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Cortisol and other stress hormones in ADHD

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Abstract from ADxS.org
Symptoms
Consequences of ADHD
Origin
Stress
Neurological aspects
Neurophysiological correlates of ADHD symptoms
Aggression in ADHD - neurophysiological correlates
Drive problems in ADHD - neurophysiological correlates
Arousal and activation in ADHD - neurophysiological correlates
Attention problems in ADHD - neurophysiological correlates
Thinking blocks and decision-making problems in ADHD - neurophysiological correlates
Emotional dysregulation - neurophysiological correlates
Frustration intolerance in ADHD - neurophysiological correlates
Hyperactivity in ADHD - Neurophysiological correlates
Impulsivity in ADHD - neurophysiological correlates
Learning problems in ADHD - neurophysiological correlates
Motivation in ADHD - neurophysiological correlates
Organizational and executive function problems in ADHD - neurophysiological correlates
Sleep problems in ADHD - neurophysiological correlates
Social phobia - neurophysiological correlates
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Cortisol and other stress hormones in ADHD

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1. Stress hormones in ADHD

Various stress hormones are altered in ADHD.
The stress hormones cortisol, ACTH and CRH discussed below are the 3rd, 2nd and 1st increment stress hormones of the HPA axis. Alpha-amylase is a biomarker for the activity of the autonomic nervous system.

In summary, it must be assumed that the cortisol response to acute stressors, which is often flattened in ADHD-HI and very often excessive in ADHD-I, is a biomarker for a pathological change in the HPA axis, but that the change in the cortisol response is not the cause of ADHD. Comparable experiences have been made in the treatment of depression.1

However, too many studies suffer from the fact that in ADHD, as in depression, the externalizing subtypes (ADHD-HI, atypical depression) and the internalizing subtypes (ADHD-I, melancholic depression) are not recorded separately.

2. Cortisol responses to stress and personality traits

2.1. High cortisol response: internalizing, low cortisol response: externalizing

We have collected a number of sources showing that high or low cortisol stress responses in healthy people correlate with gender and various general personality traits.
More on this at ⇒ Cortisol stress responses and personality traits in healthy people In the section ⇒ Stress response patterns in healthy people of the article ⇒ Stress theories and stress phenotypes: a possible explanation of ADHD subtypes.

2.2. Cortisol reactions as an expression of the stress phenotype

The available research strongly suggests that externalizing or disruptive behaviors such as aggression with or without the presence of (comorbid) Oppositional Defiant Disorder (ODD) or symptomatically more severe Conduct Disorder (CD) are associated with lower basal cortisol levels and a flattened cortisol response to acute stress.

Elevated basal blood cortisol levels in 15-year-old persons with ADHD (decrease in the late afternoon) correlated with aggression in boys, but not in girls.2 Another study found a correlation of aggression with flattened cortisol responses to acute stress, while basal cortisol levels remained unchanged.3

Depression or depressive personality traits45 6 as well as anxiety78 correlate with increased morning (CAR) or serum cortisol levels.
⇒ Cortisol in other disorders

If - as we assume - not only ADHD, but also the other mental disorders mentioned here are understood as dimensional disorders and furthermore ADHD-HI is understood as an externalizing stress phenotype and ADHD-I as an internalizing stress phenotype, it is reasonable to assume that primarily the stress phenotype could determine the cortisol response to acute stress (or that the cortisol response to acute stress could predict the stress phenotype).
This view further leads to the conclusion that dexamethasone testing of the HPA axis for cortisol reactivity could only determine whether an HPA axis disorder is present and whether this leads to an externalizing or an internalizing stress phenotype, but not which mental disorder is present within the respective spectrum.

It is argued that cortisol stress responses are more predictive of comorbidities than ADHD. According to this view, blunted cortisol responses to stress are associated with comorbid DBD (disruptive behavioral disorder), while high cortisol responses are associated with comorbid anxiety disorders.910 This is consistent with our view of the correlation of blunted cortisol stress responses with externalizing disorders and elevated cortisol stress responses with internalizing disorders.

A reduced exchange between the brain hemispheres (especially in PTSD) appears to be a cause of a reduced cortisol stress response, as well as alexithymia.11 Furthermore, a coincidence of reduced basal cortisol levels (despite normal cortisol response to ACTH) and alexithymia is reported in some persons with ADHD, from which the authors concluded that ACTH-independent mechanisms reduce cortisol levels.12

2.3. Cortisol stress responses over time

The problem is that the individual stress cortisol response maximum differs by up to 20 minutes. In a group of 54 healthy adults, the cortisol maximum in the early group occurred directly at the end of the 15-minute TSST stressor (cortisol increase from 0.04 to 0.21 ng/ml), whereas in the late group it did not occur until 20 minutes later (from 0.05 to 0.22 ng/ml). If both groups had been examined directly after the end of the TSST, the late group would have been incorrectly categorized as reacting to stress with a flattened cortisol increase with an increase from 0.05 to 0.07.13 In most studies, a cortisol measurement 20 minutes after the end of the TSST is common. The question arises as to whether the rise in cortisol in the early group lasts long enough to be properly recorded in a measurement after 20 minutes.
In many studies, not enough cortisol samples are taken at the end of the stress test to take this into account.

According to one source, the cortisol levels of people with ADHD only deviate (upwards) from those of people without ADHD, even under stress, if relationship-related issues were the subject of the stress test (increased sensitivity to relationship issues), but not in the case of purely cognitive stressors.14 This is not confirmed by most studies. To clarify this, a distinction is made below between cognitive and emotional stressors.

2.4. Cortisol stress responses by gender

Cortisol responses to stress also differ according to gender.15

2.5. Cortisol responses to stress in non-affected people

  • Among 102 five-year-old children not diagnosed with ADHD, HPA activity was significantly higher in girls than in boys. Emotional stress (retelling a story) caused a significant increase in cortisol in all children, which was even higher in girls than in boys. Increased HPA system activity (basal and stress-reactive) correlated significantly with hyperactivity/impulsivity and emotional problems in the boys and with positive emotions in the girls.16
  • Chronic stress reduces the morning cortisol maximum (CAR, typically 30 to 60 minutes after waking up) in healthy young men (average age 22.5 years).17 Even low levels of stress increased the baseline value on waking and significantly reduced the CAR maximum (30 min after waking). Severe stress led to an even higher baseline value with a flattened CAR, which also occurred 16 minutes after waking.
  • The cortisol response to physical stress depends on
    • The individual resting cortisol concentration and previous exposure1819
    • Of muscle mass. The cortisol response to physical exertion is relatively lower with larger muscle mass than with smaller muscle mass.20 We hypothesize that this could simply be due to the lower relative load when the same work is performed by more muscle mass.
    • The current blood glucose concentration and insulin availability before the start of exercise 21
      • The increase in cortisol during physical exertion is mainly triggered by an adrenergically mediated increase in ACTH22
      • In addition, glucose-sensitive receptors in the liver and brain modulate the exercise-induced
        Cortisol response through activation of the pituitary-adrenocortical axis22
    • A meta-analysis of 29 studies on 2601 subjects found no correlation between externalizing behaviour and a (flattened) cortisol stress response, as should exist according to the hypothesis we advocate.23

2.6. Interplay between cortisol and dopamine

Glucocorticoid receptors are found on numerous dopaminergic cells in the midbrain and hypothalamus.24 It is assumed that cortisol can influence the release of dopamine in the basal ganglia and in nigrostriatal and mesolimbic pathways.25
Cortisol inhibits tyrosine hydroxylase, an enzyme that limits catecholamine synthesis by acting as a catalyst for the conversion of tyrosine to DOPA. Tyrosine hydroxylase is inhibited by cortisol (as well as by dopamine and noradrenaline themselves (negative feedback).26
This indicates a reciprocal interplay between dopamine and cortisol release.

A retrospective analysis found a correlation between the use of inhaled corticosteroids in younger children with moderate to severe asthma. This correlation was not found in older children.27

2.7. Interplay between CRH and noradrenaline

The hypothalamus, which secretes CRH, is closely connected to the nucleus coeruleus, which produces noradrenaline. CRH activates the release of noradrenaline, while at the same time noradrenaline stimulates CRH production.26

3. Changes in cortisol levels in ADHD

A large number of studies have been devoted to the question of whether and how the HPA axis reacts differently in ADHD. There is now massive evidence that there are lasting changes in the HPA axis in ADHD.

Epidemiologic and preclinical studies have shown that the disorder of the HPA axis in ADHD may result from excessive cortisol exposure in the fetal and early postnatal period (early childhood stress). Glucocorticoid administration at this stage of life may permanently alter glucocorticoid receptors in the brain, causing dysregulation of HPA axis activity, disorders in the biosynthesis of neurotransmitters and their receptors, and alterations in intracellular pathways. Glucocorticoids (cortisol) enhance the activity of the dopaminergic system. Reduced expression of glucocorticoids could thus cause hypofunction of the dopaminergic system.28

A fundamental distinction must be made between basal cortisol levels and cortisol responses (reactions) to acute stress. While the subtypes of ADHD differ from non-affected persons by reduced basal cortisol values, but not by deviations from each other, the cortisol response to acute stress of ADHD-HI/ADHD-C on the one hand and ADHD-I subtype on the other hand differs considerably and systematically from each other and deviates in various directions from the values of non-affected persons.
Basal cortisol levels therefore distinguish people with ADHD from those without, and cortisol responses also differentiate between subtypes.

It is also striking that the stress-induced increase in cortisol is significantly higher in ADHD-I (without hyperactivity/impulsivity) than in those not affected, while acute stress triggers a significantly lower cortisol response in ADHD-HI (with hyperactivity) and ADHD-C than in those not affected.

This could be relevant for treatment, as cortisol not only mediates the stress response of the HPA axis, but also acts as a feedback loop to calm and deactivate the stress systems (the HPA axis and the central nervous system).

We hypothesize that a one-time higher cortisol administration in ADHD-HI could shut down the stress systems again. If the cortisol response that signals the shutdown of the stress systems is missing, it would at least be worth considering compensating for this with a single cortisol substitution. Since a high cortisol stress response is a healthy reaction to shut down the HPA axis again, a one-off intermittent administration should not necessarily have any disadvantages. For people with ADHD-I, on the other hand, this should naturally not make sense.

Dexamethasone could be recommended for this, as it addresses GR 30 times more strongly than MR. If necessary, a combination with an MR antagonist such as eplerenone, as used in a study for the treatment of back pain, would be conceivable.29

Cortisol administration could not only downregulate the HPA axis, but also support the downregulation of the PFC.
Stress-induced elevated noradrenaline inhibits PFC and working memory function via noradrenaline α1 receptors to shift action control from slow analytical control by the PFC to fast instinctive control by older brain regions, because this is advantageous during fight or flight.
A stress-induced high release of cortisol leads to a stimulation of the same noradrenaline α1 receptors in the PFC. The simultaneous addressing of these receptors intensifies the effect caused by high noradrenaline levels.30
In healthy individuals, the endocrine stress responses of noradrenaline and cortisol correlate, so that a coincidence of high noradrenaline and high cortisol levels can trigger PFC deactivation.

Cortisol plays a role in ADHD,31 but not in relation to inhibition.32

3.1. Cortisol responses to stress in ADHD altered in a subtype-specific manner

A number of studies have looked at the cortisol response of people with ADHD to stress by measuring cortisol levels before and after a stressful event.

However, a distinction must be made between ADHD-HI (with hyperactivity) and ADHD-I (without hyperactivity). If this differentiation is omitted, even meta-studies find no difference in the cortisol stress response between ADHD and non-affected individuals.33

Chronic stress reduces the expression of the glucocorticoid receptor (GR), which switches the HPA axis off again after a stress response. A slower decrease in the cortisol level to the baseline value after an acute stressor was observed, i.e. a longer time to recovery34

3.1.1. Reactions to cognitive stress in ADHD

  • 51 of 68 children with ADHD (average age 8.8 years) showed no increase in cortisol in an unspecified “psychological test as a stressor”. It is possible that the Hamburg-Wechsler Intelligence Test (WISC-III) was also used as a stressor. The 17 test subjects with an increase in cortisol under stress had a higher IQ, although the report does not clearly state whether this was the IQ value measured after stress or the IQ value without stress. The level of cortisol before the test correlated with IQ. The lower the cortisol level after the test, the lower the IQ of the test subjects.35
  • 20 children with ADHD and comorbid Oppositional Defiant Disorder (ODD) and Disorder of Social Behavior (CD), thus with high levels of aggression, showed no increase in cortisol to a cognitive stressor at the age of 4 to 6 years as well as 2 years later at the age of 6 to 8 years. People with ADHD whose problem persisted showed a flattened cortisol response.36 This is consistent with the other studies in that ODD and Disorder of Social Behavior are typical comorbidities of the hyperactive/impulsive ADHD-HI subtype, for which a reduced/absent cortisol rise is often reported.
  • Of 48 children who were exposed to the Korean Hamburg-Wechsler Intelligence Test (KEDI-WISC) as a stressor, 28 showed a drop in cortisol and 15 showed an increase in cortisol levels.37 Children with a drop in cortisol made more errors of omission and incorrect responses, which is thought to demonstrate impulsivity problems. This suggests the hyperactive-impulsive ADHD-HI subtype. The children with an elevated cortisol stress response made more incorrect responses in the attention test, indicating attention problems. Non-affected children were not compared.
  • Of 49 children with ADHD without other comorbidities between the ages of 6 and 17, 33 children showed no increase in cortisol on the Korean Hamburg-Wechsler Intelligence Test (KEDI-WISC) and the TOVA test as (cognitive) stressors, while 16 showed an increase in cortisol.3 The 33 children with a decrease in cortisol had an IQ of over 110, the 16 children with an increase had an IQ of less than 110 (IQ average: 92.3). A decrease in cortisol also correlated with higher aggression scores and lower attention scores in the K-CBCL. Children with an increase in cortisol tended to have a more withdrawn character and fewer social problems. This also fits the picture of a reduced/absent cortisol response in the hyperactive-impulsive ADHD-HI subtype. Non-affected individuals were not compared.
  • 68 of 90 children with ADHD did not show an elevated cortisol response to stress by the Korean-Wechsler Intelligence Scale for Children-Third Edition (K-WISC-III). Elevated cortisol responses to a stressor correlated with increased variance in response time.38 Non-affected individuals were not compared.
    An increased variance in response times could be explained by an impairment in the performance of the PFC, as is particularly pronounced in the ADHD-I subtype.
    Prolonged reaction times correlated with ADHD-I.39
  • 38 children with ADHD showed a significantly higher increase in cortisol in response to the Continuous Performance Test (CPT) as a stressor than 38 children without ADHD, regardless of subtype.40 A follow-up study of the same subjects 4 years later showed that the cortisol stress responses of the people with ADHD had decreased and now corresponded to those of the non-affected children.41

Rating:

We consider stress testing by means of an intelligence test to be of little use. The fact that people with a higher IQ are less stressed by an IQ test than people with a lower IQ is probably the inherent purpose of an IQ test. We also assume that children with reduced intelligence are more stressed by cognitive tests and intelligence tests because they expect a negative assessment, which means that ultimately only the expected social evaluation would trigger stress. For the question of which circumstances trigger cortisolergic stress in the first place, see above.

Furthermore, the ADHD-HI (hyperactive/impulsive) and ADHD-I (without hyperactivity) subtypes are likely to react differently to different stressors due to their different stress phenotypes. We suspect that the more extroverted ADHD-HI type will be less stressed and possibly even more stimulated by social exposure (finishing a story and doing mental arithmetic aloud while being observed/judged by others) than the more introverted ADHD-I type, whose stress response is an inward flight.
This is consistent with the findings of van West.42

3.1.2. Reactions to emotional stress in ADHD

  • A study of 9 ADHD-HI, 10 ADHD-I and 14 ADHD-C sufferers and 33 non-affected people (6 to 8 years, mean 6.3 years) using TSST-C also found a significantly reduced cortisol response in the ADHD-HI sufferers and a comparatively higher cortisol response in ADHD-I sufferers. All subtypes showed a lower baseline cortisol level than non-affected individuals. Non-affected individuals did not show a strong cortisol response.43 The latter could indicate problems with the test set-up. In addition, the number of subjects per subtype was too small for reliable conclusions.
  • A study of 18 adults with ADHD and 18 people without ADHD came to no clear conclusion. Only a general tendency towards a reduced cortisol response to acute stress and an increased subjective perception of stress in people with ADHD was reported.44 This may have been due to the small number of test subjects and the lack of separation according to subtypes.
  • A study of young adults without differentiation between ADHD-HI and ADHD-I found generally increased cortisol stress responses in ADHD.45
  • A study that used simple sensory items rather than the TSST as stressors to investigate high sensitivity in ADHD found no significant differences in cortisol stress response between non-affected, people with ADHD without and people with ADHD with high sensitivity.46 It would have been interesting to see whether the responses to the TSST would have differed.
3.1.2.1. ADHD-HI, ADHD-C and comorbid externalizing disorders
  • A study of 96 adults with ADHD and 25 non-affected individuals found a flattened cortisol response in ADHD-C compared to non-affected individuals, and an increased stress-induced cortisol response in the ADHD-I subtype.47
  • Children (6 to 12 years, mean 8.6 years) with the ADHD-HI-ADHD-C were significantly less likely to have the cortisol increase to emotional stress (Public Speaking Task, PST and Trier Social Stress Test, TSST) (expected in healthy individuals) than non-affected individuals, while the predominantly inattentive ADHD-I subtype showed a significantly stronger cortisol response than non-affected individuals.48 Only 35% of people with ADHD-C showed elevated cortisol levels due to stress, compared to 92% of people with ADHD-I and 88% of non-affected people. This study also confirmed a connection between aggression, externalization problems and a reduced cortisol stress response.
  • People with ADHD with high hyperactivity/impulsivity symptoms showed reduced cortisol suppression after the dexamethasone test.49 This may result from a flattened cortisol stress response or from less addressable glucocorticoid receptors.
  • With a low alpha-amylase release (marker of the sympathetic stress system) in response to acute stress by the TSST, a simultaneous low cortisol response correlates with high levels of aggression; with a high alpha-amylase release in response to acute stress, the cortisol response has no correlation with aggression.50
  • Of 202 male adolescents (10 to 17 years, mean 14 years), the 107 who had a comorbid disorder of social behavior (CD) responded to a psychosocial stressor with significantly more reduced cortisol stress reactivity compared to the 97 ADHD-HI only persons with ADHD.
    The more severe the ADHD symptoms were, the lower the basal cortisol level was. Disorder of social behavior, on the other hand, was associated with increased basal cortisol levels and a decreased cortisol stress response. Impaired cortisol reactivity may reflect fearlessness and be associated with poor emotion regulation and inhibition of aggressive and antisocial behavior.51 Unfortunately, no unaffected individuals were included as controls.
  • 7-12 year old (mean: 10 years) children with oppositional defiant disorder (ODD) have reduced activity patterns of the autonomic nervous system or HPA axis. 15 children with ODD, 31 children with ODD and AD, and 23 ADHD-only children were compared with 26 unaffected children. Cortisol response to competition-induced stress (non-relationship stress) was significantly reduced in ODD children with or without ADHD-HI and was equally normal in ADHD-only and unaffected children. Pulse rate was significantly decreased in ODD persons with ADHD with and without stress. ODD, ODD/ADHD-HI and ADHD-HI persons with ADHD all had equally significantly lower skin conductance values under stress.52 As MPH medication was not suspended for the study, the results are likely to be biased. That 17 of the 23 ADHD-HI-only children received MPH could explain the normalization of the stress-induced cortisol response.
  • Oppositional defiant behavior in ADHD correlated with aberrant cortisol responses to acute stress.53
  • The stronger the psychopathic traits (callous unemotional traits = CU traits) such as lack of empathy, emotional coldness, etc., the flatter the cortisol response to the TSST in children with ADHD.54
  • 22 children with DBD (Disruptive Behavior Disorder) showed decreasing and increasing cortisol responses to stress, with the children with decreasing cortisol responses showing more severe symptoms than the children with increasing cortisol responses.55
  • Disorder of social behavior (CD) correlates with a flattened cortisol stress response.56

Since externalizing disorders correlate with ADHD-HI (with hyperactivity), we consider a tendency toward a flattened cortisol stress response in ADHD-HI and ADHD-C a plausible possibility.

3.1.2.2. ADHD-I and comorbid internalizing disorders
  • A study of 96 adults with ADHD and 25 non-affected individuals found a higher stress-induced cortisol response in the ADHD-I subtype than in non-affected individuals, and a flattened cortisol response in ADHD-C.47
  • People with ADHD-I of the purely inattentive subtype showed an excessive cortisol response to acute stress.57
  • A study of 20 persons with ADHD-I and 19 non-affected persons (8 to 13 years, mean 10.3 years) using TSST-C58 revealed that the 7 persons with ADHD-I with severe inattention symptoms showed a significantly reduced cortisol response to the stressor, unlike the 13 persons with ADHD-I with moderate symptoms and the 19 non-affected persons.
    A similar study found a greater reduction in cortisol response in persons with ADHD with severe inattention symptoms than in those with less severe inattention symptoms.59
    These results contradict our analysis that ADHD-I is characterized by an excessive cortisol stress response.
  • One study found a strongly flattened cortisol stress response to the TSST in boys with pronounced inattention. Girls with marked inattention also showed a flattened cortisol stress response during and after the TSST, with elevated levels before the TSST. The basal cortisol levels were unchanged.60 The study also mentions that flattened cortisol stress responses are common in chronic stress.
    The children were categorized as ADHD-I based on inattention scores alone, not on the absence of hyperactivity/impulsivity. This could explain the results if the subjects were also showing strong hyperactivity/impulsivity scores. Comorbid externalizing or internalizing disorders did not influence the results.
  • In healthy adults, lower novelty seeking (which is more consistent with the ADHD-I subtype) correlated with increased cortisol responses to the TSST (as typically exhibited by ADHD-I), but not with ACTH levels.61
  • This also applies to higher risk aversion (which also tends to fit the ADHD-I subtype).62
  • Anxiety, depression, subjective perception of stress, impulsivity, and a higher ADHD symptom total score correlated with increased cortisol responses to acute stress in a study of adults (which was surprising in relation to impulsivity).63

3.1.3. Reactions to physical stress

  • Of 170 elementary school-aged children with ADHD, venipuncture as a stressor led to an increase in cortisol in those with comorbid anxiety problems, while those with comorbid DBD and oppositional defiant disorder had a decreased cortisol response. ADHD-HI subtypes did not elicit different cortisol responses.64
  • Of 62 children with ADHD, the ADHD-HI type showed an identical cortisol level to non-affected children before venipuncture, while the ADHD-I subtype showed an increased cortisol level compared to non-affected children even before venipuncture. Since basal cortisol levels are lower in both ADHD-I and ADHD-HI affected people than in non-affected people, this could be an anxiety response in anticipation of the stressor.65 The same pattern was seen in relation to alpha-amylase as a representative of the autonomic nervous system.
  • In the same 62 children with ADHD, the ADHD-HI subtype showed a reduction in cortisol levels 10 minutes after venipuncture, while it increased slightly in the 40 non-affected children and increased more in the ADHD-I affected children.65 The same pattern was seen in relation to alpha-amylase as a representative of the autonomic nervous system.
  • Children with ADHD tended to show increased cortisol stress responses to venipuncture on the first procedure in a home setting and significantly lower basal cortisol levels and significantly flattened cortisol stress responses on the second procedure in a clinic setting compared to non-affected individuals.66
  • Children with ADHD showed a lower increase in cortisol in response to a visit to the dentist as a stressor than children without ADHD. The increase in cortisol was particularly low in children with high levels of hyperactivity/impulsivity.67

3.2. Basal cortisol levels reduced in ADHD

The results on basal cortisol levels in ADHD show reduced levels in the majority of cases.

3.2.1. Reduced basal cortisol levels: 18 studies

Several studies found that basal (constant, basic) cortisol levels are generally reduced in ADHD, with the reduction in cortisol levels being even more pronounced in ADHD-HI and in ADHD-C than in the ADHD-I subtype.286869

3.2.1.1. Hair cortisol levels

The hair cortisol concentration is a measure of long-term cortisol secretion.70

Decreased basal cortisol levels in the hair of 4-year-old children over several months are a good predictor of an increase in ADHD symptoms in boys (but not in girls) in the following year.71 Similarly, Pauli-Pott et al.72 Another study found that HCC in children correlate between parental psychopathology and major depression and ADHD in the children.73 One study found a correlation between low hair cortisol levels and low working memory scores and low intelligence performance only in boys, but not in girls. In boys, hair cortisol fully explained the correlations of ADHD inattention symptoms with working memory and intelligence performance.74
Higher hair cortisol levels correlated with better attention/memory performance, particularly in boys70
Hair cortisol levels were not associated with executive functions or ADHD symptoms.
Childhood maltreatment was associated with inattention symptoms in adolescents with ADHD.

3.2.1.2. Morning blood cortisol level, cortisol wake-up reaction

Several other studies found reduced morning blood cortisol levels in ADHD.757667777879

The salivary cortisol level of 5- to 9-year-old boys directly after getting up at around 06:30 was on average 0.4 ng/ml lower than that of non-affected persons. However, the individual range of cortisol levels in people is significantly greater than the statistical difference (non-affected people 0.7 to 10.5 ng/ml; people with ADHD 1.3 to 8.1 ng/ml).80
In 109 adults with ADHD, 64% were found to have a normal morning cortisol awakening response (with no significant differences between subtypes), compared with 84% in unaffected controls.81

3.2.1.3. Other methods of measuring the basal cortisol level

248 adolescents with ADHD showed lower basal cortisol levels and higher perceived stress, although basal cortisol levels and perceived stress did not correlate.82

Of 202 male adolescents (10 to 17 years old, mean 14 years old), the 107 who had a comorbid social behavior disorder (CD) responded to a psychosocial stressor with significantly more reduced cortisol stress reactivity compared to the 97 ADHD-HI only sufferers. The more severe the ADHD symptoms were, the lower the basal cortisol level was. Disordered social behavior, on the other hand, was associated with increased basal cortisol levels and a decreased cortisol stress response. Impaired cortisol reactivity may reflect fearlessness and be associated with poor emotion regulation and inhibition of aggressive and antisocial behavior.51 Unfortunately, no unaffected individuals were included as controls.
Low basal stress levels (basal = not stress-induced) are interpreted as an adaptive response of the HPA axis (stress axis) to chronic stress experience. Not only children with ADHD, but also their mothers showed a reduced cortisol level at 9 a.m. compared to people with ADHD.

Reduced blood cortisol levels in 15-year-old persons with ADHD (decrease in the late afternoon) correlated significantly with aggressiveness and impulsivity in boys, but only tendentially in girls.83

Several studies show that reduced basal cortisol levels are not an exclusive feature of ADHD. They also correlate with (comorbid) social behavior disorders.848586
However, the measure of aggression does not result in different basal cortisol levels.3

3.2.2. Unchanged basal cortisol levels: 5 studies

In people with ADHD-I, a study found no changes in daily cortisol levels.59
Three other studies also found no change in basal cortisol levels in people with ADHD compared to those without the condition.875349
One study that considered ADHD subtypes/presentations found:88

  • reduced hair cortisol in boys with ADHD-I (no longer significant after controlling for early trauma)
  • increased hair cortisol in girls with ADHD-C (no longer significant after controlling for early trauma)
  • attenuated reactivity of the sympathetic nervous system in boys with ADHD and comorbid ODD/CD

3.2.3. Elevated basal cortisol levels: 3 studies

In contrast, people with ADHD with high inattention symptoms showed an increased cortisol awakening response (CAR), although this was predominantly due to comorbid anxiety or depression disorders.49
In healthy adults, lower novelty seeking (which is more consistent with the ADHD-I subtype) correlated with elevated baseline cortisol levels, but not with elevated ACTH levels.89
One study found consistently elevated basal cortisol levels.90

3.3. Decrease in cortisol levels without stress induction in ADHD?

A relatively small study came to the conclusion that a steeper drop in cortisol levels from 06:30 to 09:00 is typical for ADHD. In 19 people with ADHD, the drop in cortisol levels was 66% steeper than that of 40 people without ADHD, which was 56% steeper.91
Another study also reported abnormal changes in cortisol levels throughout the day, which correlate with the level of hyperactivity.92

3.4. GR variant influences cortisol effect and ADHD risk

See also ⇒ Gene variants of the GR In the article ⇒ Cortisol and other stress hormones in AD(H)S

4. ACTH for ADHD

  • No differences in basal ACTH levels were found between 128 people with ADHD and 30 unaffected children. The ADHD subtypes did not differ either.76

  • In healthy adults, lower novelty seeking (which is more consistent with the ADHD-I subtype) correlated with increased cortisol responses to the TSST (as is very common in the ADHD-I subtype), but not with altered ACTH levels.89

  • This also applies to a higher risk aversion (which also correlates with the ADHD-I subtype).62

  • In one study, sexually abused girls were found to have reduced basal ACTH levels and reduced ACTH responses to CRH stimulation, while the cortisol response was unremarkable.93

  • Early childhood stress causes permanent changes in the HPA axis, which are reflected in altered basal and stress-induced cortisol levels. Children with internalizing problems often showed increased cortisol stress responses, while adults who had experienced early childhood psychological stress often showed decreased basal cortisol levels and increased ACTH responses to acute stress.94

  • Disorders of the ACTH receptor systems can occur during early stress experiences, preventing the anxiety experience from being extinguished and thus causing long-term stress. This could be improved by administering ACTH.95 In our opinion, the change in ACTH receptor systems could possibly be a consequence of a down/upregulation response. ⇒ Downregulation / upregulation

  • Rats that were separated from their mother at an early age or received little care showed96

    • Elevated basal ACTH levels
    • Increased ACTH levels due to acute stress
    • More than doubled CRH levels on inflammation
    • Reduced density of CRH receptors in the anterior pituitary gland
    • Changes in extrahypothalamic CRH systems
      • 59% increase in the number of CRH receptor binding sites in the raphe nuclei
      • Increase in immunoreactive CRH concentrations in the parabrachial nucleus by 86
    • Behavioral abnormalities such as97
      • Increased anxiety
      • Anhedonia
      • Increased alcohol preference
      • Sleep disorders
      • Cognitive impairments
      • Increased sensitivity to pain

  • 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.98

5. CRH for ADHD

  • Young monkeys that grew up under early attachment stress had increased CRH and decreased adrenaline levels at the age of 4 years.99100
  • After its release, cortisol initially mediates stress symptoms. Furthermore, a high cortisol level has the effect of shutting down the HPA axis and noradrenaline.
    However, as the GR cortisol receptors are less sensitive after prolonged stress due to downregulation, they do not perceive this signal. The stress systems are not switched off.101 Consequences: CRH levels remain permanently elevated and permanently trigger the symptoms mediated by CRH. This mechanism has already been described for depression.102103
  • Prolonged stress caused chronic demethylation of the CRH gene in adult mice.104

6. α-Amylase for ADHD

The alpha-amylase level represents the activity of the primarily adrenergically controlled autonomic nervous system. Alpha-amylase reacts very strongly to a psychosocial stressor, but does not correlate with other so-called stress markers such as cortisol, noradrenaline or heart rate. Alpha-amylase is therefore suitable for recording physical changes caused by stress.105106107108 In contrast, concentration tasks (Stroop test) as a stressor do not increase the alpha-amylase level.109

  • In ADHD, the basal alpha-amylase level is usually reduced, with the α-amylase level reduction being even more pronounced in ADHD-HI and ADHD-C than in the ADHD-I subtype. This pattern is consistent with the reduced basal cortisol level (a representative of the HPA axis).65
    *In 62 children with ADHD, venipuncture only significantly increased the α-amylase levels in the control group, but not the cortisol levels.65 The same pattern was seen with regard to cortisol as a representative of the HPA axis.
  • In the same 62 children with ADHD, the ADHD-HI subtype showed a decrease in α-amylase levels 10 minutes after venipuncture, while it increased slightly in the 40 non-affected and more in the ADHD-I affected.65 The same pattern was seen with regard to cortisol as a representative of the HPA axis.

Alpha-amylase is an enzyme in the intestine that is responsible for breaking down carbohydrates into sugar. There could be a link between stress and eating problems or obesity.

6.1. Correlation between alpha-amylase and cortisol

An investigation of the time course of the occurrence of alpha-amylase as a representative of the autonomic nervous system and cortisol as a representative of the HPA axis in response to a TSST as a stressor indicates mutual dependencies between the two stress hormones:110

  • An increase in alpha-amylase was moderately often followed by an increase in cortisol 14 minutes later.
  • A rise in cortisol was slightly often followed by a drop in alpha-amylase 14 minutes later.
  • An increase in alpha-amylase was moderately often followed by a decrease in cortisol 42 minutes later.

7. Diagnosis and treatment of ADHD with cortisol / dexamethasone?

Dexamethasone is an (artificial) glucocorticoid that binds to the glucocorticoid receptors of the pituitary gland in healthy volunteers, thereby inhibiting the ACTH precursor protein POMC. Consequences are that the release of ACTH from the anterior pituitary gland is reduced. As ACTH normally stimulates the release of cortisol, a healthy response to the administration of dexamethasone would be to reduce cortisol levels - known as suppression.
Nonsuppression (a lack of cortisol reduction by dexamethasone) indicates a misalignment of the HPA axis, in the form of a lack of response of the glucocorticoid receptors that mediate HPA axis deactivation. We hypothesize such HPA axis misalignment as a possible cause of ADHD, and we believe the lack of HPA axis deactivation is typical of ADHD-HI.

The dexamethasone/CRH test, a further development of the previously used pure dexamethasone test, can be used to determine whether there is a problem with the shutdown of the HPA axis in the form of cortisol nonsupression.

For the procedure and evaluation of the dexamethasone test, see ⇒ Dexamethasone/CRH test and ⇒ Dexamethasone test in the chapter ⇒ Pharmacological endocrine function tests.

In melancholic depression, which like ADHD-I is very often characterized by an excessive cortisol response, but probably also frequently in atypical depression, which is characterized by a flattened cortisol stress response, the dexamethasone test shows insufficient negative feedback of the HPA axis and therefore insufficient cortisol suppression in response to dexamethasone administration.

We hypothesize that in ADHD-I (unlike melancholic depression) the excessive cortisol response leads to a frequent shutdown of the HPA axis. This could be a misconception, or could indicate a difference between melancholic depression and ADHD-I.

In support of the hypothesized difference between depression and ADHD-I, a large study (n = 2307) found reduced cortisol suppression to dexamethasone in hyperactivity/impulsivity (ADHD-HI), while inattention (ADHD-I) showed no correlation to nonsuppression.111 This is consistent with the results of a smaller study that found nonsuppression in only some of the people with ADHD and found that nonsuppression correlated with higher levels of hyperactivity.112 Another small study, but involving only 9 children with ADHD, found suppression in ADHD.113 Another smaller study found nonsuppression in 22.7% of people with ADHD with hyperactivity, which is 4-fold higher than the 5.7% in healthy people.114
However, the fact that dexamethasone shows a reduction in ADHD-HI symptoms in rats that serve as an animal model for ADHD-HI (with hyperactivity) (spontaneous hypertensive rat) speaks against a general nonsupression.115116 SHR have a genetically determined excessive expression of mineralocorticoid receptors (MR) and a normal expression of glucocorticoid receptors (GR).117

These results suggest that glucocorticoid receptors are not desensitized in ADHD-I.

The results further indicate that in ADHD-HI, in addition to the reduced cortisol response, which naturally leads to an insufficient shutdown of the HPA axis, there is also a (relative) overactivity of the MR or a desensitization of the GR. The nonsuppression of the HPA axis observed in hyperactivity when dexamethasone is administered proves that there is also nonsuppression in the case of a short-term high cortisol level, i.e. an inadequate shutdown of the HPA axis.

To summarize, we interpret this as follows:

  • Melancholic / psychotic depression:
    l High cortisol stress response
    • Nevertheless no shutdown of the HPA axis
    • → Desensitization of the GR or overactivity of the MR
  • ADHD-I
    HSHigh cortisol stress response
    • Shutting down the HPA axis
    • → No desensitization of the GR or overactivity of the MR
  • Atypical depression
    typeLow cortisol stress response
    • No shutdown of the HPA axis
      • Not only due to a lack of sufficient cortisol stress response
      • Also with artificial glucocorticoid administration (dexamethasone)
        ch→ more frequent desensitization of GR (more likely) or overactivity of MR (less likely, as dexamethasone addresses GR 30 times more strongly than MR and yet nonsupression occurs)
  • ADHD-HI
    HSLow cortisol stress response
    • More often no shutdown of the HPA axis
      • Not only due to a lack of sufficient cortisol stress response
      • Also with artificial glucocorticoid administration (dexamethasone)
        ch→ more frequent desensitization of GR (more likely) or overactivity of MR (less likely, as dexamethasone addresses GR 30 times more strongly than MR and yet nonsupression occurs)

8. Treatment of ADHD with cortisol / dexamethasone?

8.1. Dexamethasone as a medication for ADHD

Another strong indication that the HPA axis, and cortisol in particular, plays a central role in ADHD is provided by a study that found that dexamethasone (as a medication) in SHR rats (which are considered an animal model for ADHD-HI (with hyperactivity)) was able to significantly reduce their ADHD-HI symptoms.118
However, it must be taken into account that ADHD with hyperactivity can be caused by a variety of different gene constellations and the SHR only represent a single gene constellation, so the result cannot be easily generalized for every ADHD-HI.
W
The dopamine D1 transporter in the PFC, which is damaged in schizophrenia, can be reactivated by cortisol in animal models, which normalizes the dopamine level.119

Dexamethasone has so far only been studied for its basic efficacy in rats. With regard to ADHD, there have been no studies on its use in humans or the effects of long-term use, which could potentially have side effects (e.g. on the immune system).

On the other hand, balancing cortisol levels that are too low in ADHD and especially in ADHD-HI - provided that only the existing deficit is compensated - could also have a positive influence in other ways.

We have developed the idea of a dexamethasone shock treatment as a hypothesis: ⇒ Dexamethasone for ADHD

8.2. Cortisol as a drug for emotional stabilization in ADHD?

In one study, the administration of 20 mg to 40 mg cortisol significantly reduced feelings of sadness, activity, alertness to acute stress and improved relaxation. Fatigue was also reduced.120

Cortisol (together with other mechanisms) influences attention, vigilance and memory.121 The hippocampus, which is responsible for memory storage and retrieval processes, has the highest cortisol receptor density in the brain.121

An administration of 10 mg cortisol before learning vocabulary significantly worsened memory recall performance. Whether this only occurred in men or also in women, who could be protected against this by their sex hormones, remains to be seen.122 People with ADHD-I react to acute stress with an increased release of cortisol. Their memory recall performance is also impaired after stress - but only in men.122

While the existing medications for ADHD (stimulants, atomoxetine, guanfacine) primarily improve attention and hyperactivity problems, we believe that they are not able to reduce internal tension as effectively. According to our hypothesis, infrequent high-dose administration of cortisol should be able to calm the HPA axis again. Long-term or regular administration, on the other hand, is detrimental because it can cause effects similar to chronic severe stress.
Due to the considerable disadvantages of corticoids that act on the mineralocorticoid receptors, only corticoids that selectively address the glucocorticoid receptors (such as dexamethasone, which addresses GR to MR in a ratio of 30:1) should be considered.

8.3. Mode of action of dexamethasone

Dexamethasone is a selective glucocorticoid receptor (GR) agonist and therefore has the effect of increasing cortisol levels.118
The cortisol receptor agonist dexamethasone promotes PACAP mRNA transcription, cell proliferation and DA synthesis, while a cortisol receptor antagonist inhibits this.123

Cortisol acts on the β-adrenoceptor -cAMP/protein kinase A (PKA) signaling pathway to facilitate the synthesis and release of norepinephrine, which binds postsynaptically to ɑ1-adrenoceptor and β-adrenoceptor. A β-adrenoceptor directly coupled to adenylate cyclase (AC) can stimulate cAMP production and trigger certain responses that can be regulated by the ɑ1-adrenoceptor. Glucocorticoid receptors, together with the ɑ1-adrenoceptor, have an influence on the β-adrenoceptor-cAMP system.124 and can activate the NE system by activating the NE group of neurons in the brainstem. GR can also regulate transcription.
The activated GR bound to the glucocorticoid response element (GRE) influences gene expression as well as transcription factors, such as NF-kB, AP-1, CREB, etc., which in turn influence the combination of cAMP and PKA regulatory subtypes that model DA neuron production and survival and regulate DA activity and secretion.125

8.4. Dexamethasone for ADHD-HI, GR antagonists for ADHD-I?

The studies that found dexamethasone to be effective as an ADHD medication used SHR rats, which are considered a typical model of ADHD-HI (with hyperactivity).
This raises the theoretical question of whether, just as the GR agonist dexamethasone could function as an active ingredient in ADHD-HI, a GR antagonist could possibly be effective in ADHD-I.

This is unlikely to be the case.

A GR antagonist would prevent the HPA axis from shutting down. However, firstly, the resilencing of the HPA axis after a stress response is usually a healthy response and secondly, it is probably not impaired in ADHD-I.

Research on the dexamethasone test in ADHD shows that problems with HPA axis deactivation correlate with levels of hyperactivity, but not inattention.
More on this under Medication for ADHD, here *⇒ Dexamethasone for ADHD.*ß

  1. Büchs (2009): Einfluss von Mirtazapin auf die Hypothalamus-Hypophysen-Nebennierenrindenachse bei depressiven Patienten; Dissertation, Seite 126 ↥

  2. Poustka, Maras, Hohm, Fellinger, Holtmann, Banaschewski, Lewicka, Schmidt, Esser, Laucht (2010): Negative association between plasma cortisol levels and aggression in a high-risk community sample of adolescents. J Neural Transm 117:621–627, n = 245 ↥

  3. Yang, Shin, Noh, Stein (2007): Cortisol is inversely correlated with aggression for those boys with attention deficit hyperactivity disorder who retain their reactivity to stress. Psychiatry Res. Sep 30; 153( 1):55-60 ↥ ↥ ↥

  4. Mannie, Harmer, Cowen (2007): Increased waking salivary cortisol levels in young people at familial risk of depression. Am J Psychiatry 164:617–621 ↥

  5. Moore B (2002): Cortisol, stress and depression. Br J Psychiatry 181:348–353 mwNw ↥

  6. Piwowarska, Wrzosek, Radziwon-Zaleska, Ryszewska-Pokrasniewicz, Skalski, Matsumoto, Biernacka-Bazyluk, Szelenberger, Pachecka (2009): Serum cortisol concentration in patients with major depression after treatment with clomipramine. Pharmacol Rep 2(61):604–611 ↥

  7. (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 ↥

  8. 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 ↥

  9. Corominas, Ramos-Quiroga, Ferrer, Saez-Francas, Palomar, Bosch, Casas (2012): Cortisol responses in children and adults with attention deficit hyperactivity disorder (ADHD): a possible marker of inhibition deficits, ADHD Atten Def Hyp Disord (2012) 4:63–75. DOI 10.1007/s12402-012-0075-59, Seite 70 ↥

  10. Fairchild (2012): Hypothalamic-pituitary-adrenocortical axis function in attention-deficit hyperactivity disorder. Curr Top Behav Neurosci. 2012;9:93-111. doi: 10.1007/7854_2010_101. ↥

  11. Henry (1997): Psychological and physiological responses to stress: the right hemisphere and the hypothalamo-pituitary-adrenal axis, an inquiry into problems of human bonding. Acta Physiol Scand Suppl. 1997;640:10-25. PMID: 9401599. REVIEW ↥

  12. Mason, Giller, Kosten, Yehuda (1990), zitiert nach Henry (1997): Psychological and physiological responses to stress: the right hemisphere and the hypothalamo-pituitary-adrenal axis, an inquiry into problems of human bonding. Acta Physiol Scand Suppl. 1997;640:10-25. PMID: 9401599. REVIEW ↥

  13. Lopez-Duran, Mayer, Abelson (2014): Modeling neuroendocrine stress reactivity in salivary cortisol: adjusting for peak latency variability. Stress. 2014 Jul;17(4):285-95. doi: 10.3109/10253890.2014.915517. ↥

  14. Vuksanovic: Traumatische Erfahrungen, Stress und ADHS. Was können wir von der Neuroendokrinologie lernen? ↥

  15. Daoust, Kotelnikova, Kryski, Sheikh, Singh, Hayden (2018). Child sex moderates the relationship between cortisol stress reactivity and symptoms over time. Comprehensive Psychiatry, 87, 161–170. doi:10.1016/j.comppsych.2018.10.009 ↥

  16. Hatzinger, Brand, Perren, von Wyl, von Klitzing, Holsboer-Trachsler (2007): Hypothalamic-pituitary-adrenocortical (HPA) activity in kindergarten children: importance of gender and associations with behavioral/emotional difficulties. J Psychiatr Res., 41(10):861-70 ↥

  17. Duan, Yuan, Zhang, Qin, Zhang, Buchanan, Wu (2013): Chronic stress exposure decreases the cortisol awakening response in healthy young men. Stress. 2013 Nov;16(6):630-7. doi: 10.3109/10253890.2013.840579. ↥

  18. Galbo (1983). Hormonal and metabolic adaptation to exercise: Disputats. Thieme Medical Publishers. ↥

  19. Porta, Emsenhuber, Petek, Purstner, Vogel, Schwaberger, Salwitsch, Korstako (1993): Detection and evaluation of persisting stress-induced hormonal disturbances by a post stress provocation test in humans; Life Sciences, Volume 53, Issue 21, 1993, Pages 1583-1589; https://doi.org/10.1016/0024-3205(93)90181-2 ↥

  20. Few, Cashmore, Turton (1980): Adrenocortical response to one-leg and two-leg exercise on a bicycle ergometer; European Journal of Applied Physiology and Occupational Physiology; August 1980, Volume 44, Issue 2, pp 167–174 ↥

  21. Brechtel (1998): Das parasympathikotone Übertrainingssyndrom – Ein Modell zur Maladaption an Streß – Diagnostik und Pathophysiologie. Dissertation. Seite 198 ↥

  22. Brechtel (1998): Das parasympathikotone Übertrainingssyndrom – Ein Modell zur Maladaption an Streß – Diagnostik und Pathophysiologie. Dissertation. Seite 198, mit weiteren Nachweisen ↥ ↥

  23. Alink, van Ijzendoorn, Bakermans-Kranenburg, Mesman, Juffer, Koot (2008): Cortisol and externalizing behavior in children and adolescents: mixed meta-analytic evidence for the inverse relation of basal cortisol and cortisol reactivity with externalizing behavior. Dev Psychobiol. 2008 Jul;50(5):427-50. doi: 10.1002/dev.20300. ↥

  24. Härfstrand, Fuxe, Cintra, Agnati, Zini, Wikstrom, Okret (1986): Glucocorticoid receptor immunoreactivity in monoaminergic neurons of rat brain. Proceedings of the National Academy of Sciences of the USA, 83, 24: 9779-9783. ↥

  25. Fuxe, Agnati, Jannsson, von-Euler, Tanganelli (1990): Regulation of endocrine function by the nicotinic cholinergic receptor. Ciba-Foundation-Symposium, pp. 127-130. ↥

  26. Bieger (2011): Neurostressguide, Seite 11 ↥ ↥

  27. Xie L, Gelfand, Mathew, Atem, Delclos, Messiah (2022): Association of Corticosteroid Use and Attention Deficit/Hyperactivity Disorder in Asthmatic Children Varies by Age. J Asthma. 2022 Jun 13:1-13. doi: 10.1080/02770903.2022.2089995. PMID: 35696551. ↥

  28. Budziszewska, Basta-Kaim, Kubera, Lasoń (2010); [Immunological and endocrinological pattern in ADHD etiopathogenesis]. Przeglad Lekarski [01 Jan 2010, 67(11):1200-1204], PMID:21442976 ↥ ↥

  29. Ibrahim, Xie, Strong, Tonello, Berta, Zhang (2018): Mineralocorticoid Antagonist Improves Glucocorticoid Receptor Signaling and Dexamethasone Analgesia in an Animal Model of Low Back Pain. Front Cell Neurosci. 2018;12:453. doi:10.3389/fncel.2018.00453 ↥

  30. Shansky, Lipps (2013): Stress-induced cognitive dysfunction: hormone-neurotransmitter interactions in the prefrontal cortex. Front. Hum. Neurosci. 7, 123. http://dx.doi.org/10.3389/fnhum.2013.00123 ↥

  31. Scassellati, Bonvicini, Faraone, Gennarelli (2012). Biomarkers and attention-deficit/hyperactivity disorder: a systematic review and meta-analyses. J Am Acad Child Adolesc Psychiatry. 2012 Oct;51(10):1003-1019.e20. doi: 10.1016/j.jaac.2012.08.015. PMID: 23021477. ↥

  32. Corominas, Ramos-Quiroga, Ferrer, Sáez-Francàs, Palomar G, Bosch, Casas (2012): Cortisol responses in children and adults with attention deficit hyperactivity disorder (ADHD): a possible marker of inhibition deficits. Atten Defic Hyperact Disord. 2012 Jun;4(2):63-75. doi: 10.1007/s12402-012-0075-5. PMID: 22576746. ↥

  33. Kamradt, Momany, Nikolas (2017): A meta-analytic review of the association between cortisol reactivity in response to a stressor and attention-deficit hyperactivity disorder. Atten Defic Hyperact Disord. 2018 Jun;10(2):99-111. doi: 10.1007/s12402-017-0238-5. ↥

  34. van der Knaap, Oldehinkel, Verhulst, van Oort, Riese (2015): Glucocorticoid receptor gene methylation and HPA-axis regulation in adolescents. The TRAILS study. Psychoneuroendocrinology. 2015 Aug;58:46-50. doi: 10.1016/j.psyneuen.2015.04.012. PMID: 25951242. ↥

  35. Shin, Lee (2007): Blunted hypothalamo-pituitary-adrenal axis reactivity is associated with the poor intelligence; Performance in children with attention-deficit/hyperactivity disorder. Neuropediatrics., 38(6):298-303 ↥

  36. King, Barkley, Barrett (1998) Attention-Deficit Hyperactivity Disorder and the Stress Response. Biol Psychiatry 73 , 44:72-74; n = 20 ↥

  37. Hong HJ, Shin DW, Lee EH, Oh YH, Noh KS (2003): Hypothalamic-pituitary-adrenal reactivity in boys with attention deficit hyperactivity disorder. Yonsei Med J. 2003 Aug 30;44(4):608-14. doi: 10.3349/ymj.2003.44.4.608. PMID: 12950115. ↥

  38. Lee, Shin, Stein (2010): Increased cortisol after stress is associated with variability in response time in ADHD children. Yonsei Med J 51:206–211 ↥

  39. Ünsel-Bolat, Ercan, Bolat, Süren, Bacanlı, Yazıcı, Rohde (2019): Comparisons between sluggish cognitive tempo and ADHD-restrictive inattentive presentation phenotypes in a clinical ADHD sample. Atten Defic Hyperact Disord. 2019 Mar 25. doi: 10.1007/s12402-019-00301-y. n = 155 ↥

  40. Palma, Fernandes, Muszkat, Calil (2012): The response to stress in Brazilian children and adolescents with attention deficit hyperactivity disorder. Psychiatry Res. 2012 Aug 15;198(3):477-81. doi: 10.1016/j.psychres.2011.10.016. n = 76 ↥

  41. Palma, Natale, Calil (2015): A four-year follow-up controlled study of stress response and symptom persistence in Brazilian children and adolescents with attention deficit disorder and hyperactivity (ADHD). Psychiatry Res. 2015 Dec 15;230(2):227-32. doi: 10.1016/j.psychres.2015.08.044. n = 59 ↥

  42. van West, Claes, Deboutte (2009): Differences in hypothalamic-pituitary-adrenal axis functioning among children with ADHD predominantly inattentive and combined types. Eur Child Adolesc Psychiatry. 2009 Mar 18. ↥

  43. Maldonado, Trianes, Cortes, Moreno, Escobar (2009): Salivary cortisol response to a psychosocial Stressor on children diagnosed with attention-deficit/hyperactivity disorder: differences between diagnostic subtypes. Span J Psychol. 2009 Nov;12(2):707-14. n = 33 ↥

  44. Lackschewitz, Hüther, Kröner-Herwig (2008): Physiological and psychological stress responses in adults with attentiondeficit/hyperactivity disorder (ADHD). Psychoneuroendocrinology; 33:612–624, n = 36 ↥

  45. Raz, Leykin (2015): Psychological and cortisol reactivity to experimentally induced stress in adults with ADHD. Psychoneuroendocrinology. 2015 Oct;60:7-17. doi: 10.1016/j.psyneuen.2015.05.008. n = 49 ↥

  46. Lane, Reynolds, Thacker (2010): Sensory Over-Responsivity and ADHD: Differentiating Using Electrodermal Responses, Cortisol, and Anxiety. Front Integr Neurosci. 2010 Mar 29;4:8. doi: 10.3389/fnint.2010.00008. eCollection 2010. ↥

  47. Corominas-Roso, Palomar, Ferrer, Real, Nogueira, Corrales, Casas, Ramos-Quiroga (2015): Cortisol Response to Stress in Adults with Attention Deficit Hyperactivity Disorder.Int J Neuropsychopharmacol. 2015 Mar 17;18(9). pii: pyv027. doi: 10.1093/ijnp/pyv027, n = 121 ↥ ↥

  48. West, Glaes, Deboutte (2009): Differences in hypothalamic-pituitary-adrenal axis functioning among children with ADHD predominantly inattentive and combined types. Eur Child Adolesc Psychiatry. 2009 Mar 18. ↥

  49. Vogel, Bijlenga, Verduijn, Bron, Beekman, Kooij, Penninx (2018): Attention-deficit/hyperactivity disorder symptoms and stress-related biomarkers. Psychoneuroendocrinology. 2017 May;79:31-39. doi: 10.1016/j.psyneuen.2017.02.009. ↥ ↥ ↥

  50. Gordis, Granger, Susman, Trickett (2006): Asymmetry between salivary cortisol and alpha-amylase reactivity to stress: relation to aggressive behavior in adolescents. Psychoneuroendocrinology. 2006 Sep;31(8):976-87.. n = 67 ↥

  51. Northover, Thapar, Langley, Fairchild, van Goozena (2016): Cortisol levels at baseline and under stress in adolescent males with attention-deficit hyperactivity disorder, with or without comorbid conduct disorder; Psychiatry Res. 2016 Aug 30; 242: 130–136; doi: 10.1016/j.psychres.2016.05.052; PMCID: PMC4986851 ↥ ↥

  52. Snoek, Van Goozen, Matthys, Buitelaar, van Engeland (2004).Stress responsivity in children with externalizing behavior disorders. Dev Psychopathd 16(2): 389-406. ↥

  53. Christiansen, Oades, Psychogiou, Hauffa, Sonuga-Barke (2010): Does the cortisol response to stress mediate the link between expressed emotion and oppositional behavior in Attention-Deficit/Hyperactivity-Disorder (ADHD)? Behav Brain Funct 6:45 ↥ ↥

  54. 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 ↥

  55. Van de Wiel, Van Goozen, Matthys, Snoek, Van Engeland (2004): Cortisol and treatment effect in children with disruptive behavior disorders: A preliminary study. Journal of the American Academy of Child and Adolescent Psychiatry, 43, 1011–1018. n = 22 ↥

  56. Fairchild, van Goozen, Stollery, Brown, Gardiner, Herbert, Goodyer (2008): Cortisol diurnal rhythm and stress reactivity in male adolescents with early-onset or adolescence-onset conduct disorder. Biol Psychiatry. 2008 Oct 1;64(7):599-606. doi: 10.1016/j.biopsych.2008.05.022 ↥

  57. Abelson, Curtis, Cameron (1996): Hypothalamic-pituitary-adrenal axis activity in panic disorder: Effects of alprazolam on 24 h secretion of adrenocorticotropin and cortisol, Journal of Psychiatric Research, Volume 30, Issue 2, March–April 1996, Pages 79-93, zitiert nach Park, Jung, Park, Yang, Kim (2018): Melatonin inhibits attention-deficit/hyperactivity disorder caused by atopic dermatitis-induced psychological stress in an NC/Nga atopic-like mouse model. Sci Rep. 2018 Oct 8;8(1):14981. doi: 10.1038/s41598-018-33317-x. ↥

  58. Randazzo, Dockray, Susman (2008): The stress response in adolescents with inattentive type ADHD symptoms; Child Psychiatry Hum Dev. 2008 Mar;39(1):27-38. ↥

  59. Pesonen, Kajantie, Heinonen, Pyhala, Lahti, Jones, Matthews, Eriksson, Strandberg, Raikkonen (2012): Sex-specific associations between sleep problems and hypothalamic–pituitary–adrenocortical axis activity in children. Psychoneuroendocrinology 37:238–248 ↥ ↥

  60. Pesonen, Kajantie, Jones, Pyhälä, Lahti, Heinonen, Eriksson, Strandberg, Räikkönen (2011): Symptoms of attention deficit hyperactivity disorder in children are associated with cortisol responses to psychosocial stress but not with daily cortisol levels, Journal of Psychiatric Research, Volume 45, Issue 11, 2011, Pages 1471-1476, ISSN 0022-3956, https://doi.org/10.1016/j.jpsychires.2011.07.002. ↥

  61. Tyrka, Wier, Anderson, Wilkinson, Price, Carpenter (2007): Temperament and response to the Trier Social Stress Test; Published in final edited form as: Acta Psychiatr Scand. 2007 May; 115(5): 395–402; doi: 10.1111/j.1600-0447.2006.00941.x; PMCID: PMC4469468; NIHMSID: NIHMS698884 ↥

  62. Tyrka, Wier, Price, Rikhye, Ross, Anderson, Wilkinson, Carpenter (2008): Cortisol and ACTH Responses to the Dex/CRH Test: Influence of Temperament; Horm Behav. 2008 Apr; 53(4): 518–525; doi: 10.1016/j.yhbeh.2007.12.004; PMCID: PMC2637444; NIHMSID: NIHMS45728 ↥ ↥

  63. Hirvikoski, Lindholm, Nordenström, Nordström, Lajic (2009): High self-perceived stress and many stressors, but normal diurnal cortisol rhythm, in adults with ADHD (attention-deficit/hyperactivity disorder). Horm Behav 55:418–424, n = 56 ↥

  64. Hastings, Fortier, Utendale, Simard, Robaey (2009): Adrenocortical Functioning in Boys with Attention-Deficit/Hyperactivity Disorder: Examining Subtypes of ADHD and Associated Comorbid Conditions. J Abnorm Child Psychol 37:565-578 ↥

  65. Angeli, Korpa, Johnson, Apostolakou, Papassotiriou, Chrousos, Pervanidou (2018):Salivary cortisol and alpha-amylase diurnal profiles and stress reactivity in children with Attention Deficit Hyperactivity Disorder. Psychoneuroendocrinology. 2018 Apr;90:174-181. doi: 10.1016/j.psyneuen.2018.02.026. ↥ ↥ ↥ ↥ ↥

  66. McCarthy, Hanrahan, Scott, Zemblidge, Kleiber, Zimmerman (2011): Salivary cortisol responsivity to an intravenous catheter insertion in children with attention-deficit/hyperactivity disorder. J Pediatr Psychol. 2011 Sep;36(8):902-10. doi: 10.1093/jpepsy/jsr012. n = 29 AD(H)S-Betroffene und 339 Kontrollprobanden ↥

  67. Blomqvist, Holmberg, Lindblad, Fernell, Ek, Dahllöf (2007): Salivary cortisol levels and dental anxiety in children with attention deficit hyperactivity disorder. European Journal of Oral Sciences, 115 (1), S. 1–6 ↥ ↥

  68. Angeli, Korpa, Johnson, Apostolakou, Papassotiriou, Chrousos, Pervanidou (2018):Salivary cortisol and alpha-amylase diurnal profiles and stress reactivity in children with Attention Deficit Hyperactivity Disorder. Psychoneuroendocrinology. 2018 Apr;90:174-181. doi: 10.1016/j.psyneuen.2018.02.026. n = 102 ↥

  69. Blomqvist M, Holmberg K, Lindblad F, Fernell E, Ek U, Dahllöf G (2007): Salivary cortisol levels and dental anxiety in children with attention deficit hyperactivity disorder. Eur J Oral Sci. 2007 Feb;115(1):1-6. doi: 10.1111/j.1600-0722.2007.00423.x. PMID: 17305710. ↥

  70. Llorens M, Barba M, Torralbas-Ortega J, Nadal R, Armario A, Gagliano H, Urraca L, Pujol S, Montalvo I, Gracia R, Polo D, González-Riesco L, Matalí JL, Palao D, Pàmias M, Labad J (2023): Relationship between hair cortisol concentrations and cognitive functioning in adolescents with ADHD. Eur J Psychotraumatol. 2023;14(2):2281752. doi: 10.1080/20008066.2023.2281752. PMID: 38154075. ↥ ↥

  71. Schloß, Ruhl, Müller, Becker, Skoluda, Nater, Pauli-Pott (2018): Low hair cortisol concentration and emerging attention-deficit/hyperactivity symptoms in preschool age. Dev Psychobiol. 2018 Mar 23. doi: 10.1002/dev.21627., n = 125 ↥

  72. Pauli-Pott, Schloß, Ruhl, Skoluda, Nater, Becker (2017):. Hair cortisol concentration in preschoolers with attention-deficit/hyperactivity symptoms-Roles of gender and family adversity. Psychoneuroendocrinology. 2017 Dec;86:25-33. doi: 10.1016/j.psyneuen.2017.09.002. PMID: 28910602. ↥

  73. Ferro, Gonzalez (2020): Hair cortisol concentration mediates the association between parent and child psychopathology. Psychoneuroendocrinology. 2020 Apr;114:104613. doi: 10.1016/j.psyneuen.2020.104613. PMID: 32088544. ↥

  74. Mann, Schloß, Cosan, Becker, Skoluda, Nater, Pauli-Pott (2021): Hair cortisol concentration and neurocognitive functions in preschool children at risk of developing attention deficit hyperactivity disorder. Psychoneuroendocrinology. 2021 Jun 12;131:105322. doi: 10.1016/j.psyneuen.2021.105322. PMID: 34175557. n = 122 ↥

  75. Jue H, Fang-Fang L, Dan-Fei C, Nuo C, Chun-Lu Y, Ke-Pin Y, Jian C, Xiao-Bo X (2023): A bidirectional Mendelian randomization study about the role of morning plasma cortisol in attention deficit hyperactivity disorder. Front Psychiatry. 2023 Jun 14;14:1148759. doi: 10.3389/fpsyt.2023.1148759. PMID: 37389173; PMCID: PMC10303788. ↥

  76. Ma, Chen, Chen, Liu, Wang (2011): The function of hypothalamus-pituitary-adrenal axis in children with ADHD. Brain Res. 2011 Jan 12;1368:159-162. doi: 10.1016/j.brainres.2010.10.045. n = 158 ↥ ↥

  77. Shin, Lee (2007): Blunted hypothalamo-pituitary-adrenal axis reactivity is associated with the poor intelligence performance in children with attention-deficit/hyperactivity disorder. Neuropediatrics, 38 (6), S. 298–303 ↥

  78. Kariyawasam, Zaw, Handley (2002): Reduced salivary cortisol in children with comorbid attention deficit hyperactivity disorder and oppositional defiant disorder. Neuro Endocrinol Lett 23: 45–48 ↥

  79. Chen, Chen, Liu, Lin, Wei, Chen (2009): [Function of the hypothalamus-pituitary-adrenal axis in children with attention deficit hyperactivity disorder].[Article in Chinese].Zhongguo Dang Dai Er Ke Za Zhi. 2009 Dec;11(12):992-5. n = 128 ↥

  80. Vuksanovic (2013): Die Aktivität der Hpothalamus-Hypophysen-Nebennierenrinden-Achse bei Aufmerksamkeits-Defizit und Hyperaktivitäts-Störung, Dissertation, Seite 64 ↥

  81. Ramos-Quiroga, Corominas-Roso, Palomar, Ferrerd, Valero, Corrales, Richarte, Casas (2016): Cortisol awakening response in adults with attention deficit hyperactivity disorder: Subtype differences and association with the emotional lability; European Neuropsychopharmacology, Volume 26, Issue 7, July 2016, Pages 1140-1149, https://doi.org/10.1016/j.euroneuro.2016.03.014 ↥

  82. Isaksson, Nilsson, Lindblad (2015): The Pressure-Activation-Stress scale in relation to ADHD and cortisol. Eur Child Adolesc Psychiatry. 2015 Feb;24(2):153-61. doi: 10.1007/s00787-014-0544-9. n = 248 ↥

  83. Poustka, Maras, Hohm, Fellinger, Holtmann, Banaschewski, Lewicka, Schmidt, Esser, Laucht (2010): Negative association between plasma cortisol levels and aggression in a high-risk community sample of adolescents. J Neural Transm 117:621–627, n = 245 ↥

  84. Freitag, Hänig, Palmason, Meyer, Wüst, Seitz (2009): Cortisol awakening response in healthy children and children with ADHD: Impact of comorbid disorders and psychosocial risk factors. Psychoneuroendocrinology, 34 (7), S. 1019–28. ↥

  85. Snoek, Van Goozen, Matthys, Buitelaar, van Engeland (2004): Stress responsivity in children with externalizing behavior disorders. Dev Psychopathol. 2004;16(2):389-406. doi:10.1017/s0954579404044578 ↥

  86. Hastings, Fortier, Utendale, Simard, Robaey (2009): Adrenocortical functioning in boys with AttentionDeficit/Hyperactivity Disorder: Examining subtypes of ADHD and associated comorbid conditions. Journal of Abnormal Child Psychology, 37, S. 565–578. ↥

  87. Schulz, Halperin, Newcorn, Sharma, Gabriel (1997): Plasma cortisol and aggression in boys with ADHD; J Am Acad Child Adolesc Psychiatry. 1997 May;36(5):605-9., n = 50 ↥

  88. Pauli-Pott U, Skoluda N, Nater UM, Becker K, Derz F, Kaspar E, Kasperzack D, Kehm K, Kött M, Mann C, Schurek P, Pott W, Schloß S (2023): Long-term cortisol secretion in attention deficit hyperactivity disorder: roles of sex, comorbidity, and symptom presentation. Eur Child Adolesc Psychiatry. 2023 Mar 14. doi: 10.1007/s00787-023-02180-1. PMID: 36917355. ↥

  89. Tyrka, Wier, Anderson, Wilkinson, Price, Carpenter (2007): Temperament and response to the Trier Social Stress Test; Acta Psychiatr Scand. 2007 May; 115(5): 395–402; doi: 10.1111/j.1600-0447.2006.00941.x; PMCID: PMC4469468; NIHMSID: NIHMS698884 ↥ ↥

  90. Berens A, LeMoult J, Kircanski K, Gotlib IH (2022): ADHD symptoms and diurnal cortisol in adolescents: The importance of comorbidities. Psychoneuroendocrinology. 2022 Nov 26;148:105990. doi: 10.1016/j.psyneuen.2022.105990. PMID: 36462296. n = 138 ↥

  91. Vuksanovic (2013): Die Aktivität der Hpothalamus-Hypophysen-Nebennierenrinden-Achse bei Aufmerksamkeits-Defizit und Hyperaktivitäts-Störung, Dissertation, Seite 64; kleine Probandenzahl: n = 19 ↥

  92. Kaneko, Hoshino, Hashimoto, Okano, Kumashiro (1993): Hypothalamic-pituitary-adrenal axis function in children with attention-deficit hyperactivity disorder. J Autism Dev Disord 23:59–65 ↥

  93. De Bellis, Chrousos, Dorn, Burke, Helmers, Kling, Trickett, Putman (1994): Hypothalamic–pituitary–adrenal axis dysregulation in sexually abused girls. J. Clin. Endocrinol. Metab. 78, 249–255, n = 26 ↥

  94. Tarullo, Gunnar (2006): Child maltreatment and the developing HPA axis. Horm. Behav. 50: 632-639 ↥

  95. Massey, Lerner, Holmes, Scott, Hernan, (2016):ACTH Prevents Deficits in Fear Extinction Associated with Early Life Seizures; Front Neurol. 2016; 7: 65. doi: 10.3389/fneur.2016.00065; PMCID: PMC4852169 ↥

  96. Ladd, Owens, Nemeroff (1996): Persistent changes in corticotropin-releasing factor neuronal systems induced by maternal deprivation. Endocrinology 1996; 137: 1212–18. ↥

  97. Egle, Joraschky, Lampe, Seiffge-Krenke, Cierpka (2016): Sexueller Missbrauch, Misshandlung, Vernachlässigung – Erkennung, Therapie und Prävention der Folgen früher Stresserfahrungen; 4. Aufl., Schattauer, S. 48 ↥

  98. 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. ↥

  99. Coplan, Andrews, Rosenblum, Owens, Friedman, Gorman, Nemeroff (1996): Persistent elevations of cerebrospinal fluid concentrations of corticotropin-releasing factor in adult nonhuman primates exposed to early-life stressors: implications for the patho-physiology of mood and anxiety disorders. Proc Natl Acad Sci 1996; 93: 1619–23. ↥

  100. Coplan, Smith, Altemus, Scharf, Owens, Nemeroff, Gorman, Rosenblum (2001): Variable foraging demand rearing: sustained elevations in cisternal cerebrospinal fluid corticotropin-releasing factor concentration in adult primates. Biol Psychiatry 2001; 50: 200–4. ↥

  101. Rensing, Koch, Rippe, Rippe (2006): Mensch im Stress; Psyche, Körper Moleküle; Elsevier (jetzt Springer), Seiten 120, 151 ↥

  102. Holsboer (2001): Stress, hypercortisolism and corticosteroid receptors in depression: implications for therapy. J Affect Disord. 2001 Jan;62(1-2):77-91. ↥

  103. Miller, Ancoli-Israel, Bower, Capuron, Irwin (2008): Neuroendocrine-Immune Mechanisms of Behavioral Comorbidities in Patients With Cancer; J Clin Oncol. 2008 Feb 20; 26(6): 971–982. doi: 10.1200/JCO.2007.10.7805, PMCID: PMC2770012, NIHMSID: NIHMS147295 ↥

  104. Elliott, Gili, Limor, Neufeld-Cohen (2010): Resilience to social stress coincides with functional DANN methylation of the CRF gene in adult mice. Nat Neurosci 2010; 13: 1351–53. ↥

  105. Nater, La Marca, Florin, Koller, Ehlert (2003): The relationship between salivary alpha-amylase and plasma catecholamines. Journal of Psychophysiology. ↥

  106. Nater, Rohleder, Gaab, Berger, Jud, Kirschbaum, Ehlert (2003). Alpha-Amylase im Speichel als biologischer Indikator einer psychosozialen Stressreaktion. Verhaltenstherapie, 13 (Suppl. 1), 42. ↥

  107. Nater, Rohleder, Gaab, Berger, Jud, Kirschbaum, Ehlert (2003): Alpha-Amylase in saliva as a useful indicator of autonomic stress reaction. Psychosomatic Medicine, 65 (1), 28. ↥

  108. Nater, Rohleder, Gaab, Berger, Jud, Kirschbaum, Ehlert (2005): Reactivity of human salivary alpha-amylase in a psychosocial stress paradigm. Journal of Psychophysiology. ↥

  109. Reinhardt (2007): Endokrinologische Veränderungen (Cortisol und Amylase) im Speichel bei akutem und chronischem Stress während einer stationären Psychotherapie; Dissertation; Seite 83; n = 75 ↥

  110. Engert, Vogel, Efanov, Duchesne, Corbo, Ali, Pruessner (2011): Investigation into the cross-correlation of salivary cortisol and alpha-amylase responses to psychological stress; Psychoneuroendocrinology (2011) 36, 1294—1302; n = 50 ↥

  111. Vogel, Bijlenga, Verduijn, Bron, Beekman, Kooij, Penninx (2017): Attention-deficit/hyperactivity disorder symptoms and stress-related biomarkers. Psychoneuroendocrinology. 2017 May;79:31-39. doi: 10.1016/j.psyneuen.2017.02.009. n = 2307 ↥

  112. Kaneko, Hoshino, Hashimoto, Okano, Kumashiro (1993): Hypothalamic-pituitary-adrenal axis function in children with attention-deficit hyperactivity disorder; Journal of Autism and Developmental Disorders; March 1993, Volume 23, Issue 1, pp 59–65 ↥

  113. Gispen-de Wied, Jansen, Wynne, Matthys, van der Gaag, Thijssen, van Engeland (1998): Differential effects of hydrocortisone and dexamethasone on cortisol suppression in a child psychiatric population. Psychoneuroendocrinology. 1998 Apr;23(3):295-306. ↥

  114. Steingard, Biederman, Keenan, Moore (1990): Comorbidity in the interpretation of dexamethasone suppression test results in children: a review and report. Biol Psychiatry. 1990 Aug 1;28(3):193-202. ↥

  115. Chen, Zheng, Xie, Huang, Ke, Zheng, Lu, Hu (2017): Glucocorticoids/glucocorticoid receptors effect on dopaminergic neurotransmitters in ADHD rats. Brain Res Bull. 2017 May;131:214-220. doi: 10.1016/j.brainresbull.2017.04.013. ↥

  116. Lu, Zhang, Hong, Wang, Huang, Zheng, Chen (2018): [Effect of glucocorticoid receptor function on the behavior of rats with attention deficit hyperactivity disorder] [Article in Chinese]; Zhongguo Dang Dai Er Ke Za Zhi. 2018 Oct;20(10):848-853. ↥

  117. Brocca, Pietranera, de Kloet, De Nicola (2018): Mineralocorticoid Receptors, Neuroinflammation and Hypertensive Encephalopathy. Cell Mol Neurobiol. 2018 Aug 16. doi: 10.1007/s10571-018-0610-9. ↥

  118. Chen, Zheng, Xie, Huang, Ke, Zheng, Lu, Hu (2017): Glucocorticoids/glucocorticoid receptors effect on dopaminergic neurotransmitters in ADHD rats; Brain Research Bulletin; Volume 131, May 2017, Pages 214-220 ↥ ↥

  119. Roozendaal, Williams, McGaugh (1999): Glucocorticoid receptor activation in the rat nucleus of the solitary tract facilitates memory consolidation: Involvement of the basolateral amygdala. Eur J Neurosci, 11:1317-1323 ↥

  120. Reuter (2002); Impact of Cortisol on Emotions under Stress and Nonstress Conditions: A Pharmacopsychological Approach. Neuropsychobiology 2002;46:41-48, n = 100 ↥

  121. Kirschbaum (2001): Das Stresshormon Cortisol – Ein Bindeglied zwischen Psyche und Soma? in: Jahrbuch der Heinrich-Heine-Universität Düsseldorf, 2001, 150-156 ↥ ↥

  122. Kirschbaum (2001): Das Stresshormon Cortisol – Ein Bindeglied zwischen Psyche und Soma? in: Jahrbuch der Heinrich-Heine-Universität Düsseldorf, 2001, 150-156, mwNw ↥ ↥

  123. McArthur, McHale, Dalley, Buckingham, Gillies (2005): Altered mesencephalic dopaminergic populations in adulthood as a consequence of brief perinatal glucocorticoid exposure. Journal of Neuroendocrinology 17(8):475-82 · September 2005 ↥

  124. Kassel, Herrlich (2002): Crosstalk between the glucocorticoid receptor and other transcription factors: molecular aspects. Mol Cell Endocrinol. 2007 Sep 15;275(1-2):13-29. ↥

  125. Yang, Tsao, Li, Wu, Hsu, Cheng (2007): Changes of dopamine content and cell proliferation by dexamethsone via pituitary adenylate cyclae-activating polypeptide in PC12 cell. Neurosci Lett, 426(1):45-48. ↥

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