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Cortisol and stress axis changes in other disorders

Cortisol and stress axis changes in other disorders

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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 persons with ADHD, the dexamethasone test showed an excessive cortisol response.1

Due to the lack of cortisol response, people with ADHD generally showed increased levels of inflammatory biomarkers (inflammatory values).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 flattened out at 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 / ADHD-C on the one hand and ADHD-I on the other, depression has two different manifestations, which also differ on the basis 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 / ADHD-C).
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 / ADHD-C, 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 marker 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 twins of the test subjects who were not people with ADHD 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 people with ADHD 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 found in unipolar psychotic depression could speak in favor of this being 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 increased high-frequency heart rate variability (HF-HRV) as a stress response in addition to a flattened cortisol stress response in people with ADHD, while both HF-HRV and cortisol levels were reduced at rest.17

Unlike persons with ADHD, people with bipolar 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 persons with ADHD found around 80 % nonsuppression. With regard to pure mania, in 15 studies with a total of around 330 subjects, around half of the people with ADHD showed suppression and the other half nonsuppression on the dexamethasone test. 20
An excessive cortisol response (nonsupression) to the dexamethasone/CRH test was found in both remitted and non-remitted people with ADHD.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 people with ADHD 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 people with ADHD and schizophrenia with the glucocorticoid antagonist mifepristone initially led to a significant increase in cortisol levels in the first 7 days and to a significant drop in cortisol levels from day 21 onwards.24

In bipolar-1, an excessive ACTH response to CRH (in lithium-treated, mood-balanced persons with ADHD 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 people with ADHD and bipolar-2 and in controls without bipolar relatives showed26

  • A decrease in cortisol and an improvement in mood in bipolar-2 relatives
  • A decrease in cortisol and a deterioration in mood in bipolar-1 relatives and controls
  • Increased manic symptoms in lithium-treated manic patients
  • No changes were found in people with ADHD 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 may 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 barely associated 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 persons with ADHD without comorbid PTSD, the DST showed an increased ACTH response, while in borderline persons with comorbid PTSD, the ACTH response was significantly attenuated.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

Persons with ADHD who had suffered early maltreatment showed significantly higher cortisol responses to the TSST as a psychosocial stressor than people with ADHD 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

Children with ADHD 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. The more psychopathic they were.51

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

Callolus unemotional traits in ADHD correlated with higher HRV resting state and response scores. This could indicate comparatively less impaired self-regulatory ability in a reward-related context.53

Callolus unemotional traits (CU) play a role in both conduct disorder (CD) and oppositional defiant disorder (ODD).
Impulse control in CD and ODD symptoms depends on CU. With increased CU, CD correlated with a more cautious decision-making style, while ODD correlated with more efficient decision-making.54

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.1955

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 increment of the HPA axis) by means of inflammatory cytokines. If cortisol secretion (third increment of the HPA axis) is too low, inflammation is not sufficiently inhibited.56

Too little cortisol (hypocortisolism) causes inflammatory problems:57

  • Neurodermatitis
  • Fibromyalgia5859
  • Intestinal inflammatory disorders59
  • 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.60

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.60

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 consequence of severe viral infections, e.g. Epstein-Barr or XMRV. It is suspected that these cause the immune system to become unbalanced 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.59

In CFS, the cortisol awakening response (CAR) (only in women) and the basal cortisol level are reduced.59 The CAR is particularly pronounced in early sexual abuse.59

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.61 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.62

Fatigue could be explained by a central activation of pro-inflammatory cytokines. The following are mentioned:63

  • 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.64

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

In multiple sclerosis, the cortisol response of the HPA axis to dexamethasone is usually excessive, while the ACTH response to CRH is unchanged. In MS patients, too, some show a greatly increased cortisol response and others a flattened one.65

20. Dementia, Alzheimer’s disease

Daily cortisol levels appear to be significantly increased in dementia and Alzheimer’s disease.66

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).67

22. High blood pressure

Hypertension is associated with ADHD-HI and ADHD-C, not ADHD-I. We therefore suspect that hypertension is more likely to be associated with a flattened cortisol response to acute stressors.
In ADHD-HI and ADHD-C, we hypothesize that a reduced cortisol stress response causes insufficient deactivation of the HPA axis at the end of the stress response, so that the HPA axis remains persistently overactivated.

Hypertension can be treated by mineralocorticoid antagonists,68 which indicates an imbalance of too many / too active mineralocorticoid receptors (MR) versus too few / too inactive GR. This may also contribute to insufficient deactivation of the HPA axis, as cortisol preferentially binds to the 10-fold more cortisol-affine MR and, in the case of excess MPR, too little cortisol remains to bind sufficiently to the GR.
In SHR, the main model animal for ADHD-C, the highly selective glucocorticoid agonist dexamethasone normalizes the excessive blood pressure and reduces ADHD symptoms.

23. Allergies

Cortisol activates the immune defense against foreign bodies (bacteria, parasites):57

  • 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.57

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

24. Overtraining

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

  • 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.69

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 stimulation70
  • Reduced ACTH sensitivity of the adrenal cortex.71

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 of72

  • 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.73

26. Autism

In autism (ASD), there appears to be a more complex picture of the cortisol stress response.
Overall, ASD seems to correlate more with a flattened cortisol stress response. Differentially, stressors with a social evaluation threat appear to correlate with an underreaction, whereas stressors with unpleasant stimuli or relatively harmless social situations correlate with an overreaction of the HPA axis.74

Social interaction (e.g. TSST)

  • Adolescents with ASD (10 to 13 years) showed a significantly flattened cortisol stress response to the TSST75

  • High-functioning autism (HFA) correlated with

    • with a flattened cortisol stress response to the TSST76
    • with a normal high cortisol stress response

  • ASA correlated with a flattened cortisol stress response on the social stress-oriented TSST as well as on the friendly communication-oriented TSST-F (aka f-TSST), in which controls show no cortisol stress response77

  • in social interaction were shown by boys with ASD aged 8 to 12 years:78

    • Younger people showed 5.8 times more approach behavior and a lower cortisol stress response than older people
    • verbal contact correlated with higher cortisol response
    • Older people showed the highest stress reactivity

  • Exposure to social situations:79

    • ASS like controls: normal cortisol stress response
    • Controls showed habituation to the stressor, ASA maintained the cortisol increase as a stress response, with stronger individual differences
    • Age was a positive moderator for stress in the ASD group
    • IQ a negative moderator for the controls

  • Face-to-Face-Still-Face-Paradigm (FTFSF)80

    • FTFSF tests the internalization of social expectations in infants
      • Parent interacts with the child for 3 minutes
      • then the parent interrupts the social communication and shows an expressionless face for 2 to 3 minutes
      • it then continues the typical game for another 2 minutes
    • Infants aged 3 show
      • already show social expectations of their parents’ availability
      • reduce their positive behavior and increase their withdrawal during the parents’ silent face
      • show after-effects during the “reparation phase” of reunification
    • Preschool children showed
      • the typical reaction
      • simpler regulation strategies (self-soothing, approach search)
      • less complex strategies such as diverting attention or substitute play
      • The presence of the mother suppressed the cortisol stress response in children with ASD, while it was normally elevated in the absence of the mother
      • The cortisol stress response was synchronized with that of the interacting parent (mother and father)
        • another study found synchronous daytime cortisol levels, particularly in relation to the father81
      • for us, the values read like a flattened cortisol stress response in FTFS by both mother and father

  • Children with ASD aged 8 to 12 years showed82

    • increased cortisol stress responses in the social interaction paradigm (PIP)
    • higher sensory sensitivity according to the Short Sensory Profile correlated with low cortisol levels
    • higher stress values in the Stress Survey Schedule correlated with higher cortisol values

  • in a semi-structured video game-based social interaction setting, there was no difference in the cortisol stress response in ASD83

Physical stressors

  • to a previously unknown blood draw as a stressor, 3- to 10-year-old children with ASD showed a significantly elevated cortisol stress response, with girls again showing a significantly higher cortisol stress response than boys84

According to the study situation, the cortisol stress response to ASA does not appear to be clear.
An indication that it could depend on the stress phenotype, as in other disorders (ADHD, depression, narcissism), in that externalizing stress reactions tend to correlate with a flattened and internalizing ones with an increased cortisol stress response, results from the correlation of irritability in ASD with the cortisol stress response.
High irritability in boys with high-functioning autism (HFA) correlated with a flattened cortisol stress response, while low irritability correlated with a normally elevated cortisol stress response. The effects of irritability on heart rate, but not on cortisol levels, were explained by the trait “anxiety”.85
In contrast, one study found a flattened cortisol stress response in ASD only in boys with comorbid anxiety disorder.86

Girls with high-functioning ASA (HFA) were more likely to show a reverse cortisol awakening response87

Multiple complex developmental disorder (MCDD) is a symptomatically distinct group in the ASD spectrum. Unlike children with ASD, some children with MCDD develop schizophrenia in adulthood. MCDD is characterized by impaired regulation of anxiety and affective states, impaired social behavior/social sensitivity and thought disorders. MCDD and ASD show abnormal reactions to their social environment.
MCDD correlates with a flattened cortisol stress response to psychosocial stress.88 In comparison, ASA showed a higher cortisol stress response.89

Away from cortisol: respiratory sinus arrhythmia (RSA)

  • Adults with ASD were more likely to show an anticipatory stress response, while adolescents with ASD were more likely to show a reactive stress response90
    • Overall, the RSA was significantly reduced before, during and after the TSST, but the relative change was identical. The cortisol stress response was not measured.
  • another study also found a reduced RSA with ASA without significant differences in the RSA stress response77

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