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Aggression in ADHD - Neurophysiological correlates


Aggression in ADHD - Neurophysiological correlates

A distinction must be made between hot (impulsive) and cold (considered) aggression.

Aggression is controlled in the brain by a system of brain regions working together.

The determining neurotransmitters are testosterone, cortisol and serotonin. A high testosterone value with a simultaneously low cortisol value promotes aggression. A low serotonin level promotes impulsivity, which also promotes aggression. A low dopamine level also promotes aggression, although it must be questioned in which brain regions a reduced dopamine level causes this, since dopamine levels are not the same throughout the brain.

1. The 2 types of aggression

There are two types of aggression:

1.1. Hot (reactive) aggression

  • Defensive reaction when attacked by self or other member of the group
  • Reactive, impulsive affect-driven aggression1
  • Signs of anger, activates sympathetic nervous system
  • Involved brain region: dorsal part of the central cavernous gray (periaqueductal gray)
  • Decreased serotonin level2
  • Overreactivity of the amygdala3

1.2. Cold (proactive) aggression

  • Reaction to attacks of a different kind
  • Also called purposeful, proactive or instrumental aggression1
  • Prey behavior
  • No anger/rage signs, efficient attack, no sympathetic activation
  • Involved brain region: ventral part of the central cavernous gray
  • Is associated with reduced emotionality (callous unemotional traits, reduced empathy)3
  • No decreased serotonin level2
  • Reduced reactivity of the amygdala3

Aggression must always be distinguished from dominance behavior.

Aggression in ADHD is quite typically hot aggression. Aggression correlates with ADHD-HI and ADHD-C, less so with ADHD-I.
Cold aggression is not a typical ADHD symptom.

That aggression and impulsivity are distinct constructs is also evident in mice with an Adgrl3 gene defect, which show increased impulsivity and decreased aggression.4

2. Aggression brain system

Aggression is significantly regulated in the brain by an interaction of several brain regions:5

  • Hypothalamus
  • Amygdala
  • Orbitofrontal cortex (OFC)
  • Central cave gray (periaqueductal gray, PAG)

Both types of aggression are activated by different stimulation of the periaqueductal gray (central cavernous gray) in the midbrain. The gating is done by hypothalamus and amygdala, while the control is done by the PFC.6

Androgen receptors that bind the androgenic steroid hormones testosterone and dihydrotestosterone are commonly found in7

  • Amygdala
  • Hippocampus
  • Cerebral cortex

Testosterone (especially in conjunction with low cortisol levels) increases responses in the brain’s aggression system (especially in the amygdala) to angry faces shown.89 Amygdalar activity can be predicted (among other things) by salivary testosterone levels and a specific adrenoreceptor gene polymorphism.10

A high cortisol response, on the other hand, dampens the amygdala because cortisol, which is secreted at the end of the HPA axis response, not only inhibits the HPA axis but also slows down the HPG axis, at the end of which testosterone is secreted. Thus, an acute high exogenous cortisol level has the result of reducing aggression and anxiety.1

Impulsive-aggressive sufferers exhibit reduced connectivity between the amygdala and PFC.1112
Neurofeedback could be suitable to improve such connectivities.

Reactive aggression in ADHD correlated with high activity in:13

  • right insula
  • Hippocampus
  • middle and upper frontal areas

3. Aggression inhibition by serotonin

Serotonin cannot cross the blood-brain barrier. The following illustration concerns only serotonin in the brain.

Aggression inhibition is mediated by the PFC via serotonin at 5-HT1A and 5-HT1B serotonin receptors.
High serotonin levels in the PFC cause low aggression. High serotonin levels reduce aggression and impulsivity.1415161718

In male prisoners, aggression correlated with:19

  • Tryptophan serum level decreased
  • Kynurenine serum level decreased
  • 5-HT serum level increased
  • 5-HT/(Trp∗1000) ratio increased
    • Correlated with the number of severely aggressive acts (r=0.593, P<0.001)
  • Impulsivity increased
  • ADHD symptoms increased
  • IQ decreased
  • Global function values reduced
  • Mood disorders more common
  • Substance abuse/dependence more common
  • Borderline more often
  • Conduct disorder more often (Conduct disorder)
  • Antisocial behavior more often

Especially the 3 features

  • 5-HT/(Trp∗1000) ratio increased
  • Antisocial behavior increased
  • Global function values reduced

were (jointly) predictors of aggressive behavior. The model combining these three predictors had an area under the ROC curve of 0.851 (95% CI 0.806-0.895).

Zuckermann’s theory that impulsivity is accompanied by increased dopamine levels, however, does not seem to be confirmed. Rather, Cloninger’s theory seems to be confirmed, according to which impulsivity is promoted by low serotonin and low dopamine levels.20 According to the inverse-U theory, according to which excessive as well as reduced neurotransmitter levels cause almost identical deficits in the respective brain region, these two theories are not mutually exclusive.

Low serotonin levels also correlate with lower social skills.
Destruction of the raphe nuclei, where serotonin is produced in the brain, causes indirect triggering of aggression via serotonin deficiency in the PFC, which is now unable to inhibit aggression and impulsivity due to lack of serotonin.

The euphoric and hallucinogenic effects of serotonin agonists such as LSD are mediated by activation of 5-HT2A receptors.21

Reduced numbers of (2A) serotonin transporters have been found in impulsive-aggressive men as well as women.222324 For more on this, see Montova et al.25

4. Aggression as a result of high testosterone/cortisol ratio

A high ratio of testosterone to cortisol is thought to promote the emergence of hot aggression (reactive, impulsive, affect-driven aggression), whereas serotonin modulates between hot and cold aggression (cold: goal-directed aggression).126

Testosterone is the hormone of the last stage of the hypothalamic-pituitary-gonodal (HPG) axis, while cortisol is the hormone of the last stage of the hypothalamic-pituitary-adrenocortical (HPA) axis. These two stress axes influence each other by inhibiting each other.27

Cortisol inhibits all stages of the HPG axis. Testosterone inhibits the HPA axis only at the (first) stage of the hypothalamus.282927

This mutual interaction of the HPG and HPA axes easily swings toward a dominance of one of the two hormone systems (cortisol or testosterone). However, HPG dominance is much more common in men because the production of sex hormones (such as testosterone) is controlled solely by the HPG axis in men, whereas in women they are produced approximately in half by the HPG axis and the adrenal cortex (HPA axis),30 so the significance of this issue in women is considerably less.

A prolonged ratio of high testosterone to low cortisol further causes expression of genes that promote social aggression while impairing cortical control.2

Since basal cortisol levels are on average somewhat more depressed in ADHD-HI (with hyperactivity) than in ADHD-I, whereas the cortisol response to acute stress is often flattened in ADHD-HI and very often elevated in ADHD-I, testosterone levels elevated by a particularly low cortisol level could possibly explain sex addiction developing in ADHD-HI sufferers. According to this hypothesis, sex addiction would occur less frequently in ADHD-I.

High cortisol causes CRH gene expression in the amygdala, which promotes anxiety/anxiety and social phobia.3132 In line with this, high cortisol responses are associated with internalizing stress phenotypes (e.g., ADHD-I, more frequent anxiety) and low cortisol responses are associated with externalizing stress phenotypes (e.g., ADHD-HI, less frequent anxiety).

D-amphetamine medications such as lisdexamfetamine medications (Elvanse) increase cortisol levels but not testosterone levels.33

Increased were

  • Glucocorticoids (as caused by methylphenidate)
    • Cortisol
    • Cortisone
    • Corticosterone
    • 11-dehydrocorticosterone,
    • 11-Deoxycortisol
  • The androgens
    • Dehydroepiandrosterone
    • Dehydroepiandrosterone sulfate,
    • Δ4-androstene-3,17-dione (androstenedione)
  • Progesterone (this only in men)


  • Mineralocorticoids
    • Aldosterone
    • 11-Deoxycorticosterone
  • The androgen
    • Testosterone

An increase in plasma glucocorticoid levels by guanfacine is likely.34 Studies on the effect of guanfacine on testosterone levels are not yet known to us.

Stimulants (methylphenidate and amphetamine drugs) decrease the concentration of androgens.
There is a correlation between ADHD-HI and a polymorphism of the androgen receptor gene leading to its higher expression.35

An increase in testosterone levels alleviates depression. This also affects patients with normal testosterone levels.36

5. Aggression, adrenaline and noradrenaline

  • Aggression and outward anger correlate with elevated norepinephrine37
  • Anxiety, on the other hand, correlates with increased adrenaline37

6. Irritability and dopamine

Low dopaminergic activity in the PFC is thought to be a predictor of irritability.38

7. Behavioral correlates of aggression

Aggression correlates with

  • High urge for reward39
  • Low sensitivity to punishment (prototypical for psychopathy)3940
  • Novelty seeking41
  • One large study compared the correlation of various symptoms with aggressiveness.42
    Externalizing symptoms showed here a significantly higher correlation to aggression than internalizing symptoms, which, however, may well be present alongside aggression.
    Correlation to aggressiveness (descending):
    • Emotional reactivity: 65 %
    • Rule breaks: 63 %
    • Social problems: 60 %
    • Emotional lability: 51 %
    • Hyperactivity with impulsivity: 51 %
    • ADHD: 45 %
      Here, ADHD-HI and ADHD-I do not seem to have been considered separately. If they were considered separately, we would expect a significantly increased correlation with ADHD-HI and a significantly decreased correlation with ADHD-I.
    • Hyperactivity: 43 %
    • ODD: 43 %
    • Anxious-depressive: 43 %
    • Seclusion: 42 %
    • Cognitive problems / thinking disorders: 42 %
    • Inattention 39 % to 54
      Inattention seems to be independent of externalizing or internalizing tendencies. Thus, it exists equally strongly in both ADHD-HI and ADHD-I.
    • Autism spectrum disorder: 38 %
    • Sleep problems: 38 %
    • Withdrawn-depressed: 38 %
    • Fear: 37 %43
    • Somatic complaints: 30 %
    • Physical coordination problems (gross/fine motor skills): 30%
    • Depression 27.5
    • Emotional-anxious: 26 %
    • Peer problems (social problems in the group): 24 %
    • Social phobia 14 %
    • OCD / Coercion: 11 %
    • Social isolation: 11 %
    • Dependency: 4%
    • Prosocial behavior: -25% (minus = negative correlation)
  • Another study confirmed the correlation of anger to externalizing problems.44
  • No correlation was found between45
    • Aggression and depression
      The extent to which internalizing and externalizing subtypes of depression were considered separately in this study is not known to us.
    • Aggression and academic performance.
  • Suicidality is more strongly associated with hot (reactive) aggression than with cold (proactive) aggression. The association between hot aggression and suicidality presupposed high hyperactivity/impulsivity.46

8. Other correlations

Low cortisol levels and low anxiety correlate with

  • High willingness to take risks / risky decisions40
  • While administration of cortisol increased risk taking.47

High levels of testosterone correlated with

  • High urge for rewards48
  • Low sensitivity to penalties48
  • Higher rejection of offers in the Ultimatum Game (explanation below) by men49 as by women50.

Low testosterone levels were correlated with

  • Low urge for rewards48
  • High sensitivity to penalties48

The effect of testosterone levels, meanwhile, appears to be sex-dependent.
In the Ultimatum Game, a partner is offered a portion of the game amount. If the partner accepts, both keep the divided sum; if the partner refuses, both receive nothing. Whereas testosterone administration in men resulted in more unfair offers,51 testosterone administration in women increased the rate of fairer (more generous) offers (but not rejection of unfair offers).52 The study authors of the study in women hypothesize that testosterone in women promotes the pursuit of higher social status, which is associated with avoidance of conflict. This could be related to “tend and befriend” behavior as a stress symptom, according to our unverified hypothesis.

Anxiety correlated with

  • High sensitivity to punishment39
  • Low urge for reward39

Low autonomic nervous system arousal has been associated with low behavioral inhibition (lack of inhibition).41

All these facts indicate that certain ADHD symptoms can be assigned to the individual subtypes, which can be distinguished on the basis of the ratio of testosterone and cortisol levels. Additionally, the serotonin level could (co-)explain the measure of impulsivity.

Testosterone appears to directly affect the activity of dopaminergic neurons,53 as does cortisol.54

Emotional dysregulation, irritability, anger, and agitation in ADHD correlate with ADHD-specific genes and not with genes specifically associated with affective disorders (depression).55

  1. Montoya ER, Terburg D, Bos PA, van Honk J. Testosterone, cortisol, and serotonin as key regulators of social aggression: a review and theoretical perspective.Motiv Emot 2012;36(1):65–73.

  2. van Honk, Harmon-Jones, Morgan, Schutter (2010): Socially explosive minds: the triple imbalance hypothesis of reactive aggression. J Pers. 2010 Feb;78(1):67-94. doi: 10.1111/j.1467-6494.2009.00609.x.

  3. Blair (2010): Neuroimaging of psychopathy and antisocial behavior: a targeted review. Curr Psychiatry Rep. 2010 Feb;12(1):76-82. doi: 10.1007/s11920-009-0086-x.

  4. Mortimer, Ganster, O’Leary, Popp, Freudenberg, Reif, Artigas, Ribasés, Ramos-Quiroga, Lesch, Rivero (2019): Dissociation of impulsivity and aggression in mice deficient for the ADHD risk gene Adgrl3: Evidence for dopamine transporter dysregulation. Neuropharmacology. 2019 Mar 5. pii: S0028-3908(19)30078-4. doi: 10.1016/j.neuropharm.2019.02.039.

  5. Nelson, Trainor (2009): Neural mechanisms of aggression. Nat Rev Neurosci. 2007 Jul;8(7):536-46.

  6. Siegel et al (1999), zitiert nach Studentenskript zur Vorlesung NEUROPSYCHOLOGIE Zimmer WS 2011/12 Uni Köln

  7. Sarkey, Azcoitia, Garcia-Segura, Garcia-Ovejero, DonCarlos (2008): Classical androgen receptors in non-classical sites in the brain. Horm Behav. 2008 May;53(5):753-64. doi: 10.1016/j.yhbeh.2008.02.015.

  8. Hermans, Ramsey, van Honk (2007): Exogenous testosterone enhances responsiveness to social threat in the neural circuitry of social aggression in humans. Biol Psychiatry. 2008 Feb 1;63(3):263-70.

  9. Derntl, Windischberger, Robinson, Kryspin-Exner, Gur, Moser, Habel (2009): Amygdala activity to fear and anger in healthy young males is associated with testosterone.Psychoneuroendocrinology. 2009 Jun;34(5):687-93. doi: 10.1016/j.psyneuen.2008.11.007.

  10. Manuck, Marsland, Flory, Gorka, Ferrell, Hariri (2010): Salivary testosterone and a trinucleotide (CAG) length polymorphism in the androgen receptor gene predict amygdala reactivity in men. Psychoneuroendocrinology. 2010 Jan;35(1):94-104. doi: 10.1016/j.psyneuen.2009.04.013.

  11. Decety, Michalska, Akitsuki, Lahey (2009): Atypical empathic responses in adolescents with aggressive conduct disorder: a functional MRI investigation. Biol Psychol. 2009 Feb;80(2):203-11. doi: 10.1016/j.biopsycho.2008.09.004.

  12. Marsh, Finger, Mitchell, Reid, Sims, Kosson, Towbin, Leibenluft, Pine, Blair (2008): Reduced amygdala response to fearful expressions in children and adolescents with callous-unemotional traits and disruptive behavior disorders. Am J Psychiatry. 2008 Jun;165(6):712-20. doi: 10.1176/appi.ajp.2007.07071145.

  13. Jakobi, Arias-Vasquez, Hermans, Vlaming, Buitelaar, Franke, Hoogman, van Rooij (2022): Neural Correlates of Reactive Aggression in Adult Attention-Deficit/Hyperactivity Disorder. Front Psychiatry. 2022 May 19;13:840095. doi: 10.3389/fpsyt.2022.840095. PMID: 35664483; PMCID: PMC9160326.

  14. Nelson, Trainor (2007): Neural mechanisms of aggression. In: Nature Reviews Neuroscience. Band 8, Nr. 7, Juli 2007, S. 536–546, doi:10.1038/nrn2174, PMID 17585306

  15. Stadler, Zepf, Demisch, Schmitt, Landgraf, Poustka (2007): Influence of rapid tryptophan depletion on laboratoryprovoked aggression in children with ADHD. Neuropsychobiology 56:104–110

  16. Carrillo, Ricci, Coppersmith, Melloni (2009): The effect of increased serotonergic neurotransmission on aggression: a critical meta-analytical review of preclinical studies. Psychopharmacology (Berl). 2009 Aug;205(3):349-68. doi: 10.1007/s00213-009-1543-2.

  17. Ferrari, Palanza, Parmigiani, de Almeida, Miczek (2005): Serotonin and aggressive behavior in rodents and nonhuman primates: predispositions and plasticity. Eur J Pharmacol. 2005 Dec 5;526(1-3):259-73.

  18. Huber, Smith, Delago, Isaksson, Kravitz (1997): Serotonin and aggressive motivation in crustaceans: altering the decision to retreat. Proc Natl Acad Sci U S A. 1997 May 27;94(11):5939-42.

  19. Comai, Bertazzo, Vachon, Daigle, Toupin, Côté, Turecki, Gobbi (2016): Tryptophan via serotonin/kynurenine pathways abnormalities in a large cohort of aggressive inmates: markers for aggression. Prog Neuropsychopharmacol Biol Psychiatry. 2016 Oct 3;70:8-16. doi: 10.1016/j.pnpbp.2016.04.012. PMID: 27117820. n = 361

  20. Wanke (2003): Impulsivität und dopaminerge resp. serotonerge Reagibilität. Ein Vergleich der Impulsivitätskonzepte von Cloninger und Zuckerman; Dissertation

  21. Nichols (2004): Hallucinogens. In: Pharmacology & Therapeutics. Band 101, Nr. 2, Februar 2004, S. 131–181, doi:10.1016/j.pharmthera.2003.11.002, PMID 14761703

  22. Siever, Buchsbaum, New, Spiegel-Cohen, Wei, Hazlett, Sevin, Nunn, Mitropoulou (1999): d,l-fenfluramine response in impulsive personality disorder assessed with [18F]fluorodeoxyglucose positron emission tomography. Neuropsychopharmacology. 1999 May;20(5):413-23.

  23. Frankle, Lombardo, New, Goodman, Talbot, Huang, Hwang, Slifstein, Curry, Abi-Dargham, Laruelle, Siever (2005): Brain serotonin transporter distribution in subjects with impulsive aggressivity: a positron emission study with [11C]McN 5652. Am J Psychiatry. 2005 May;162(5):915-23.

  24. Rosell, Thompson, Slifstein, Xu, Frankle, New, Goodman, Weinstein, Laruelle, Abi-Dargham, Siever (2010): Increased serotonin 2A receptor availability in the orbitofrontal cortex of physically aggressive personality disordered patients. Biol Psychiatry. 2010 Jun 15;67(12):1154-62. doi: 10.1016/j.biopsych.2010.03.013.

  25. Montoya, Terburg, Bos, van Honk (2012): Testosterone, cortisol, and serotonin as key regulators of social aggression: a review and theoretical perspective.Motiv Emot 2012;36(1):65–73.

  26. Manigault, Zoccola, Hamilton, Wymbs (2019): Testosterone to cortisol ratio and aggression toward one’s partner: Evidence for moderation by provocation. Psychoneuroendocrinology. 2019 Jan 18;103:130-136. doi: 10.1016/j.psyneuen.2019.01.018.

  27. Viau (2002): Functional cross-talk between the hypothalamic-pituitary-gonadal and -adrenal axes. J Neuroendocrinol. 2002 Jun;14(6):506-13.

  28. Johnson, Kamilaris, Chrousos, Gold (1992): Mechanisms of stress: a dynamic overview of hormonal and behavioral homeostasis. Neurosci Biobehav Rev. 1992 Summer;16(2):115-30.

  29. Tilbrook, Turner, Clarke (2000): Effects of stress on reproduction in non-rodent mammals: the role of glucocorticoids and sex differences. Rev Reprod. 2000 May;5(2):105-13.

  30. Burger (2002): Androgen production in women. Fertil Steril. 2002 Apr;77 Suppl 4:S3-5.

  31. Schulkin (2007): Autism and the amygdala: an endocrine hypothesis. Brain Cogn. 2007 Oct;65(1):87-99.

  32. Schulkin, Gold, McEwen (1998): Induction of corticotropin-releasing hormone gene expression by glucocorticoids: implication for understanding the states of fear and anxiety and allostatic load. Psychoneuroendocrinology. 1998 Apr;23(3):219-43.

  33. Strajhar, Vizeli, Patt, Dolder, Kratschmar, Liechti, Odermatt (2018): Effects of lisdexamfetamine on plasma steroid concentrations compared with d-amphetamine in healthy subjects: A randomized, double-blind, placebo-controlled study. J Steroid Biochem Mol Biol. 2018 Oct 28. pii: S0960-0760(18)30645-9. doi: 10.1016/j.jsbmb.2018.10.016.

  34. Gazzola, Spiers (2002): Effects of the α2-adrenoceptor agonist, guanfacine, on growth rate, glucose, corticosterone, insulin and energy partitioning in rats. Animal Science, 74(3), 455-459. doi:10.1017/S1357729800052607

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

  36. Walther, Breidenstein, Miller (2018): Association of Testosterone Treatment With Alleviation of Depressive Symptoms in Men. A Systematic Review and Meta-analysis. JAMA Psychiatry. doi:10.1001/jamapsychiatry.2018.2734, n = 1.890

  37. Woodman (1979): Biochemistry of psychopathy. J Psychosom Res. 1979;23(6):343-60. doi: 10.1016/0022-3999(79)90046-1. PMID: 549972, 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

  38. Laakso, Wallius, Kajander, Bergman, Eskola, Solin, Ilonen, Salokangas, Syvälahti, Hietala (2003): Personality traits and striatal dopamine synthesis capacity in healthy subjects. Am J Psychiatry. 2003 May;160(5):904-10. doi: 10.1176/appi.ajp.160.5.904. PMID: 12727694.

  39. Arnett (1997): Autonomic responsivity in psychopaths: a critical review and theoretical proposal. Clin Psychol Rev. 1997 Dec;17(8):903-36.

  40. van Honk, Schutter, Hermans, Putman (2003): Low cortisol levels and the balance between punishment sensitivity and reward dependency. Neuroreport. 2003 Oct 27;14(15):1993-6.

  41. Raine (1996): Autonomic nervous system factors underlying disinhibited, antisocial, and violent behavior. Biosocial perspectives and treatment implications. Ann N Y Acad Sci. 1996 Sep 20;794:46-59.

  42. Bartels, Hendriks, Mauri, Krapohl, Whipp, Bolhuis, Conde, Luningham, Fung Ip, Hagenbeek, Roetman, Gatej, Lamers, Nivard, van Dongen, Lu, Middeldorp, van Beijsterveldt, Vermeiren, Hankemeijer, Kluft, Medland, Lundström, Rose, Pulkkinen, Vuoksimaa, Korhonen, Martin, Lubke, Finkenauer, Fanos, Tiemeier, Lichtenstein, Plomin, Kaprio, Boomsma (2018): Childhood aggression and the co-occurrence of behavioural and emotional problems: results across ages 3-16 years from multiple raters in six cohorts in the EU-ACTION project. Eur Child Adolesc Psychiatry. 2018 Sep;27(9):1105-1121. doi: 10.1007/s00787-018-1169-1.

  43. ähnlich: Raine (1996): Autonomic nervous system factors underlying disinhibited, antisocial, and violent behavior. Biosocial perspectives and treatment implications. Ann N Y Acad Sci. 1996 Sep 20;794:46-59.

  44. Leaberry, Rosen, Slaughter, Reese, Fogleman (2019): Temperamental negative affect, emotion-specific regulation, and concurrent internalizing and externalizing pathology among children with ADHD. Atten Defic Hyperact Disord. 2019 Mar 23. doi: 10.1007/s12402-019-00294-8.

  45. Evans, Frazer, Blossom, Fite (2018): Forms and Functions of Aggression in Early Childhood. J Clin Child Adolesc Psychol. 2018 Jul 27:1-9. doi: 10.1080/15374416.2018.1485104.

  46. Abel, Poquiz, Fite, Doyle (2019): Reactive Aggression and Suicidal Behaviors in Children Receiving Outpatient Psychological Services: The Moderating Role of Hyperactivity and Inattention. Child Psychiatry Hum Dev. 2019 Jun 20. doi: 10.1007/s10578-019-00905-5.

  47. Putman, Antypa, Crysovergi, van der Does (2009): Exogenous cortisol acutely influences motivated decision making in healthy young men. Psychopharmacology (Berl). 2010 Feb;208(2):257-63. doi: 10.1007/s00213-009-1725-y.

  48. van Honk, Schutter, Hermans, Putman, Tuiten, Koppeschaar (2004): Testosterone shifts the balance between sensitivity for punishment and reward in healthy young women. Psychoneuroendocrinology. 2004 Aug;29(7):937-43.

  49. Burnham (2007): High-testosterone men reject low ultimatum game offers. Proc Biol Sci. 2007 Sep 22;274(1623):2327-30.

  50. Mehta, Beer (2019): Neural mechanisms of the testosterone-aggression relation: the role of orbitofrontal cortex. J Cogn Neurosci. 2010 Oct;22(10):2357-68. doi: 10.1162/jocn.2009.21389.

  51. Zak, Kurzban, Ahmadi, Swerdloff, Park, Efremidze, Redwine, Morgan, Matzner (2009): Testosterone administration decreases generosity in the ultimatum game. PLoS One. 2009 Dec 16;4(12):e8330. doi: 10.1371/journal.pone.0008330.

  52. Eisenegger C1, Naef M, Snozzi R, Heinrichs M, Fehr (2010): Prejudice and truth about the effect of testosterone on human bargaining behaviour. Nature. 2010 Jan 21;463(7279):356-9. doi: 10.1038/nature08711. n = 60

  53. Wood (2008): Anabolic-androgenic steroid dependence? Insights from animals and humans. Front Neuroendocrinol. 2008 Oct;29(4):490-506. doi: 10.1016/j.yfrne.2007.12.002.

  54. Piazza, Le Moal (1997): Glucocorticoids as a biological substrate of reward: physiological and pathophysiological implications. Brain Res Brain Res Rev. 1997 Dec;25(3):359-72.

  55. Nigg, Karalunas, Gustafsson, Bhatt, Ryabinin, Mooney, Faraone, Fair, Wilmot (2019): Evaluating chronic emotional dysregulation and irritability in relation to ADHD and depression genetic risk in children with ADHD. J Child Psychol Psychiatry. 2019 Oct 12. doi: 10.1111/jcpp.13132.