Dear reader of ADxS.org, please excuse the disruption.

ADxS.org needs about $63500 in 2024. In 2023 we received donations of about $ 32200. Unfortunately, 99.8% of our readers do not donate. If everyone who reads this request makes a small contribution, our fundraising campaign for 2024 would be over after a few days. This donation request is displayed 23,000 times a week, but only 75 people donate. If you find ADxS.org useful, please take a minute and support ADxS.org with your donation. Thank you!

Since 01.06.2021 ADxS.org is supported by the non-profit ADxS e.V..

$18094 of $63500 - as of 2024-04-30
28%
Header Image
Cortisol and stress axis changes in other disorders

Sitemap

Cortisol and stress axis changes in other disorders

The cortisol responses to acute stress show a rough pattern in different disorders: mental disorders with internalizing symptoms predominantly show an excessive cortisol response to acute stress, while disorders with externalizing symptoms tend to have a flattened cortisol stress response.

1. Early childhood stress

In those affected by early childhood stress, the dexamethasone test showed an excessive cortisol response.1

People affected by early childhood stress generally showed increased levels of inflammatory biomarkers (inflammation values) due to the lack of cortisol response.23

1.1. Premature births

Preterm infants - and here even more so girls - had a higher cortisol level on waking, a flatter CAR and an excessive cortisol response to the TSST-C as a stressor compared to full-term infants. Preterm infants also had more emotional problems and poorer memory performance. The authors conclude that early childhood stress alters the response values of the HPA axis and thus causes susceptibility to stress.4

1.2. Anxiety / stress of the mother during pregnancy

The mother’s level of anxiety during pregnancy correlated with the intensity of the infant’s stress response: the babies’ cortisol response was elevated 5 weeks after birth, but had leveled off by 8 weeks and 12 months. The correlation with the mothers’ cortisol levels was comparatively lower.5

The functions of the PFC are divided hemispherically. The right side of the PFC is responsible for controlling stress and negative emotions, while the left side is responsible for controlling positive emotions. If the EEG activity of the right hemisphere is particularly strong, this causes increased anxiety and leads to particularly defensive behavior. In these individuals, basal blood cortisol levels and cerebral CRH levels are significantly elevated. Cortisol responses to acute stressors are also significantly elevated.6

1.3. Attachment problems

In 78 young adult women, attachment problems correlated with a higher cortisol response to the TSST-G as a stressor, regardless of age, smoking status, menstrual phase and body mass index. An insecure attachment style (high insecurity and high attachment seeking) caused a higher cortisol reactivity than an avoidant (high insecurity and low attachment seeking) or secure attachment style. The time of the cortisol peak or the cortisol decrease after the stress did not correlate with an attachment style.7

2. Depression

Like ADHD-HI and ADHD-I, depression has two different manifestations, which also differ in terms of the cortisol stress response.

Melancholic (endogenous) and psychotic depression are characterized by an excessive cortisol stress response (like ADHD-I). Atypical depression and bipolar depression (bipolar disorder) are characterized by a flattened cortisol stress response (like ADHD-HI).
More on this at Melancholic and atypical depression

In depression, the proinflammatory cytokines

  • Tumor necrosis factor
  • Interleukin 1β (IL-1β)
  • Interleukin IL-6
    is increased, as is the protein
  • C-reactive protein (CRP)8

In depression, the glucocorticoid receptor appears to be endowed with reduced sensitivity, whereas in PTSD the glucocorticoid receptor shows increased sensitivity. In mice, an HDAC6 inhibitor normalized glucocorticoid receptor sensitivity and social behavior without altering the glucocorticoid response to the DEX/CRH test.9

3. Dysthymia

In children with dysthymia - in contrast to depression - a reduced basal cortisol level was found.10

4. Premenstrual dysphoric disorder (PMD)

In mild depression in the period before menstruation, a flattened cortisol response to stress was observed.11 Only during the luteal phase of menstruation (from menstruation to ovulation) is the sensitivity to benzodiazepines, ethanol (alcohol) and GABA steroids reduced in PMD, but not in the follicular phase between ovulation and menstruation, which indicates a temporary receptor downregulation.12

5. Burnout

In burnout, an exaggerated suppression of cortisol was observed on the low-dose dexamethasone test (0.5 mg instead of 1 mg DEX).13

6. Bipolar disorder / bipolar depression

For bipolar depression, the studies predominantly show a flattened cortisol stress response, otherwise a normal cortisol stress response. This is consistent with the distribution in ADHD-HI, where a flattened cortisol stress response also predominates, but normal cortisol stress responses were also found. In addition, there appears to be an excessive amylase stress response, which suggests involvement of the autonomic nervous system in bipolar disorder.

Studies on the cortisol stress response in bipolar depression

In type 1 bipolar depression, a flattened cortisol and elevated amylase stress response was found, which correlated with antipsychotic medication.14
From this, the authors conclude that the changes in stress responses are a consequence of the medication rather than a characteristic of the disease itself.

An excessive amylase response was also found in another study in bipolar women and men.15

In our opinion, the fact that the unaffected twins of the test subjects showed normal stress responses suggests that this is a consequence of the illness and not a genetic disposition. This is further supported by the fact that the children of parents affected by bipolar do not show a different cortisol stress response than children of healthy parents.16
In our opinion, the fact that an excessive cortisol stress response is usually observed in unipolar psychotic depression could indicate that this is a consequence of the illness and not a consequence of the medication. If antipsychotic medication caused a flattened cortisol response, this would also be found to be typical in psychotic unipolar depression.

Another study found an increased high-frequency heart rate variability (HF-HRV) as a stress response in bipolar patients in addition to a flattened cortisol stress response, while the HF-HRV as well as the cortisol level were reduced in the resting state.17

Unlike non-affected people, bipolar sufferers showed a flattened cortisol response to tryptophan administration.18

In other studies, a normal cortisol stress response was found in bipolar.1915

The cortisol level on awakening and the cortisol awakening response were also normal.19

5 studies on a total of 120 bipolar patients found around 80 % nonsuppression. With regard to pure mania, in 15 studies with a total of around 330 test subjects, around half of those affected by mania showed suppression, while the other half showed nonsuppression on the dexamethasone test. 20
An excessive cortisol response (nonsupression) to the dexamethasone/CRH test was found in both remitted and non-remitted bipolar patients.21

It is possible that the cortisol response changes depending on the phase of the illness. In an older long-term study, a cortisol nonsupression to the dexamethasone test was found in half of the bipolar patients during the depressive phases, but in none of the bipolar patients in a euthymic (balanced) or manic phase.22

Bipolar depressives (depression with manic phases) have a higher risk of depression than unipolar depressives (depression without manic phases):23

  • No deviations in the basal cortisol values
    • Cortisol stress responses were unfortunately not investigated
  • CAR cortisol increase / cortisol decrease over the day increased in men, not in women
  • Deviations in the C-reactive protein
  • 8 % (men: 48 % instead of 40 %) to 10 % (women: 46 % instead of 36 %) more active smokers
  • Slightly lower alcohol consumption
  • Slightly increased physical activity
  • Slightly increased BMI
  • Reduced sleep
  • Inflammation values
    • For men
      • Inflammation values increased (not significant)
      • Increased use of anti-inflammatory medication (not significant)
    • For women
      • Inflammation values unchanged
      • Reduced use of anti-inflammatory medication (not significant)

Treatment of bipolar and schizophrenia patients with the glucocorticoid antagonist mifepristone initially led to a considerable increase in cortisol levels in the first 7 days and to a considerable drop in cortisol levels from the 21st day onwards.24

In bipolar 1, an excessive ACTH response to CRH (in lithium-treated, mood-balanced patients without acute symptoms) could predict the likelihood of a (hypo)manic phase in the following 6 months.25

Acute tryptophan depletion (resulting in serotonin deficiency) in lifelong symptom-free direct relatives of bipolar 1 and bipolar 2 sufferers and in controls without bipolar relatives showed26

  • A decrease in cortisol and an improvement in mood in bipolar 2 relatives
  • In bipolar 1 relatives and controls a decrease in cortisol and a deterioration in mood
  • Increased manic symptoms in lithium-treated manic patients
  • No changes were observed in bipolar sufferers who had been symptom-free for 1 to 15 years

7. Mania

In mania, the cortisol response of the HPA axis to dexamethasone generally appears to be increased, as is the ACTH response to CRH. in one study, cortisol levels had normalized 6 months after the mania symptoms had subsided, but ACTH levels had not.27

8. Traumas

Traumatic childhood experiences correlate with a flattened cortisol response to stress.28

In adults with post-traumatic stress disorder, the corticoid receptors are hypersensitive. This is accompanied by reduced cortisol levels in the blood.29

In trauma, exaggerated suppression of cortisol on the low-dose dexamethasone test (0.5 mg rather than 1 mg DEX) has been observed, e.g. in adolescents exposed to earthquake-related trauma,30 women with childhood sexual abuse31 and in women with childhood sexual abuse and chronic pelvic pain,32 although this could also be the result of reported decreased adrenocortical responsiveness.

9. PTSD - Post-traumatic stress disorder

In PTSD, an increase in noradrenaline in the spinal fluid correlates with the severity of the symptoms.33

In PTSD, a reduced basal cortisol level, an increased number of lymphatic glucocorticoid receptors, an increased cortisol suppression to dexamethasone and an increased release of ACTH to metapyrone were found.343536
In PTSD, basal CRH levels continued to be elevated without CRH correlating directly with PTSD symptoms. In contrast, basal cortisol levels were reduced and the reduction correlated significantly with PTSD symptoms. 37

Most studies have found an increased cortisol response to acute stress in PTSD, with dexamethasone leading to increased cortisol suppression, suggesting that the cortisol response to ACTH is enhanced.3839

In another small study of (only 18) women, a flattened cortisol response was found in PTSD and no change in the ACTH response. Furthermore, the ACTH and cortisol response to dexamethasone was flattened.40

The majority of the studies are consistent with other findings that PTSD is primarily associated with internalizing symptoms and hardly with externalizing symptoms.41 The small second study contradicts this.

In contrast, the results on basal cortisol levels in PTSD are contradictory (not increased or decreased).42

The contradictory results could be interpreted to mean that different stress phenotypes also occur in PTSD.

In a stress test on rats, changes in the glucocorticoid/mineralocorticoid ratio were found that could explain the changes in PTSD.43

In depression, the glucocorticoid receptor appears to be endowed with reduced sensitivity, whereas in PTSD the glucocorticoid receptor shows increased sensitivity. In mice, an HDAC6 inhibitor normalized glucocorticoid receptor sensitivity and social behavior without altering the glucocorticoid response to the DEX/CRH test.9

10. Borderline

In borderline sufferers without comorbid PTSD, the DST showed an increased ACTH response, in borderline sufferers with comorbid PTSD a significantly weakened ACTH response.44

11. Anxiety disorders

Anxiety disorders correlate with increased morning (CAR) or serum cortisol levels.4546

A meta-analysis of 732 adults with acute (partly social) anxiety disorder showed a reduced cortisol response to acute stress in women and an increased cortisol response in men.47

People with social anxiety disorder who had suffered early maltreatment showed significantly higher cortisol responses to the TSST as a psychosocial stressor than people with social anxiety disorder without early maltreatment, than PTSD sufferers without early maltreatment and than non-affected people.48

12. Panic disorders

In panic disorders, the cortisol response of the HPA axis to dexamethasone is increased, as is the ACTH response to CRH.49

13. Repressors

Repression is a coping style characterized by low anxiety and a high need to defend oneself. This could be associated with externalizing behaviour. Women with a high repressor score were significantly more likely to show a flattened cortisol stress response and lower subjective stress perception on the TSST.50

14. Psychopathy

ADHD-affected children showed a flattened cortisol stress response to the TSST the more they showed psychopathic traits (callous unemotional traits/CU traits) such as lack of empathy, coldness of feeling, etc.51

In a group of subjects with high CU trait values, resting cortisol levels were found to be greatly reduced.52

15. Schizophrenia

A flattened cortisol stress response was found in schizophrenia. The higher the anxiety in people with schizophrenia, the lower the cortisol stress response.19

The cortisol level on awakening and the cortisol awakening response were normal.19

16. Neurodermatitis and other inflammatory diseases

Atopic immune disorders (such as atopic dermatitis) could be due to an excessive immune response caused by low cortisol levels. Cortisol inhibits the inflammation promoted by CRH (first stage of the HPA axis) by means of inflammatory cytokines. If the release of cortisol (third stage of the HPA axis) is too low, inflammation is not sufficiently inhibited.53

Too little cortisol (hypocortisolism) causes inflammatory problems:54

  • Neurodermatitis
  • Fibromyalgia5556
  • Intestinal inflammatory disorders56
  • Asthma

A study on cortisol response to the TSST-C in children with atopic neurodermatitis showed significantly attenuated cortisol responses compared to a non-atopic control group. The reduced cortisol responses to the stressor could not be explained by corticosteroid medication or differences in personality variables. This confirms that atopic dermatitis is an inflammatory response.57

A study on cortisol response to the TSST-C in children with allergic asthma also showed significantly attenuated cortisol responses compared to a non-atopic control group. The reduced cortisol responses to the stressor could not be explained by corticosteroid medication or differences in personality variables.57

17. Chronic fatigue syndrome (CFS)

CFS is characterized by

  • Does not already exist for life
  • Lasting at least 6 months
  • States of exhaustion that cannot be explained medically in any other way,
    which are not the result of special stress
  • Is not reduced by rest
  • Causes substantial restriction of professional and social activities
  • In addition, at least 4 of the following symptoms are fulfilled:
    • Non-restorative sleep
    • Memory / concentration problems
    • Muscle pain (myalgia)
    • Joint pain (arthralgia)
    • Sore throat
    • Pressure-sensitive lymph nodes on the neck / under the armpits
    • Headache
    • Particularly intense and persistent fatigue after exertion

CFS, like other inflammatory disorders, often occurs as a result of severe viral infections, e.g. after Epstein-Barr or XMRV. It is suspected that these infections unbalance the immune system in conjunction with the stress response system that models it. Elevated levels of pro-inflammatory cytokines, e.g. IL-6 or TNF-alpha, have been found, indicating subtle chronic inflammatory processes. IL-6 triggers symptoms of fatigue.56

In CFS, the cortisol awakening response (CAR) (only in women) and the basal cortisol level are reduced.56 The CAR is particularly pronounced in early sexual abuse.56

One study found normal basal cortisol levels and cortisol awakening responses in CFS, but increased and prolonged cortisol suppression in response to a reduced dexamethasone dose of 0.5 mg.58 In the dexamethasone test, an administration of 1 mg DEX is usual.

In CFS, an increased sensitivity of the adrenal cortex to ACTH with a simultaneously limited cortisol response has been described.59

Fatigue could be explained by a central activation of pro-inflammatory cytokines. The following are mentioned:60

  • Interleukin 1ß (IL-1ß)
  • IL-6
  • IL-8
  • CD40L
  • IFN-alpha.

In addition

  • C-reactive protein (CRP)

be increased.

A reduction is reported by

  • IL-16
  • IL-17
  • VEGF.

As CFS is a neuroinflammatory disorder, the measurement of cytokines in the blood is not useful.

18. Chronic lower abdominal pain

Women with chronic lower abdominal pain exhibit changes in the HPA axis. They show a significantly reduced cortisol response to CRH test stimulation.61

19. Neurological diseases (e.g. multiple sclerosis)

In multiple sclerosis, the cortisol response of the HPA axis to dexamethasone is generally excessive, while the ACTH response to CRH is unchanged. In MS patients, too, some have a greatly increased cortisol response and others a flattened one.62

20. Dementia, Alzheimer’s disease

Daily cortisol levels appear to be significantly increased in dementia and Alzheimer’s disease.63

21. Obesity

Men with a high waist-to-hip ratio (WHR) tend to have an increased cortisol response to stress. Exposure to stress and increases in WHR are specifically associated with poorer performance on declarative memory tasks (spatial recognition memory and pair-associated learning).64

22. High blood pressure

Hypertension is associated with ADHD-HI, not ADHD-I. On this side, it is therefore assumed that high blood pressure is associated with a flattened cortisol response to acute stressors.
In ADHD-HI, it is assumed on this side that there is a lack of or an underfunction of the glucocorticoid receptors, which is why the HPA axis is not properly switched off.

Hypertension can be treated by mineralocorticoid antagonists,65 which indicates an imbalance of too many / too active mineralocorticoid receptors (MR) versus too few / too inactive GR.

23. Allergies

Cortisol activates the immune defense against foreign bodies (bacteria, parasites):54

  • Cortisol inhibits the promotion of inflammation triggered by CRH again (inhibition of pro-inflammatory cytokines)
  • Instead, cortisol promotes contra-inflammatory (anti-inflammatory) cytokines (T-helper type 2 cytokines, e.g. interleukin IL-4, IL-5, IL-6 and IL-10).
  • The TH-2 cytokines promoted by cortisol ward off extracellular pathogens (bacteria, parasites) and promote basophils, mast cells and eosinophils, which can promote allergies if excessive.
  • The change from TH1 inhibition to TH2 promotion triggered by cortisol is also known as the TH1/TH2 shift

Too much cortisol (hypercortisolism), as is typical in ADHD-I, is therefore conducive to allergies.54

“Allergic” asthma, on the other hand, seems to be more of an inflammatory reaction, which is a typical consequence of hypocortisolism, such as occurs in ADHD-HI.

24. Overtraining

When athletes are in a state of overtraining, the studies show in some cases

  • Increased basal cortisol levels and a reduced cortisol stress response to further physical stress
    and partly
  • Reduced basal cortisol levels and an increased cortisol stress response to further physical stress.66

These two response profiles could support this hypothesis of different stress phenotypes in humans. It would be compatible with this hypothesis that a flattened cortisol response in the overtraining state could be attributed to a

  • Reduced ACTH stimulation67
  • Reduced ACTH sensitivity of the adrenal cortex.68

The explanation with different stress phenotypes, as they are also known in healthy people and in some mental disorders (ADHD-I/ADHD-HI; melancholic/atypical depression), seems in any case more conclusive than the explanations of the flattened cortisol response to physical overload by means of69

  • Depletion of the adrenal cortex
  • Reversible adrenocortical insufficiency
  • Addisonoid overtraining
  • Stage of resistance according to Selye’s model
  • Non-specific stressors after physical training
    or
  • Increased cortisol elimination rate under stress

25. Learning disorders

Stress-related elevated cortisol levels make it more difficult for the hippocampus to process learned activities at night.70


  1. Carpenter, zitiert nach Egle, Joraschky, Lampe, Seiffge-Krenke, Cierpka (2016): Sexueller Missbrauch, Misshandlung, Vernachlässigung – Erkennung, Therapie und Prävention der Folgen früher Stresserfahrungen; 4. Aufl., Schattauer, S. 49

  2. Danese, Moffitt, Pariante, Ambler, Poulton, Caspi. Elevated inflammation levels in depressed adults with a history of childhood maltreatment. Arch Gen Psychiatry 2008; 65: 409–15.

  3. Danese A, Caspi A, Williams B, Ambler A, Sugden, Mika, Werts, Freeman, Pariante, Moffitt, Arseneault (2011): Biological embedding of stress through infl-mmation processes in childhood. Mol Psychiatry 2011; 16: 244–6.

  4. Quesada, Tristão, Pratesi, Wolf (2014): Hyper-responsiveness to acute stress, emotional problems and poorer memory in former preterm children. Stress. 2014 Sep;17(5):389-99. doi: 10.3109/10253890.2014.949667.

  5. Tollenaar, Beijers, Jansen, Riksen-Walraven, de Weerth (2011): Maternal prenatal stress and cortisol reactivity to stressors in human infants.Stress. 2011 Jan;14(1):53-65. doi: 10.3109/10253890.2010.499485.

  6. Steckler, Kalin, Reul (2005): Handbook of Stress and the Brain, Teil 1; Elsevier, Seite 811

  7. Smyth, Thorn, Oskis, Hucklebridge, Evans, Clow (2015): Anxious attachment style predicts an enhanced cortisol response to group psychosocial stress. Stress. 2015;18(2):143-8. doi: 10.3109/10253890.2015.1021676.

  8. Miller, Raison (2016): The role of inflammation in depression: from evolutionary imperative to modern treatment target. Nature Rev Immunol 2016; 16: 22-34

  9. McClung (2015): Glucocorticoid Receptor Function and Resilience: A Tale of Mice and Men, Biological Psychiatry, Volume 77, Issue 4, 2015, Pages 310-311, ISSN 0006-3223, https://doi.org/10.1016/j.biopsych.2014.11.009.

  10. Gispen-de Wied, Jansen, Wynne, Matthys, van der Gaag, Thijssen, van Engeland (1997): Differential Effects of Hydrocortisone and Dexamethasone on Cortisol Suppression in a Child Psychiatric Population; Psychoneuroendocrinology, April 1998, Volume 23, Issue 3, Pages 295–305, DOI: https://doi.org/10.1016/S0306-4530(97)00097-8

  11. Evans, Marneros (2007): Depressionen und bipolare Erkrankungen in der psychiatrischen und allgemeinärztlichen Praxis: ein Leitfaden, Seite 285

  12. Bäckstrom, Birzniece, Fernandez, Johansson, Kask, Lindblad, Lundgren, Hyberg, Ragagnin, Sundström-Poromaa, Strömberg, Turkman, Wang, von Boekhoven, van Wingen: Neuroactive Seorids: Effects on Cognitive Functions; in: Weizman (Herausgeber) (2008): Neuroactive Steroids in Brain Function, Behavior and Neuropsychiatric Disorders: Novel Strategies for Research and Treatment; Chapter 5, S 103 ff

  13. Pruessner, Hellhammer, Kirschbaum (1999): Burnout, Perceived Stress, and Cortisol Responses to Awakening; Psychosomatic Medicine: March/April 1999 – Volume 61 – Issue 2 – p 197-204

  14. Houtepen, Boks, Kahn, Joëls, Vinkers (2016): Antipsychotic use is associated with a blunted cortisol stress response: a study in euthymic bipolar disorder patients and their unaffected siblings. Eur Neuropsychopharmacol. 2015 Jan;25(1):77-84. doi: 10.1016/j.euroneuro.2014.10.005.

  15. Tanaka, Maruyama, Ishitobi, Kawano, Ando, Ikeda, Inoue, Imanaga, Okamoto, Kanehisa, Ninomiya, Tsuru, Akiyoshi (2013): Salivary alpha-amylase and cortisol responsiveness following electrically stimulated physical stress in bipolar disorder patients. Neuropsychiatr Dis Treat. 2013;9:1899-905. doi: 10.2147/NDT.S48722.

  16. Ellenbogen, Hodgins, Walker, Couture, Adam (2006): Daytime cortisol and stress reactivity in the offspring of parents with bipolar disorder. Psychoneuroendocrinology. 2006 Nov;31(10):1164-80.

  17. Casement, Goldstein, Gratzmiller, Franzen (2018): Social stress response in adolescents with bipolar disorder. Psychoneuroendocrinology. 2018 May;91:159-168. doi: 10.1016/j.psyneuen.2018.02.017.

  18. Nurnberger, Berrettini, Simmons-Alling, Lawrence, Brittain (1990): Blunted ACTH and cortisol response to afternoon tryptophan infusion in euthymic bipolar patients. Psychiatry Res. 1990 Jan;31(1):57-67.

  19. Girshkin, O’Reilly, Quidé, Teroganova, Rowland, Schofield, Green (2016): Diurnal cortisol variation and cortisol response to an MRI stressor in schizophrenia and bipolar disorder. Psychoneuroendocrinology. 2016 May;67:61-9. doi: 10.1016/j.psyneuen.2016.01.021.

  20. Cassidy, Ritchie, Carroll (1998): Plasma dexamethasone concentration and cortisol response during manic episodes. Biol Psychiatry. 1998 May 15;43(10):747-54.

  21. Watson, Gallagher, Ritchie, Ferrier, Young (2004): Hypothalamic-pituitary-adrenal axis function in patients with bipolar disorder. Br J Psychiatry. 2004 Jun;184:496-502. n = 81

  22. Maj, Ariano, Arena, Kemali (1984): Plasma cortisol, catecholamine and cyclic AMP levels, response to dexamethasone suppression test and platelet MAO activity in manic-depressive patients. A longitudinal study. Neuropsychobiology. 1984;11(3):168-73. n = 15

  23. Becking, Spijker, Hoencamp, Penninx, Schoevers, Boschloo (2015): Disturbances in Hypothalamic-Pituitary-Adrenal Axis and Immunological Activity Differentiating between Unipolar and Bipolar Depressive Episodes. PLoS One. 2015 Jul 21;10(7):e0133898. doi: 10.1371/journal.pone.0133898. eCollection 2015. n = 764

  24. Gallagher, Watson, Dye, Young, Ferrier (2008): Persistent effects of mifepristone (RU-486) on cortisol levels in bipolar disorder and schizophrenia. J Psychiatr Res. 2008 Oct;42(12):1037-41. doi: 10.1016/j.jpsychires.2007.12.005.

  25. Vieta, Martínez-De-Osaba, Colom, Martínez-Arán, Benabarre, Gastó (1999): Enhanced corticotropin response to corticotropin-releasing hormone as a predictor of mania in euthymic bipolar patients. Psychol Med. 1999 Jul;29(4):971-8.

  26. Sobczak, Honig, Nicolson, Riedel (2002): Effects of acute tryptophan depletion on mood and cortisol release in first-degree relatives of type I and type II bipolar patients and healthy matched controls. Neuropsychopharmacology. 2002 Nov;27(5):834-42.

  27. Schmider, Lammers, Gotthardt, Dettling, Holsboer, Heuser (1995): Combined dexamethasone/corticotropin-releasing hormone test in acute and remitted manic patients, in acute depression, and in normal controls. Biological Psychiatry 38: 797–802; Vorsicht, geringe Probandenzahl von n = 6

  28. Suzuki A1, Poon L2, Papadopoulos AS2, Kumari V3, Cleare (2014): Long term effects of childhood trauma on cortisol stress reactivity in adulthood and relationship to the occurrence of depression. Psychoneuroendocrinology. 2014 Dec;50:289-99. doi: 10.1016/j.psyneuen.2014.09.007. n = 70

  29. Rensing, Koch, Rippe, Rippe (2006): Mensch im Stress; Psyche, Körper Moleküle; Elsevier (jetzt Springer), Seite 312

  30. Goenjian, Yehuda, Pynoos, Steinberg, Tashjian, Yang, Najarian, Fairbanks (1996): Basal Cortisol, Dexamethasone Suppression of Cortisol, and MHPG in Adolescents After the 1988 Earthquake in Armenia. Am J Psychiatry 1996;153: 929–34.

  31. Stein, Yehuda, Koverola, Hanna (1997): Enhanced Dexamethasone Suppression of Plasma Cortisol in Adult Women Traumatized by Childhood Sexual Abuse, Biological Psychiatry, Volume 42, Issue 8, 1997, Pages 680-686, ISSN 0006-3223, https://doi.org/10.1016/S0006-3223(96)00489-1.

  32. Heim, Ehlert, Hanker, Hellhammer (1998): Abuse-related posttraumatic stress disorder and alterations of the hypothalamic-pituitary-adrenal axis in women with chronic pelvic pain. Psychosom Med 1998; 60: 309–18.

  33. Geracioti, Baker, Ekhator, West, Hill, Bruce, Schmidt, Rounds-Kugler, Yehuda, Keck, Kasckow (2001): CSF Norepinephrine Concentrations in Posttraumatic Stress Disorder; https://doi.org/10.1176/appi.ajp.158.8.1227

  34. Yehuda, Levengood, Schmeidler, Wilson, Guo, Gerber (1996): Increased pituitary activation following metyrapone administration in post-traumatic stress disorder, Psychoneuroendocrinology, Volume 21, Issue 1, 1996, Pages 1-16, ISSN 0306-4530, https://doi.org/10.1016/0306-4530(95)00055-0.

  35. Yehuda, Southwick, Krystal, Bremner, Charney, Mason (1993): Enhanced suppression of cortisol following dexamethasone administration in posttraumatic stress disorder. The American Journal of Psychiatry, 150(1), 83-86. http://dx.doi.org/10.1176/ajp.150.1.83, n = 33

  36. Yehuda, Boisoneau, Lowy, Giller (1995): Dose-Response Changes in Plasma Cortisol and Lymphocyte Glucocorticoid Receptors Following Dexamethasone Administration in Combat Veterans With and Without Posttraumatic Stress Disorder. Arch Gen Psychiatry. 1995;52(7):583–593. doi:10.1001/archpsyc.1995.03950190065010; n = 40

  37. Baker, West, Nicholson, Ekhator, Kasckow, Hill, Bruce, Orth, Geracioti (1999): Serial CSF Corticotropin-Releasing Hormone Levels and Adrenocortical Activity in Combat Veterans With Posttraumatic Stress Disorder; American Journal of Psychiatry 1999 156:4, 585-588, n = 23

  38. de Kloet, Vermetten, Geuze, Kavelaars, Heijnen, Westenberg (2006): Assessment of HPA-axis function in posttraumatic stress disorder: pharmacological and non-pharmacological challenge tests, a review. J Psychiatr Res. 2006 Sep;40(6):550-67. Metaanayse

  39. Yehuda, Giller, Southwick, Lowy, Mason (1991): Hypothalamic-pituitary-adrenal dysfunction in posttraumatic stress disorder. Biol Psychiatry. 1991 Nov 15;30(10):1031-48.

  40. Wingenfeld (2003): EINE UNTERSUCHUNG DER ENDOKRINEN UND PSYCHOLOGISCHEN VERÄNDERUNGEN BEI PTSD UND STRESSABHÄNGIGEN KÖRPERLICHEN BESCHWERDEN, Dissertation; Betreuer: Hellhammer, Heim, Seite 128; n = 18

  41. Hiller, Creswell, Meiser-Stedman, Lobo, Cowdrey, Lyttle, Ehlers, Halligan (2018): A Longitudinal Examination of the Relationship between Trauma-Related Cognitive Factors and Internalising and Externalising Psychopathology in Physically Injured Children. J Abnorm Child Psychol. 2018 Sep 28. doi: 10.1007/s10802-018-0477-8.

  42. Meewisse, Reitsma, de Vries, Gersons, Olff (2007): Cortisol and post-traumatic stress disorder in adults. Systematic review and meta-analysis. The British Journal of Psychiatry Oct 2007, 191 (5) 387-392; DOI: 10.1192/bjp.bp.106.024877, Metaanalyse von 37 Studien mit n = 1628

  43. Liberzon, López, Flagel, Vázquez, Young (1999): Differential Regulation of Hippocampal Glucocorticoid Receptors mRNA and Fast Feedback: Relevance to Post-Traumatic Stress Disorder. Journal of Neuroendocrinology, 11(1), 11-17. http://dx.doi.org/10.1046/j.1365-2826.1999.00288.x

  44. Rinne, de Kloet, Wouters, Goekoop, DeRijk (2002): RH, van den Brink W. Hyperresponsiveness of hypothalamic-pituitary-adrenal axis to combined dexamethasone/corticotropin-releasing hormone challenge in female borderline personality disorder subjects with a history of sustained childhood abuse. Biol Psychiatry 2002; 52: 1102–12.

  45. Vreeburg, Zitman, van Pelt, DeRijk, Verhagen, van Dyck, Hoogendijk, Smit, Penninx (2010): Salivary cortisol levels in persons with and without different anxiety disorders. Psychosom Med 72:340–347

  46. Greaves-Lord, Ferdinand, Oldehinkel, Sondeijker, Ormel, Verhulst (2007): Higher cortisol awakening response in young adolescents with persistent anxiety problems. Acta Psychiatr Scand 116:137–144

  47. Zorn, Schür, Boks, Kahn, Joëls, Vinkers (2017): Cortisol stress reactivity across psychiatric disorders: A systematic review and meta-analysis; Psychoneuroendocrinology, 2017, Volume 77 , 25 – 36

  48. Elzinga, Spinhoven, Berretty, de Jong, Roelofs (2010): The role of childhood abuse in HPAaxis reactivity in Social Anxiety Disorder: a pilot study. Biol Psychol 2010; 83: 1–6.

  49. Schreiber, Lauer, Krumrey, Holsboer, Krieg (1996): Dysregulation of the hypothalamic-pituitary-adrenocortical system in panic disorder. Neuropsychopharmacology 15: 7–15

  50. Oskis, Smyth, Flynn, Clow (2018): Repressors exhibit lower cortisol reactivity to group psychosocial stress. Psychoneuroendocrinology. 2018 Dec 17;103:33-40. doi: 10.1016/j.psyneuen.2018.12.220.

  51. Stadler, Kroeger, Weyers, Grasmann, Horschinek, Freitag, Clement (2011): Cortisol reactivity in boys with attention-deficit/hyperactivity disorder and disruptive behavior problems: the impact of callous unemotional traits. Psychiatry Res 187:204–209, n = 36

  52. Loney, Butler, Lima, Counts, Eckel (2006): The relation between salivary cortisol, callous-unemotional traits, and conduct problems in an adolescent non-referred sample. J Child Psychol Psychiatry 47:30–36, N = 108

  53. Kirschbaum, Clemens (2001) Das Stresshormon Cortisol – Ein Bindeglied zwischen Psyche und Soma? In: Jahrbuch der Heinrich-Heine-Universität Düsseldorf 2001. Heinrich-Heine-Universität Düsseldorf, Düsseldorf, pp. 150-156. ISBN 3-9808514-0-0

  54. Egle, Joraschky, Lampe, Seiffge-Krenke, Cierpka (2016): Sexueller Missbrauch, Misshandlung, Vernachlässigung – Erkennung, Therapie und Prävention der Folgen früher Stresserfahrungen; 4. Aufl., Schattauer, S. 443, 444

  55. Heim, Miller: Depression, in: Ehlert, von Känel (2011): Psychoendokrinologie und Psychoimmunologie, Seiten 365-382

  56. Nater: Funktionelle somatische Beschwerden, in: Ehlert,von Känel (2011): Psychoendokrinologie und Psychoimmunologie, Seiten 219 – 229

  57. Buske-Kirschbaum A. (2009). Cortisol responses to stress in allergic children: interaction with the immune response. Neuroimmunomodulation;16(5):325-32

  58. Gaab, Hüster, Peisen, Engert, Schad, Schürmeyer, Ehlert (2002): Low-Dose Dexamethasone Suppression Test in Chronic Fatigue Syndrome and Health; Psychosomatic Medicine: March-April 2002 – Volume 64 – Issue 2 – p 311-318, n = 42

  59. Demitrack, Dale, Straus, Laue, Listwak, Kruesi, Chrousos, Gold (1991): Evidence for Impaired Activation of the Hypothalamic-Pituitary-Adrenal Axis in Patients with Chronic Fatigue Syndrome, The Journal of Clinical Endocrinology & Metabolism, Volume 73, Issue 6, 1 December 1991, Pages 1224–1234, https://doi.org/10.1210/jcem-73-6-1224, n = 102

  60. Bieger: ME/CFS – die unbekannte Krankheit, symptome.ch

  61. Heim, Newport, Bonsall, Miller, Nemeroff (2001): Altered pituitary-adrenal axis responses to provocative challenge tests in adult survivors of childhood abuse. Am J Psychiatry 2001; 158: 575–81.

  62. Grasser, Möller, Backmund, Yassouridis, Holsboer (1996): Heterogeneity of hypothalamic-pituitary-adrenal system response to a combined dexamethasone-CRH test in multiple sclerosis, Experimental and Clinical.Endocrinology and Diabetes 104: 31–37; n = 19

  63. Ferrari, Arcaini, Gornati, Pelanconi, Cravello, Fioravanti, Solerte, Magri (2000): Pineal and pituitary-adrenocortical function in physiological aging and in senile dementia. Exp Gerontol. 2000 Dec;35(9-10):1239-50.

  64. Lasikiewicz, Hendrickx, Talbot, Dye (2013): Exploring stress-induced cognitive impairment in middle aged, centrally obese adults. Stress. 2013 Jan;16(1):44-53. doi: 10.3109/10253890.2012.682109.

  65. Sica (2015): Mineralocorticoid Receptor Antagonists for Treatment of Hypertension and Heart Failure Methodist Debakey Cardiovasc J. 2015 Oct-Dec; 11(4): 235–239. doi: [10.14797/mdcj-11-4-235], PMCID: PMC4814010, PMID: 27057293

  66. Brechtel (1998): Das parasympathikotone Übertrainingssyndrom – Ein Modell zur Maladaption an Streß – Diagnostik und Pathophysiologie. Dissertation. Seite 199, mit weiteren Nachweisen

  67. Tharp (1975): The role of glucocorticoids in exercise. Med Sci Sports. 1975;7(1) 6-11. PMID: 1143055.

  68. Tharp, Buuck (1974): Adrenal adaptation to chronic exercise. Journal of Applied Physiology 1974 37:5, 720-722

  69. Brechtel (1998): Das parasympathikotone Übertrainingssyndrom – Ein Modell zur Maladaption an Streß – Diagnostik und Pathophysiologie. Dissertation. Seiten 200, 201, mit weiteren Nachweisen

  70. Dolfen, King, Schwabe, Swinnen, Albouy (2019): Glucocorticoid response to stress induction prior to learning is negatively related to subsequent motor memory consolidation. Neurobiol Learn Mem. 2019 Jan 10. pii: S1074-7427(19)30009-7. doi: 10.1016/j.nlm.2019.01.009.

Diese Seite wurde am 27.02.2024 zuletzt aktualisiert.