on cortisol levels that is similar in magnitude to the effect of injec- 1597
1538 merging the hand in cold water for 1–2 min (see Section 7.1 for tion of 1 ␮g/kg human corticotropin releasing hormone (hCRH), 1598
1539 further discussion). The socially evaluated cold pressor task takes although administration of 0.25 mg of ACTH1–24 led to a larger 1599
1540 the cold pressor task and adds a psychosocial element to it by film- and more sustained increase in salivary cortisol (Schmidt-Reinwald 1600
1541 ing the participant, telling them that this footage will be analysed, et al., 1999). 1601
1542 and having an experimenter watch the participant during hand Both the TSST and DST administration are sensitive to higher 1602
1543 immersion (Schwabe et al., 2008). Consistent with the finding that HPA axis responsivity in depression. The DST has been found to 1603
1544 social evaluative stress is particularly effective at increasing HPA be less likely to lead to reduced cortisol in depressed participants 1604
1545 axis activity (Dickerson and Kemeny, 2004), the socially evaluated compared to controls (Lowy et al., 1984), and patients with depres- 1605
1546 cold pressor task induces a greater cortisol response than the orig- sion who had higher cortisol levels following DST also had higher 1606
1547 inal cold pressor task. The Maastricht Acute Stress Test (Smeets catecholamine levels (Barnes et al., 1983; Sora et al., 1986). There 1607
1548 et al., 2012) combines aspects of the socially evaluated cold pressor is evidence that the DST normalises during treatment for depres- 1608
1549 task and the TSST. This comprises a preparation period, followed by sion (Carroll et al., 1976), although this was the not case for some 1609
1550 immersion of a hand in ice-cold water, combined with mental arith- patients, who may have lower levels of ACTH (Yerevanian et al., 1610
1551 metic. The Maastricht Acute Stress Test has been shown to induce 1983). Depressed patients with abnormal response to the DST were 1611
1552 a higher cortisol response than either the original or socially eval- more likely to commit suicide in a 15-year follow-up (Coryell and 1612
1553 uated cold pressor tasks, and it has similar effects to the TSST on Schlesser, 2001). The HPA axis response to the TSST may also 1613
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1614 have predictive validity; cortisol reactivity to a control version 7.1.4. The cortisol awakening response 1675
1615 of the TSST was shown to predict depressive symptoms at a six- The cortisol awakening response leads to an increase in cortisol 1676
1616 month follow-up (Morris et al., 2012). Similar to the standard dose release of 50–75% and peaks approximately 30 min after waking 1677
1617 DST, there is evidence that the HPA axis response to a low-dose (Pruessner et al., 1997b). The TSST has been found to have an 1678
1618 (0.5 mg) DST normalises in non-suppressors following remission effect on cortisol levels that is similar in magnitude to the cortisol 1679
1619 (Sarai and Matsunaga, 1986). PTSD did not alter HPA response to awakening response (Schmidt-Reinwald et al., 1999). The corti- 1680
1620 a low-dose DST in adults (Simeon et al., 2007a) or adolescents sol awakening response is a useful measure of HPA axis activity 1681
1621 (Lipschitz et al., 2003). In contrast, greater suppression of corti- for large studies, as participants can collect saliva samples while 1682
1622 sol in response to a low-dose DST occurred in women who had at home (Kudielka and Wüst, 2010). In ambulatory studies, about 1683
1623 experienced severe childhood sexual abuse (Stein et al., 1997), and 15–25% of participants do not show this response (Dockray et al., 1684
1624 older trauma survivors with PTSD (Yehuda et al., 2002). Similar to 2008; Wüst et al., 2000). However, given observed non-compliance 1685
1625 the cortisol response to the TSST, the low-dose DST differentiated in ambulatory studies and consistent presence of the cortisol awak- 1686
1626 childhood abuse survivors with depression from non-depressed ening response in sleep laboratory studies, healthy young adults 1687
1627 survivors and healthy controls, although the standard DST did not may generally show this response (Kudielka and Wüst, 2010). The 1688
1628 (Newport et al., 2004). Combining administration of dexametha- cortisol awakening response can nonetheless be moderated by fac- 1689
1629 sone the night before the day of assessment with administration of tors such as gender and health status (Fries et al., 2009). Awakening 1690
1630 CRH on the day of assessment has been found to have greater sen- has also been associated with a fall in secretory immunoglobu- 1691
1631 sitivity to major depression than the classic DST (DEX/CRH; Heuser lin A (Hucklebridge et al., 1998) as well as increased heart rate 1692
1632 et al., 1994). Although the level of sensitivity of this DEX/CRH test and low frequency/high frequency ratio, although there was not 1693
1633 has subsequently been challenged (Schüle et al., 2009), depressed a clear association between the cortisol awakening response and 1694
1634 patients show higher cortisol and ACTH following the DEX/CRH the changes in heart rate or heart rate variability (Stalder et al., 1695
1635 (Heuser et al., 1994; Ising et al., 2007; von Bardeleben and Holsboer, 2011); there is thus scope for further research on the effects of 1696
1636 1989), and higher cortisol response to the DEX/CRH test is asso- awakening on immune and cardiovascular factors as well as HPA 1697
1637 ciated with increased risk of relapse in patients with remitted axis response. The cortisol awakening response is also affected by 1698
1638 depression (Zobel et al., 1999, 2001). Similarly, men who had expe- stress-related disorders; it is higher in unmedicated participants 1699
1639 rienced childhood abuse had higher cortisol and ACTH following with current major depressive disorder (Bhagwagar et al., 2005), 1700
1640 administration of corticotrophin-releasing factor and dexametha- as well as in men with depressive symptoms but without clini- 1701
1641 sone (Heim et al., 2008). In contrast to the pro-inflammatory effect cal depression (Pruessner et al., 2003) and recovered depression 1702
1642 of the TSST, DEX/CRH reduces plasma IL-6 and TNF-␣ in depressed patients (Bhagwagar et al., 2003). 1703
1643 patients (Schuld et al., 2001).

7.1.5. Cognitive tasks 1704
Many studies use cognitive tasks to assess the psychophysiolog- 1705
ical effects of stress. For example, the Stroop test has been shown 1706
1644 7.1.2. The cold pressor task
to produce subjective stress effects, as well as changes in heart rate 1707
1645 Although the cold pressor task induces subjective stress
and heart rate variability (Delaney and Brodie, 2000) and inhibi- 1708
1646 (Schwabe et al., 2008) and distress (Kotlyar et al., 2008a), the TSST
tion of gastric activity (Huerta-Franco et al., 2012). The defined 1709
1647 leads to higher plasma cortisol and ACTH than the cold pressor task
intensity stress simulator, which requires simultaneous perfor- 1710
1648 (McRae et al., 2006). Similar to DEX/CRH challenge, the cold pres-
mance of multiple cognitive tasks, such as mental arithmetic and 1711
1649 sor task has been found to reduce the pro-inflammatory cytokine
Stroop test, leads to an increase in cortisol, although this may be 1712
1650 response via TNF-␣, IL-1␤, MCP-1 and IL-12 (Cruz-Almeida et al.,
restricted to the afternoon (Scholey et al., 2009), higher subjective 1713
1651 2012). The cold pressor task has increased heart rate and adrenaline
anxiety (Kennedy et al., 2006) and down-regulation of secretory 1714
1652 in some studies (Grassi et al., 2008; Kotlyar et al., 2008a) although
immunoglobulin A when workload is increased (Wetherell and 1715
1653 other research has not shown a significant effect on heart rate
Sidgreaves, 2005). An advantage of using computer-based cognitive 1716
1654 (Weise et al., 1993) or adrenaline (Dyson et al., 2006). An advan-
tasks is that the effects of stress on cognition can be studied using 1717
1655 tage of cold pressor task is that it is shorter than the TSST (stress
precise measures of cognitive performance, and since the cognitive 1718
1656 exposure only lasts 3 min) and only requires the presence of one
task is itself the stressor, current stress is studied, rather than post- 1719
1657 experimenter. However, as the cold pressor task is a method of
stress effects, as is the case of the TSST followed by cognitive tasks. 1720
1658 inducing pain as well as being a stressor (and a psychosocial stressor
Tasks on which the difficulty of the task can be altered precisely 1721
1659 in the case of the socially evaluated cold pressor task), conceptual
are advantageous in terms of controlling the intensity of the stres- 1722
1660 differences between the two should be borne in mind.
sor. However, comparing different types of psychological stressor, 1723
tests combining public speaking with a cognitive task (including 1724
the TSST) proved to induce larger cortisol responses than cognitive 1725
1661 7.1.3. The CO2 challenge test tasks or public speaking alone (Dickerson and Kemeny, 2004). This 1726
1662 The CO2 challenge test, which involves inhaling carbon dioxide- difference was not attributable to task duration, suggesting that the 1727
1663 enriched air, has been found to induce panic attacks in people with nature of the stressor may be the key factor. 1728
1664 panic disorder, but is also an effective physiological stressor. The
1665 CO2 challenge can induce a modest but significant increase in sub- 7.1.6. Noise 1729
1666 jective anxiety, noradrenaline and systolic blood pressure, as well Noise is frequently used as a stressor in research, in field studies 1730
1667 as a reduction in heart rate, although no effect has been detected as well as in experimental work; noise has been found to increase 1731
1668 on adrenaline or immune factors (for a review, see Vickers et al., sAA (Wagner et al., 2010), noradrenaline secretion (Babisch et al., 1732
1669 2012). Plasma and serum cortisol appear to increase following the 2001), heart rate variability (Schnell et al., 2013), and to impair cog- 1733
1670 CO2 challenge, but salivary cortisol does not (e.g. Kaye et al., 2004; nitive performance (Bengtsson et al., 2004; Jahncke et al., 2011), 1734
1671 Loft et al., 2007; Wetherell et al., 2006). It has been observed that and increase fatigue (Jahncke et al., 2011), although noise may 1735
1672 70% of participants can be classified as salivary cortisol responders enhance performance under conditions of low alertness (Smith, 1736
1673 or non-responders across testing sessions, although a majority of 2012). Although evening cortisol has been found to correlate with 1737
1674 these were non-responders (Wetherell et al., 2006). noise exposure (Fouladi et al., 2012) research has not indicated a 1738
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1739 clear effect of noise on cortisol or subjective stress (e.g. Bengtsson neuroendocrine responses (Yim et al., 2010). Although the Mon- 1802
1740 et al., 2004; Ljungberg and Neely, 2007). A novel paradigm called treal Imaging Stress Test induces stress in participants while being 1803
1741 the Mannheim Multicomponent Stress Test (Reinhardt et al., 2012) scanned by fMRI, there is a lack of a full TSST to be used in com- 1804
1742 combines noise stress with the added stressors of cognitive per- bination with fMRI. Nonetheless, the existence of virtual reality 1805
1743 formance, emotional induction and the threat of loss of money. versions of the TSST may allow for such a version to be designed 1806
1744 Participants perform serial addition while being presented with in the future. Imaging techniques may be useful for teasing apart 1807
1745 pictures which induce negative emotions and increasing decibels the cognitive effects of psychosocial stress, although careful con- 1808
1746 of white noise. They are also informed that incorrect answers result trol conditions (e.g. reading an extract aloud to a virtual committee, 1809
1747 in reduced payment. The Mannheim Multicomponent Stress Test similar to von Dawans et al., 2011) may be necessary to delineate 1810
1748 increased subjective stress, heart rate and cortisol activity. Aspects the brain areas affected by psychosocial stress and those involved 1811
1749 of this task, such as threatened reduction in payment, could easily in the performance of mental arithmetic and speech tasks. 1812
1750 be adapted to the TSST. As mentioned above, TSST research employing a repeated mea- 1813
sures design could induce more consistent stress responses over 1814
1751 7.1.7. Comparison with other methods of inducing stress and multiple testing sessions by varying the stressors to a greater 1815
1752 measuring HPA axis activity: summary extent (Foley and Kirschbaum, 2010). In a design with three vis- 1816
1753 Unlike the DST, the TSST does not require any pharmacologi- its, this could be carried out by using the job interview speech 1817
1754 cal treatment, and unlike the cold pressor task it does not expose from the classic TSST during one testing session, the personality 1818
1755 the participant to physical discomfort/pain. However, in the case of speech from the TSST-M during another session and the storytelling 1819
1756 very severe depression or social anxiety, the TSST may be more dif- speech task from the TSST-C for the third. Having each partic- 1820
1757 ficult to complete than tests such as the DST, given the performance ipant perform for different panel members during each session 1821
1758 requirements placed on the research participant for the speech and should also lessen habituation. Alternatively, researchers may wish 1822
1759 mental arithmetic tasks. The use of the interview panel can make to pre-select those high-responding participants who do not habit- 1823
1760 the TSST more labour-intensive than other methods such as the uate to repeated stress observed previously (e.g. Kirschbaum et al., 1824
1761 cold pressor task, although the amount of work required may be 1995b). A repeated measures design for the TSST which can reli- 1825
1762 reduced by the use of modified protocols such as group assessment ably induce a stress response in the HPA axis over multiple visits 1826
1763 or virtual committees. Table 3 summarises these methods of stress will be most useful for intervention studies (e.g. those investigat- 1827
1764 induction and their relative advantages and disadvantages. ing coping strategies for acute stressors or experiments on changes 1828
in diet). A repeated measures version of the TSST for children and 1829
1765 7.2. Future research adolescents may be useful in longitudinal research; the longer time 1830
lags between testing sessions should mean that habituation is less 1831
1766 It has been suggested that analysis of participants’ performance likely. 1832
1767 during the TSST could generate informative data, which may be In line with the reduction in HPA axis response to stress after 1833
1768 linked to the physiological response to the TSST (Williams et al., administration of the serotonin precursor tryptophan (Firk and 1834
1769 2004). Cognitive performance has typically been assessed follow- Markus, 2009) and enhanced sAA response following depletion of 1835
1770 ing the TSST, although performance on the mental arithmetic task tryptophan (van Veen et al., 2009), further research could estab- 1836
1771 itself has been measured; this did not indicate a significant corre- lish if SSRI’s can attenuate the HPA axis response to the TSST. As 1837
1772 lation between the lowest number reached and salivary cortisol in serotonin can act directly on the adrenal gland (Dinan, 1996), sero- 1838
1773 healthy volunteers (Simeon et al., 2007b). It is possible that per- tonin may play a role in HPA axis responses to the TSST. However, 1839
1774 formance on the maths tasks may affect other psychophysiological research using simulated public speaking has not found an effect 1840
1775 factors; given the transient effect of TSST stress on heart rate in on anxiety of tryptophan depletion, a method which reduces avail- 1841
1776 particular, such a method could be useful for assessing if heart able tryptophan (a serotonin precursor) by administering amino 1842
1777 rate changes are associated with performance on the maths task. acids which compete for access through the blood–brain barrier 1843
1778 Quality of performance on the speech task may be more difficult (Monteiro-dos-Santos et al., 2000; Shansis et al., 2000). A problem 1844
1779 to assess reliably than mathematical performance, although future with measuring tryptophan alone when studying serotonin effects 1845
1780 research could use a method such as the consensual assessment is that the large majority of tryptophan is catabolised along the 1846
1781 technique (Amabile, 1982) with experienced judges. Furthermore, kynurenine pathway without being converted to serotonin, and this 1847
1782 non-verbal behaviour during the TSST has been analysed using an alternative metabolic pathway also generates neuroactive metabo- 1848
1783 ethological scoring system developed by Troisi (1999); assertive lites (Bender, 1986; Van Donkelaar et al., 2011); measurements of 1849
1784 behaviours were associated with higher cortisol before and lower tryptophan/kynurenine ratios and downstream metabolites (e.g. 1850
1785 cortisol after the speech task, while submissive behaviours were kynurenic acid) may thus be useful. Serotonin effects may be mod- 1851
1786 associated with lower noradrenaline throughout the procedure ulated by individual differences at a genetic level; those with the 1852
1787 (Makatsori et al., 2004). Research using the same ethological scor- short/short genotype of the serotonin transporter gene have the 1853
1788 ing system has revealed that displacement behaviours (activities strongest cortisol response to the TSST (Gotlib et al., 2008; Way 1854
1789 such as face scratching or lip biting) are associated with reduced and Taylor, 2010) and clearer reduction by tryptophan adminis- 1855
1790 stress, but only in males (Mohiyeddini et al., 2013a), that displace- tration in HPA axis response to the TSST (Cerit et al., 2013), as 1856
1791 ment behaviour in men can mediate the relationship between state well as higher serum IL-6 and IL-10 at baseline and during stressor 1857
1792 anxiety and stress (Mohiyeddini and Semple, 2013), and that higher (Fredericks et al., 2010). Micro RNAs (mi-RNAs) are a potential ther- 1858
1793 levels of displacement behaviour can actually increase stress in apeutic target for the treatment of anxiety and depression effectors 1859
1794 females with high public self-consciousness (Mohiyeddini et al., (O’Connor et al., 2011); preclinical research has indicated that both 1860
1795 2013b). The lack of measurement of performance and behaviour on acute and chronic stress can produce region-specific changes in 1861
1796 the speech and mental arithmetic tasks during most TSST research miRNA levels (Meerson et al., 2010; Rinaldi et al., 2010). Genetic 1862
1797 ignores a large potential source of individual variability. research employing miRNAs combined with the TSST may give 1863
1798 More work needs to be conducted on modified versions of the insight into genetic factors underpinning sustained response to 1864
1799 TSST. Direct comparison of different versions of the TSST (e.g. TSST acute psychosocial stress. Early-life stress may be crucial in this 1865
1800 and TSST-M) within a single study would be useful in evaluating research area, not only because it can predispose individual to 1866
1801 the key aspects of the test that induce different psychological and stress-related disorders, but also because early-life stress has been 1867
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Table 3
Comparison of different methods of measuring stress/HPA axis responses in humans.
Method Description Associated effects Advantages Disadvantages
Trier social stress test Participants perform a public ↑ HPA axis activity Induces reliable, moderate Labour intensive
speech task and a mental ↑ Pro-inflammatory increase of HPA axis HPA axis habituates to
arithmetic task in front of an response activity current methods of
unresponsive audience ↑ Cardiovascular arousal Psychosocial nature allows repeated exposure
↑ Sympathetic-adrenal- for flexibility in design (e.g.
medullary system activity modifications such as
↑ Subjective stress positive versus negative
Variable effects on feedback)
cognitive performance
More research required on
gastrointestinal effects
Dexamethasone 1 mg of dexamethasone is ↓ Cortisol secretion Useful biomarker for Pharmacological

suppression test administered at night and ↑ Catecholamines (in melancholic episodes intervention
cortisol examined during the depression) Useful for assessing clinical Requires administration of
following day DEX/CRH: ↓ recovery dexamethasone and
Pro-inflammatory response within-participant assessment on different
Low dose: Lower HPA axis days
response in depression
with childhood trauma and
older trauma survivors
with PTSD
CO2 challenge Participants take maximal vital ↑ Plasma/serum cortisol Only one experimenter Inconsistent HPA axis
capacity inhalation of carbon ↑ Systolic BP required effects
dioxide-enriched air ↓ Heart rate Useful for panic disorder Need to exclude vulnerable
↑ Subjective anxiety research participants (e.g. those
with cardiovascular or
respiratory disorders)
Cold pressor test Participants immerse their ↑ HPA axis activity (smaller Only one experimenter HPA axis activation smaller
hand in ice-cold water than TSST) required than TSST
↓ Pro-inflammatory A social-evaluative Can be painful for
response element can be added participants
↑ Subjective stress
Cortisol awakening Samples collected to measure ↑ HPA axis activity Established as suitable for Reliance on participant
response HPA axis response to ↑ sIga study in field settings compliance in collecting
awakening in the morning ↑ Cardiovascular activity In non-clinical samples, samples if not conducted in
this response may nearly sleep laboratory
always be present
Cognitive tasks A variety of cognitive tasks are Variable, depending on Only one experimenter Unlikely to induce HPA axis
used to induce performance tasks employed required effects as large as those
stress, such as multitasking Cognitive performance induced by the TSST
frameworks or Stroop test measures intrinsic to task
Flexibility in altering stress
intensity
Noise Exposure to loud, unpleasant ↑ sAA Established as suitable for Unlikely to induce HPA axis
sound; can be manipulated in ↑ Noradrenaline study in field settings or subjective effects as
the laboratory or assessed in ↑ Heart rate variability consistently as the TSST
field setting
Mannheim Requires mathematical ↑ HPA axis activity Cognitive performance Less established than older
multicomponent performance under conditions ↑ Cardiovascular arousal measure intrinsic to task measures; further research
stress test of noise, imagery-based ↑ Subjective stress Flexibility in altering stress required to ascertain
negative emotional induction intensity effects
and threat of reduced payment Care needs to taken not to
if performance is poor confound stress with other
states induced by
emotional induction
1868 shown to interact with the short allele of the 5-HTTLPR in TSST effects on multiple biomarkers (see Fig. 3) and other measures 1878
1869 response in young adults (Mueller et al., 2011). have their own advantages, such as consistently responsiveness to 1879
repeated exposure to the TSST or the ability to measure continu- 1880
1870 7.3. Summary and conclusions ously during the mental arithmetic and speech tasks (see Table 1). 1881
The TSST also consistently induces subjective stress, although this 1882
1871 The TSST has become one of the most widely used means of will not necessarily be correlated with physiological outcomes, and 1883
1872 experimentally inducing acute psychosocial stress. Salivary corti- further work remains to be done on the cognitive effects of the 1884
1873 sol is a particularly useful marker of the stress response using this TSST. Given the relative advantages and disadvantages between 1885
1874 method, due to extensive evidence for its response to the TSST, measures, the possibility of interactions between them and the 1886
1875 the fact that as a marker of HPA axis activity it is selectively acti- likelihood that the timing of their effects will differ, it is impor- 1887
1876 vated by stress, rather than arousal in general, as well as the ease of tant to collect multiple biomarker outputs, as well as subjective 1888
1877 collection of saliva compared to blood. However, the TSST induces measures. 1889
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Fig. 3. Psychophysiological effects of the TSST. The TSST increases ACTH (e.g. Buske-Kirschbaum et al., 2007; Munro et al., 2005) and salivary, serum, and plasma cortisol
(e.g. Gaab et al., 2002; Kirschbaum et al., 1993, 1999), as well as DHEA and DHEA-S (Lennartsson et al., 2012b). At a subjective and behavioural level, the TSST induces
heightened subjective stress (e.g. Buske-Kirschbaum et al., 2002b; Sugaya et al., 2012), and can alter memory performance, although this latter effect can be moderated
by stimulus valence (e.g. Domes et al., 2004; Jelici et al., 2004). Complex cognition has been shown to be moderated by panel behaviour (e.g. Akinola and Mendes, 2008;
Kassam et al., 2009). The variable effects of the TSST on cognition suggest that further research using the TSST may provide insight into the complex relationship between
acute stress and cognition. The TSST increases heart rate (e.g. Jezova et al., 2004; Rimmele et al., 2007, 2009) and systolic blood pressure (e.g. Gerra et al., 2001; Jezova
et al., 2004), although variable results have been observed for heart rate variability (e.g. Lackschewitz et al., 2008; Rohleder et al., 2006). The TSST also increases adrenaline
(Gold et al., 2004; Jezova et al., 2004), noradrenaline (Schommer et al., 2003), salivary ␣-amylase (Gordis et al., 2006; Het et al., 2009) and galvanic skin response (Jezova
et al., 2004; Rohrmann et al., 1999). The HPA axis effects of the TSST can in turn lead to a heightened pro-inflammatory response, visible in the activity of cytokines such
as IL-6 (e.g. Slavich et al., 2010; von Känel et al., 2006), IL-2 (Bellingrath et al., 2010) and IL-1␤ (Yamakawa et al., 2009). There is preliminary evidence to suggest that this
stress response may also alter gastrointestinal activity, as ghrelin response has been altered in bulimia nervosa (Monteleone et al., 2012) and HPA axis responses have been
altered in irritable bowel syndrome (Kennedy et al., 2013; Suárez-Hitz et al., 2012). However, further research on the effects of the TSST on the brain–gut axis is required.
CNS, central nervous system; HRV, heart rate variability; HPA, hypothalamic-pituitary-adrenal; ACTH, adrenocorticotropic hormone; DHEA, dehydroepiandrosterone; SAM,
sympathetic-adrenal-medullary; sAA, saliva ␣-amylase; GSR, galvanic skin response.
1890 Anxiety disorders may moderate TSST effects, although this can consistently high HPA axis responses in a majority of participants. 1905
1891 vary depending on the specific anxiety disorder. The research on Grouped assessment and the use of virtual committees may reduce 1906
1892 TSST effects in depression is equivocal, perhaps due to age differ- the time commitment of confederates. The current evidence sug- 1907
1893 ences between samples in different studies. There is preliminary gests that while grouped assessment is successful in inducing 1908
1894 evidence that psychological and pharmacological therapies can stress, virtual committees may need further development before 1909
1895 alter stress responses to the TSST, although HPA axis activity should they can be treated as being as reliable as live committees. Such 1910
1896 be investigated further in this area. Genetic research as well as methods could be very useful in using the TSST to further the study 1911
1897 studies investigating tryptophan loading and SSRI use suggest that of acute stress within cognitive neuroscience. In addition to the 1912
1898 serotonin may play a role in the modulation of stress by individual TSST, a number of new paradigms are emerging which combine 1913
1899 differences and in stress-related disorders. different types of stressor in order to induce a psychophysiologi- 1914
1900 Although the “classic” TSST involves testing adult participants cal stress response, such as the Maastricht Acute Stress Test and the 1915
1901 individually using a live committee, modifications are frequently Mannheim Multicomponent Stress Test; future research will estab- 1916
1902 made to the TSST. Control versions of the TSST allow for a more com- lish the usefulness of these new methodologies in furthering the 1917
1903 plete assessment of psychosocial stress effects, although repeated study of acute stress. Until they are adequately validated, the TSST 1918
1904 measures versions may require further modification to induce remains one of the most important tools available to researchers 1919
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1920 in this area and its continued use in conjunction with a more con- Bender, D.A., 1986. The relative importance of dietary tryptophan and performed 1997
1921 sidered selection of biomarkers from those evaluated above will be nicotinic acid and nicotinamide as precursors of nicotinamide nucleotide coen- 1998
zymes. In: Bender, D.A., Joseph, M.H., Kochen, W., Steinhart, H.W. (Eds.), Progress 1999
1922 key to further advances. in Tryptophan and Serotonin Research. de Gruyter, Berlin, pp. 159–164. 2000
Bengtsson, J., Persson Waye, K., Kjellberg, A., 2004. Evaluations of effects due to 2001
low-frequency noise in a low demanding work situation. J. Sound Vibrat. 278, 2002
1923 Acknowledgements 83–99. 2003
Bhagwagar, Z., Hafizi, S., Cowen, P.J., 2003. Increase in concentration of waking 2004
1924 The Alimentary Pharmabiotic Centre is a research centre funded salivary cortisol in recovered patients with depression. Am. J. Psychiatry 160, 2005
1890–1891. 2006
1925 by Science Foundation Ireland (SFI), through the Irish Govern- Bhagwagar, Z., Hafizi, S., Cowen, P.J., 2005. Increased salivary cortisol after waking 2007
1926 ment’s National Development Plan (NDP). The authors and their in depression. Psychopharmacol. 182, 54–57. 2008
1927 work were supported by SFI (Grant Nos. 12/RC/2273, 02/CE/B124 Bijkerk, C.J., de Wit, N.J., Muris, J.W.M., Jones, R.H., Knottnerus, J.A., Hoes, A.W., 2003. 2009
Outcome measures in irritable bowel syndrome: comparison of psychometric 2010
1928 and 07/CE/B1368). G.C., J.F.C. and T.D. are also funded by the Irish
and methodological characteristics. Am. J. Gastroenterol. 98, 122–127. 2011
1929 Health Research Board (HRB) Health Research Awards (Grant No. Bishop, N.C., Gleeson, M., 2009. Acute and chronic effects of exercise on markers of 2012
1930 HRA POR/2011/23). mucosal immunity. Front. Biosci. 14, 4444–4456. 2013
Blair, J., Lancaster, G., Titman, A., Peak, M., Newlands, P., Collingwood, C., Chesters, 2014
C., Moorcroft, T., Wallin, N., Hawcutt, D., Gardner, C., Didi, M., Lacy, D., Couriel, 2015
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ARTICLE IN PRESS

Neuroscience and Biobehavioral Reviews xxx (2013) xxx–xxx

Contents lists available at ScienceDirect

Neuroscience and Biobehavioral Reviews

2 Biological and psychological markers of stress in humans:

0149-7634/$ – see front matter © 2013 Published by Elsevier Ltd.

3.1.2. Immune system measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00

important for responding to threatening situations, chronic stress is 61

can induce chronic stimulation of the HPA axis, leading to depres- 63

77 (Buynitsky and Mostofsky, 2009) and preclinical research has pro-

79 such as neurotransmitters (e.g. Browne et al., 2011; Cryan et al.,

alocorticoid receptors as well as glucocorticoid receptors, and the 149

role in mediating glucocorticoid feedback inhibition (Pariante and 151

127 well as its psychological effects (cognitive performance and subjec-

241 stressor (Izawa et al., 2013b). Lipopolysaccharide (LPS)-stimulated

310 2.1.5. Brain–gut axis effects

397 pictures (Buchanan and Tranel, 2008). TSST-induced stress led to

453 Bos et al., 2009), as well as a measure of risk-taking behaviour in

455 and Mendes, 2008; Kassam et al., 2009) used a modiﬁcation of

555 and Lewis, 2003). Consequently, every effort must be made to

stressful situations associated with factors such as unpredictabil- 629

Biomarker Non-invasive Can be measured Speciﬁcally Similar results Consistently

660 without interrupting the psychosocial stressor), although other fac-

tasks in response to increasing stress (e.g. Fisher, 1986; Matthews 719

exposing participants to the stressful speech task. 816

One explanation for gender moderating either cortisol effects 818

interacting with TSST effects (Kudielka et al., 2007). Women in 820

787 istics associated with Trier stress (e.g. novelty, unpredictability) to

878 2010). Research using the mental arithmetic component of the

905 for noradrenaline: carriers of a functional deletion variant of the

responses may have a role in the pathophysiology of depression 1071

that the manifestation of HPA axis dysfunction in depression may 1086

1037 TSST include genetic factors underpinning glucocorticoid and min-

1039 a review of corticoid receptor genetics and stress), as well as the

be necessary to show if psychophysiological responses to acute 1199

1150 than controls, although these effects were non-signiﬁcant (Dorn

1154 vosa (Monteleone et al., 2012), although stress-induced changes in

to an active control group who received an intervention which 1231

to mindfulness – MBSR did not have differing effects on subjective 1233

efﬁcacy in normalising the stress response. There is also emerg- 1307

1248 tigated the effects of pharmacological agents under conditions of

1251 can reduce anxiety at pre-stress (Graeff et al., 2003). Pre-treatment

this stressor. Conversely, a minority of participants (16%) show 1336

remained relatively stable. The lack of habituation in heart rate 1350

NBR 1866 1–31

ipants). In a control condition, participants read a scientiﬁc text 1434

1494 committee. However, such a methodology may be less stressful

1519 6.6. Hybrid versions of the TSST

1521 with dexamethasone taken at bedtime and exposure to the TSST

1643 patients (Schuld et al., 2001).

Many studies use cognitive tasks to assess the psychophysiolog- 1705

tests combining public speaking with a cognitive task (including 1724

Method Description Associated effects Advantages Disadvantages

Dexamethasone 1 mg of dexamethasone is ↓ Cortisol secretion Useful biomarker for Pharmacological

repeated exposure to the TSST or the ability to measure continu- 1880

1967 1229–1239. Psychoneuroendocrinology 37, 1810–1821. 2053

1988 3, 352. response correspond with physiological responses? Psychoneuroendocrinology 2074

1996 403–409. macological implications. Pharmacol. Ther. 130, 226–238. 2082

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