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Secure attachment beats genetic disposition in ADHD

Secure attachment beats genetic disposition in ADHD

1. No early childhood stress experience = lower risk of manifested ADHD

A genetic disposition for ADHD does not have to lead to ADHD. If early childhood stress experiences are absent, this significantly increases the chance that ADHD will not develop.
No experience of stress does not mean that children should be spoiled - that would be a serious misunderstanding.

An absence of stressors, on the other hand, does not mean keeping the child away from every (stressful) experience, because then no functional coping strategies with stressful experiences could be gathered.

Example:
If a child has injured himself while playing (e.g., skinned his knee), it is dysfunctional to scold the child or to bring up the injury in great excitement - because that would increase the significance of the injury and thus at the same time the perception of pain. Fear and pain perception are learned as well as other skills. Appropriate care for the injury and positive, unagitated consolation, which above all provides emotional security, are the most important elements of a good attachment.
A child needs the security that it is also allowed to make mistakes. If the child learns that the parents trust him, that he does not want to make mistakes, and therefore do not dramatize mistakes per se, while at the same time the parents naturally expect the child to learn from the mistakes and support him in this, he has no reason to use mistakes to provoke attention.

Since the mechanism is universal that early childhood stress increases the risk of acquiring mental disorders, this is not unique to ADHD. The model differs with respect to different mental disorders only in that different mental disorders may develop depending on the type of gene dispositions and the type and timing of stress.
Therefore, the fact that secure attachment reduces the risk that an existing genetic predisposition to a mental disorder will manifest is also universal.

2. Secure attachment helps prevent ADHD manifestation

The attachment behavior of the parents (especially the mother) has a greater influence on the emergence of mental disorders than the existence of a genetic disposition.

Animal studies show that the positive effect of a secure attachment and social behavior of the raising surrogate mother clearly outweighs the negative influences of the genes inherited from the birth mother.

  • Rats descended from attachment-deficient mothers and entrusted to attachment-strong mothers for rearing had little tendency toward disorganized attachment behavior or ADHD; conversely, rats bodily descended from attachment-strong mothers and reared by attachment-deficient mothers had significant tendencies toward disorganized attachment behavior or ADHD.1

  • Early childhood stress alters stress coping behavior in adult mice and adult male offspring. The behavioral changes are accompanied by increased glucocorticoid receptor (GR) expression and decreased DNA methylation of the GR promoter in the hippocampus. DNA methylation is also decreased in sperm from exposed males in adulthood. If animals with genetic exposure grow up without early childhood stress in a safe environment with many social contact opportunities (enriched environement), no adverse behavioral changes are observed. Rather, the aforementioned changes in GR gene expression and DNA methylation were reversed in the hippocampus of male offspring.2

  • Caring brood care in rat pups during the first week causes methylation of promoters involved in the expression of genes that positively influence stress responses and behavior throughout life.3
    In genetically identical rats, different brood care alone showed different expression of stress systems

    • Rat pups that received little grooming and physical attention from their mothers developed lower levels of the transcription factor NGFI-A (also called EGR1) in the hippocampus. This caused increased methylation and thereby lower expression of the glucocorticoid receptor gene (GR gene) in the hippocampus.4
      A lower GR expression level in the hippocampus correlated in adulthood with4
      • Elevated basal glucocorticoid levels (in mice: corticosterone, in humans: cortisol)
      • Excessive cortisol stress response
      • More anxious behavior
      • In females: lower brood care of own children
    • Rat pups that received a lot of grooming and physical attention from their mothers developed higher levels of the transcription factor NGFI-A (EGR1) in the hippocampus. This causes reduced methylation and thereby higher expression of the glucocorticoid receptor gene (GR gene) in the hippocampus.4
      Higher GR expression level in the hippocampus correlates with4 in adulthood
      • Lower basal glucocorticoid levels (in mice: corticosterone, in humans: cortisol)
      • Lower glucocorticoid stress response
      • Less anxious behavior
      • In females: increased brood care of own children
  • Similarly, it is reported from monkeys that all monkey children who were bodily descended from aggressive mothers and raised by caring mothers were in turn able to give their children a caring attachment, while 50 to 60% of the bodily children of caring mothers who were raised by violent mothers showed this violence toward their own children as well.5

  • High oxytocin receptor density in the nucleus accumbens caused increased resistance of newborns to neglect due to social isolation (a specific form of early childhood stress):67

    • Animals with few oxytocin receptors in the nucleus accumbens
      • Without neonatal neglect
        • Strong preference as adults to spend more time with their partner than with strangers
      • And neonatal neglect
        • No preference as an adult to spend more time with their partner than with strangers
    • Animals with many oxytocin receptors in the nucleus accumbens
      • Strong preference as adults to spend more time with their partner than with strangers

    This is a direct example of how parental neglect in early childhood affects attachment style.
    On the influence of attachment style on the likelihood of later mental disorders, see ADHD - Prevention and screening - What parents can do. Touch increases oxytocin release in the brain and body. Maternal licking and grooming increased maternal behavior in adulthood in infant rats, as did oxytocin injections.86

  • Offspring of rat mothers who applied high levels of care as adults:9

    • More benzodiazepine receptors in amygdala (central, lateral, basolateral) and locus coeruleus
    • More alpha2-adrenoreceptors in the locus coeruleus
    • Fewer CRH receptors in the locus coeruleus
    • A significantly lower anxiety to new stimuli
      Anxiety and fear are moderated by, among other things
      • Noradrenergic projections from the locus coeruleus to the PFC
      • CRH projections from the amygdala to the locus coeruleus (anxiety-increasing)
      • Endogenous benzodiazepines (anxiolytic)

    The authors conclude that maternal caregiving during infancy serves to “program” behavioral responses to stress in offspring by altering the development of neural systems that mediate anxiety.910

Studies in humans confirm these results as a universal pattern.11
Secure attachment behavior of parents can massively influence the behavior of children and thereby avoid the manifestation of a genetic disposition to a mental disorder.

2.1. Parents’ attachment style to the child particularly important for chance/risk genes

Several studies show that the influence of the attachment style is not the same for all children, but is much stronger for children who are endowed with certain genetic dispositions (“chance/risk genes”). In these children, the attachment style has particularly serious effects, both negative and positive.121314
Fundamental to this: the differential susceptibility hypothesis of Belsky.15 Strikingly, all genes named by Belsky as chance-risk genes were named as candidate genes for ADHD. Candidate genes in ADHD

Only a few genes have been described as specific opportunity/risk genes so far.

2.1.1. DRD4-7R - ADHD opportunity/risk gene

DRD4-7R, causes a less sensitive dopamine D4 receptor, which thereby requires 3 times the amount of dopamine to respond. This acts like a seemingly decreased dopamine level. For more on this, including evidence, see Dopamine receptor D4 gene, DRD4 (chromosome 11p15.5 exon III, VTNR) (x) In the article Candidate genes in ADHD in the chapter How ADHD develops: genes or genes + environment.

We suspect that DRD4-7R is one of the genes that mediate high sensitivity. We assume that the high sensitivity mediated by DRD4-7R is not a consequence that would only develop as a result of an additional early childhood stress experience. Rather, we assume that the high sensitivity mediated by DRD4-7R is the “lever” that makes the affected person particularly susceptible to external influences and thus mediates a particularly positive and particularly negative development (chance-risk).

In children with the DRD4-7R gene variant (also relevant for ADHD), parenting and attachment style have a serious influence. A bad attachment style triggers six times more often high aggressiveness (risk: plus 600 %). At the same time, a good attachment style, even if subsequently trained, causes above-average empathy (and non-aggressiveness), i.e. above the level of children without the DRD4-7R risk gene form.161718

Positive, sensitive handling leads to less externalizing behavior in two- to three-year-old DRD4-7R subjects, whereas a negative, controlling style leads to marked externalizing behavior.19

In children without this gene variant, on the other hand, there were hardly any differences due to changes in attachment style.161718
This supports the hypothesized association of the DRD4-7R gene form with high sensitivity.

Conversely, only children with DRD4-7R also benefited from therapeutic promotion of maternal sensitivity in child handling.20

The behavioral changes are mediated by the HPA axis (stress regulation axis).21

In children with ADHD and the ADHD risk gene disposition DRD-4-7R, training parents in how to manage their children produced a 27% improvement on a symptom scale, whereas children with ADHD without this gene disposition obtained an improvement of only 12% from the same training of their parents.22

Similarly, it was observed that children with a DRD-4-7R disposition developed a particularly affable manner (compared to non-ADHD children) when their parents provided them with a particularly sensitive parenting style.22

Further studies on DRD4-7R and secure attachment

In another study, children with the DRD4-7R gene who had received a secure parental attachment were the ones who donated the most, while those with the DRD4-7R gene who had grown up with an insecure attachment donated the least.23 Affected individuals with the DRD4-7R gene who had received secure parental attachment had lower delay aversion than the control group without this gene variant. They took a significantly higher delay to end up with a higher reward, while those with DRD4-7R who had grown up with an insecure attachment had significantly higher delay aversion than the control group.24

Attachment disorders of children in the first years of life lead to the alteration of the DRD4 gene, which is also typical for ADHD.25
Another study confirms the involvement of DRD4-7R in gene-environment interactions.26

2.1.2. 5-HTTLPR short - depression opportunity/risk gene polymorphism

People with the (short) risk variant of the serotonin transporter gene SLC6A4, the polymorphism 5-HTTLPR short,27 have a higher risk of depression. However, the increased risk of depression exists only if a 5-HTTLPR short carrier has been exposed to stressful experiences in the past.28 29 In contrast, affected individuals without such stressful experiences are less likely to become depressed than carriers of the long non-risk variant.18
About 20% of all Western Europeans have the gene polymorphism 5-HTTLPR in the short variant.30

The number of S alleles (in gene 5-HTTLPR) correlates with positive emotional traits.31

In healthy seven-year-old children, marked externalizing of internalizing behavior is related to the cumulative presence of both gene variants (DRD4-7R and 5-HTTLPR short).32

Further research confirms that those genes that cause particular vulnerability to early stress experiences are also opportunity genes with particular support during this time.333435

The neonatal stress response was associated with higher scores for negative emotionality and lower scores for orientation/regulatory ability in the 5-HTTLPR S allele than the L allele.36

2.1.3. COMT - chance/risk gene

The COMT-Val-158-Val polymorphism causes dopamine degradation 4 times faster than the COMT-Met-158-Met variant. COMT is responsible for 60% of dopamine degradation in the PFC, but only 15% of DA degradation in the striatum.

COMT-Met-158-Met carriers are compared to COMT-Val-158-Val carriers

  • Mentally more powerful (more efficient, not more intelligent)373839
  • More sensitive to stress (high dopamine levels (only) in the PFC already at rest, substantial dopamine increase (only) in the PFC already at mild stress)
  • Anxious
  • More sensitive to pain.404142

Another study confirms the leverage of the COMT gene for the effect of parenting behavior on ADHD symptoms (gene-environment interaction).43
Severe maternal anxiety during pregnancy increases the ADHD risk of the unborn child depending on its COMT gene variant (gene-environment interaction).44

COMT Val158Met correlates with ADHD.45
The Met allele of the COMT-Val158Met polymorphism was associated with higher positive affectivity/neediness (surgency) and orientation/regulatory ability and greater cortisol lowering as a stress response in newborns.36
Children with at least one COMT158Met allele were more sensitive overall to early childhood adversity. They showed more inattention and hyperactivity/impulsivity when exposed to high socioeconomic risk factors in childhood compared to Val-Val carriers.46

2.1.4. MAO-A - Aggressiveness Opportunity/Risk Gene

Boys with a variant of the MAO-A gene that puts them at risk for aggressive behavior have greater behavior problems only if they have suffered maltreatment. Without maltreatment, they were less aggressive than boys with the non-risk MAO-A variant.1847 An MAO-A variant that breaks down dopamine particularly efficiently prevented antisocial behavior in maltreated children.48

The same relationship is described for aggression with a variant of the gene MAO-A and stress in childhood.49

The response to stress in neonates was associated with higher Negative Emotionality scores, lower Orientation/Regulatory Ability scores, and lower decreases in cortisol after acute stress in the MAOA-L allele.36

2.1.5. CHRM2 - Opportunity/risk gene for socially undesirable behavior

Adolescents with risk variants of CHRM2 (risk gene for socially undesirable behavior such as aggressiveness, rule breaking, or alcoholism) had more behavior problems with parental neglect than the control group. With strongly caring parents, they had significantly fewer behavioral problems than adolescents without this gene variant.18

2.2. Increased sensitivity due to chance-risk genes DRD4-7R / 5-HTTLPR

The gene polymorphism 5-HTTLPR short causes a significant change in evoked potentials. The LA of the N1/P2 component is steeper than in people with the homozygous l/l genotype. As the intensity (loudness) of an auditory stimulus increases, the amplitude increases more rapidly in 5-HTTLPR short than in the l/l genotype. (Decrease over electrode Cz = vertex of the head).50
We understand this to mean that people with 5-HTTLPR short are more sensitive to auditory stimuli.

Details of serotonin transporters:51

5-HTTLPR-induced high (5HTTLPR long/long) and low (5HTTLPR short/short) serotonin activity indexes ADHD symptoms in the presence of added psychosocial stress, but not medium (5HTTLPR long/short) serotonin activity.52

2.3. Stress sensitivity as a risk in opportunity/risk genes

A study of preschool children revealed a particularly intense stress response (heart rate and cortisol levels) in some. These more intensely reacting children were more aggressive than the others when faced with problems at home (money problems, marital problems, strict upbringing, depression of the caregiver). Without these problems, on the other hand, the stress-sensitive children behaved more socially than the stress-robust children, got out of hand less often, and were more involved in school.53 5455

Children who had a “difficult” temperament at 6 months of age showed more behavioral problems than children with an “easy” temperament at that time if caregivers provided poor care at age 10. With good and loving care, they formed better social skills and have fewer problems than the “easy” children.
The same was true for thinking ability and academic performance.
The differential susceptibility to external influences remained in affected individuals at least into early puberty, but probably throughout life.56

There are quite a few other studies on this topic.57585459

From our point of view, this answers the question of whether discipline and harshness or empathy and warmth make the race to make children strong. In any case, a hard, strict upbringing destroys sensitive children. However, clear rules that apply not only sometimes are helpful for all children.

2.4. Anxious attachment style moderates stress sensitivity in ADHD

A study of adults with and without ADHD found that attachment anxiety moderated the association between ADHD, anxiety, and depression. Only adults with ADHD who had moderate to high attachment anxiety had higher scores for depression and anxiety. Anxious attachment style correlated with higher psychological distress in adults with ADHD.No correlations were found between ADHD, anxiety, and depression for secure attachment style, from which the authors interpreted secure attachment style as a resilience factor against psychological distress in ADHD sufferers.60

2.5. Incidence of maltreatment and ADHD development

The prevalence for child sexual abuse is 1.6%,61 for physical abuse is 8%61 and for psychological abuse ranges from 0.3 to 36.3%.62 Psychological maltreatment has the same fatal consequences in terms of genetic manifestation of predispositions, brain developmental delays and permanent stress dysregulation as physical or sexual maltreatment.63
The wide range from 0.3% to 36.3% for psychological maltreatment is likely due to different measures.
Other studies support these findings.11

According to one study, 22% of n = 364 children who suffered (sexual or physical) abuse developed ADHD.
58% (of n = 364) developed separation anxiety/anxiety disorders, 36% phobic disorders, 35% PTSD, and 22% dissocial behavior disorder.64
According to another study, of n = 9336 traumatized children, 48% developed behavior problems, 41% developed school problems, and 37% developed behavior problems in school/kindergarten, etc., each associated with ADHD. 31% of children developed attachment disorders, 11% suicidality, and 24% PTSD.65

3. Conclusions on opportunity/risk genes

It is assumed that 15 to 20 % of all people are endowed with the described chance/risk genes.66
This prevalence of opportunity/risk genes in people of 15 to 20% coincides (coincidentally?) with the prevalence figures assumed for high sensitivity: 15 to 20%67 or 15 to 25%.68

The abundance of results indicates that certain gene variants increase the “sensitivity” or the “intensity” of people, whereby these have an equal effect as a risk and as an opportunity. The only difference is that, as children, those affected are helplessly at the mercy of their parents’ attachment behavior due to a lack of influence on whether their genetic disposition will materialize as an opportunity or a risk.
The results can be interpreted in such a way that higher sensitivity implies higher vulnerability on the one hand and greater developmental potential on the other. This is consistent with our understanding about the relationship between giftedness and high sensitivity. High giftedness and ADHD

A basic pattern emerges:
Gene variants can cause changes in the brain, as can early childhood experiences. If genes and behavior cause changes in the same direction (e.g., increase or decrease of a neurotransmitter), this is very likely to lead to conditions where the healthy balance (for neurotransmitters, the optimal level) is left. This often leads to (psychological) problems. A gene variant that degrades dopamine particularly well would, in the absence of a simultaneous environmental effect that provides for an increase in dopamine by other means, cause dopamine levels to be too low, which can cause working memory problems in the PFC, for example.
Such gene variants are often the result of epigenetic changes due to early childhood stress in previous generations.

In rats, the epigenetic changes caused by first-generation early childhood stress that resulted in increased vulnerability to psychological stress in adolescence (resulting in persistent psychological problems in adulthood) were still detectable in the 4th generation.
Ultimately, this realization leads to the uncomfortable insight that only a determination of gene expressions in newborns can show which manners of handling can bring about a psychologically healthy development. (This explicitly does not include a statement as to whether this is ethically justifiable. This must be discussed elsewhere)


  1. Brisch (2004): Der Einfluss von traumatischen Erfahrungen auf die Neurobiologie und die Entstehung von Bindungsstörungen. Psychotraumatologie und Medizinische Psychologie 2, 29-44, Link auf Beitrag gleichen Namens auf Webseite Brisch, mit anderer Seitennummerierung, Link-Seite 26

  2. Gapp, Bohacek, Grossmann, Brunner, Manuella, Nanni, Mansuy (2016): Potential of Environmental Enrichment to Prevent Transgenerational Effects of Paternal Trauma

  3. Kaffman, Meaney (2007): Neurodevelopmental sequelae of postnatal maternal care in rodents: clinical and research implications of molecular insights. J Child Psychol Psychiatry 2007; 48(3–4): 224–44.

  4. Feder, Nestler, Charney (2009): Psychobiology and molecular genetics of resilience. Nat Rev Neurosci. 2009;10(6):446-57.

  5. Müller, Candrian, Kropotov (2011): ADHS – Neurodiagnostik in der Praxis, Springer, Seite 235, mit weiteren Nachweisen

  6. Barrett, Arambula, Young (2015): The oxytocin system promotes resilience to the effects of neonatal isolation on adult social attachment in female prairie voles. Transl Psychiatry. 2015 Jul 21;5(7):e606. doi: 10.1038/tp.2015.73. PMID: 26196439; PMCID: PMC5068726.

  7. Walum, Young (2018): The neural mechanisms and circuitry of the pair bond. Nat Rev Neurosci. 2018 Nov;19(11):643-654. doi: 10.1038/s41583-018-0072-6. PMID: 30301953; PMCID: PMC6283620. REVIEW

  8. Rilling, Young (2014): The biology of mammalian parenting and its effect on offspring social development. Science. 2014 Aug 15;345(6198):771-6. doi: 10.1126/science.1252723. PMID: 25124431; PMCID: PMC4306567. REVIEW

  9. Caldji, Tannenbaum, Sharma, Francis, Plotsky, Meaney (1998): Maternal care during infancy regulates the development of neural systems mediating the expression of fearfulness in the rat. Proc Natl Acad Sci U S A. 1998 Apr 28;95(9):5335-40. doi: 10.1073/pnas.95.9.5335. PMID: 9560276; PMCID: PMC20261.

  10. Teicher, Andersen, Polcari, Anderson, Navalta (2002): Developmental neurobiology of childhood stress and trauma. Psychiatr Clin North Am. 2002 Jun;25(2):397-426, vii-viii. doi: 10.1016/s0193-953x(01)00003-x. PMID: 12136507. REVIEW

  11. Seleem , Amer, Romeh, Hamoda (2019): Demographic and clinical characteristics of children seeking psychiatric services in the Nile Delta region: an observational retrospective study. Int J Ment Health Syst. 2019 Oct 23;13:66. doi: 10.1186/s13033-019-0323-6. eCollection 2019.

  12. unter anderem: Obradović, Bush, Stamperdahl, Adler, Boyce (2010): Biological Sensitivity to Context: The Interactive Effects of Stress Reactivity and Family Adversity on Socio-Emotional Behavior and School Readiness; Child Dev. Child Dev. 2010 Jan-Feb; 81(1): 270–289; doi: 10.1111/j.1467-8624.2009.01394.x; PMCID: PMC2846098; NIHMSID: NIHMS157386

  13. Belsky, Beaver (2011), Cumulative-genetic plasticity, parenting and adolescent self-regulation. Journal of Child Psychology and Psychiatry, 52: 619–626. doi:10.1111/j.1469-7610.2010.02327.x

  14. Diamond (2014): Biologische und soziale Einflüsse auf kognitive Kontrollprozesse, die vom präfrontalen Kortex abhängen; In: Kubesch (Herausgeberin): Exekutive Funktionen und Selbstregulation – Neurowissenschaftliche Grundlagen und Transfer in die pädagogische Praxis; Huber, Seite 30

  15. Differential susceptibility hypothesis in der englischprachigen Wikipedia

  16. Bakermans-Kranenburg, van IJzendoorn (2006): Gene-environment interaction of the dopamine D4 receptor (DRD4) and observed maternal insensitivity predicting externalizing behavior in preschoolers; Developmental Psychobiology, Volume 48, Issue 5, pages 406–409, July 2006, DOI: 10.1002/dev.20152

  17. Bakermans-Kranenburg, van IJzendoorn, Caspers, Philibert (2011): DRD4 genotype moderates the impact of parental problems on unresolved loss or trauma; Attachment & Human Development Volume 13, Issue 3, 2011; n = 124

  18. Glomp (2011): GLÜCKSFALL PROBLEMKIND, Bild der Wissenschaft, 11/2011, Seite 84 – Kultur & Gesellschaft

  19. Vuksanovic (2013): Die Aktivität der Hypothalamus-Hypophysen-Nebennierenrinden-Achse bei Aufmerksamkeits-Defizit und Hyperaktivitäts-Störung, Dissertation, Seite 12, unter Verweis auf Propper et al 2007

  20. Vuksanovic (2013): Die Aktivität der Hypothalamus-Hypophysen-Nebennierenrinden-Achse bei Aufmerksamkeits-Defizit und Hyperaktivitäts-Störung, Dissertation, Seite 12, unter Verweis auf Bakermans-Kranenburg et al, 2008a

  21. Vuksanovic (2013): Die Aktivität der Hypothalamus-Hypophysen-Nebennierenrinden-Achse bei Aufmerksamkeits-Defizit und Hyperaktivitäts-Störung, Dissertation, Seite 12, unter Verweis auf Bakermans-Kranenburg et al, 2008b

  22. Berndt (2013): Resilienz, Seite 142

  23. Bakermans-Kranenburg, van Ijzendoorn (2011): Differential susceptibility to rearing environment depending on dopamine-related genes: New evidence and a meta-analysis; Development and Psychopathology, Volume 23, Issue 1; February 2011, pp. 39-52; DOI: http://dx.doi.org/10.1017/S0954579410000635

  24. Sweitzer, Halder, Flory, Craig, Gianaros, Ferrell, Manuck (2012): Polymorphic variation in the dopamine D4 receptor predicts delay discounting as a function of childhood socioeconomic status: evidence for differential susceptibility; Soc Cogn Affect Neurosci (2013) 8(5): 499-508.doi: 10.1093/scan/nss020

  25. Brisch (2004): Der Einfluss von traumatischen Erfahrungen auf die Neurobiologie und die Entstehung von Bindungsstörungen. Psychotraumatologie und Medizinische Psychologie 2, 29-44, Link auf Beitrag gleichen Namens auf Webseite Brisch, mit anderer Seitennummerierung, Link-Seite 25

  26. Sánchez-Mora, Richarte, Garcia-Martínez, Pagerols, Corrales, Bosch, Vidal, Viladevall, Casas, Cormand, Ramos-Quiroga, Ribasés (2015): Dopamine receptor DRD4 gene and stressful life events in persistent attention deficit hyperactivity disorder. Am J Med Genet B Neuropsychiatr Genet. 2015 Sep;168(6):480-491. doi: 10.1002/ajmg.b.32340.

  27. Becker (2007): Zusammenhang zwischen der Lautstärkeabhängigkeit akustisch evozierter Potentiale und dem 5-HTTLPR, Dissertation, Seite 10

  28. Bennett, Lesch, Heils, Long, Lorenz, Shoaf, Champoux, Suomi, Linnoila, Higley (2002): Early experience and serotonin transporter gene variation interact to influence primate CNS function. Mol Psychiatry. 2002;7(1):118-22. doi: 10.1038/sj.mp.4000949. PMID: 11803458.

  29. Grawe (2004): Neuropsychotherapie, Seite 200

  30. Szczesny-Friedmann (2012): Taube oder Falke: Warum wir sind, wie wir sind – und was wir daran ändern können, Rowohlt

  31. Wielpuetz, Kuepper, Grant, Munk, Hennig (2013): Acute responsivity of the serotonergic system to S-citalopram and positive emotionality—the moderating role of the 5-HTTLPR; Front Hum Neurosci. 2013; 7: 486; doi: 10.3389/fnhum.2013.00486; PMCID: PMC3750213

  32. Vuksanovic (2013): Die Aktivität der Hypothalamus-Hypophysen-Nebennierenrinden-Achse bei Aufmerksamkeits-Defizit und Hyperaktivitäts-Störung, Dissertation, Seite 11, unter Verweis auf Schmidt et al 2007

  33. Heim, Binder (2012): Current research trends in early life stress and depression: review of human studies on sensitive periods, gene-environment interactions, and epigenetics. Exp Neurol; 2012; 233: 102–11.

  34. zu 5-HTTPR: Vuksanovic (2013): Die Aktivität der Hypothalamus-Hypophysen-Nebennierenrinden-Achse bei Aufmerksamkeits-Defizit und Hyperaktivitäts-Störung, Dissertation, Seite 12

  35. Grawe (2004): Neuropsychotherapie, Seite 202

  36. Bajgarova Z, Bajgar A. The relationships among MAOA, COMT Val158Met, and 5-HTTLPR polymorphisms, newborn stress reactivity, and infant temperament. Brain Behav. 2020 Feb;10(2):e01511. doi: 10.1002/brb3.1511. PMID: 31884721; PMCID: PMC7010585.

  37. Diamond (2014): Biologische und soziale Einflüsse auf kognitive Kontrollprozesse, die vom präfrontalen Kortex abhängen; In: Kubesch (Herausgeberin): Exekutive Funktionen und Selbstregulation – Neurowissenschaftliche Grundlagen und Transfer in die pädagogische Praxis; Huber, Seite 29

  38. Boyce (2007/2013): A Biology of Misfortune: Stress Reactivity, Social Context, and the Ontogeny of Psychopathology in Early Life, IN: Ann S. Masten (Editor): Multilevel Dynamics in Developmental Psychopathology: Pathways to the Future: The Minnesota Symposia on Child Psychology, Volume 34; Minnesota Symposia on Child Psychology Series.

  39. Boyce, Ellis (2005): An evolutionary–developmental theory of the origins and functions of stress reactivity; Biological sensitivity to context: https://doi.org/10.1017/S0954579405050145

  40. Diamond (2014): Biologische und soziale Einflüsse auf kognitive Kontrollprozesse, die vom präfrontalen Kortex abhängen; In: Kubesch (Herausgeberin): Exekutive Funktionen und Selbstregulation – Neurowissenschaftliche Grundlagen und Transfer in die pädagogische Praxis; Huber, Seite 28

  41. Diatchenko, Slade, Nackley, Bhalang, Sigurdsson, Belfer, Goldman, Xu, Shabalina, Shagin, Max, Makarov, Maixner (2005): Genetic basis for individual variations in pain perception and the development of a chronic pain condition; Hum Mol Genet. 2005 Jan 1;14(1):135-43.

  42. Zubieta, Heitzeg, Smith, Bueller, Ke, Xu, Koeppe, Stohler, Goldman (2003): COMT val158met Genotype Affects µ-Opioid Neurotransmitter Responses to a Pain Stressor; Science 21 Feb 2003:Vol. 299, Issue 5610, pp. 1240-1243; DOI: 10.1126/science.1078546

  43. Morgan, Caplan, Tung, Noroña, Baker, Lee (2018): COMT and DAT1 polymorphisms moderate the indirect effect of parenting behavior on youth ADHD symptoms through neurocognitive functioning. Child Neuropsychol. 2018 Aug;24(6):823-843. doi: 10.1080/09297049.2017.1346067.

  44. O’Donnell, Glover, Lahti, Lahti, Edgar, Räikkönen, O’Connor (2017): Maternal prenatal anxiety and child COMT genotype predict working memory and symptoms of ADHD. PLoS One. 2017 Jun 14;12(6):e0177506. doi: 10.1371/journal.pone.0177506. eCollection 2017.

  45. Taylor (2018): Association between COMT Val158Met and psychiatric disorders: A comprehensive meta-analysis.Am J Med Genet B Neuropsychiatr Genet. 2018 Mar;177(2):199-210. doi: 10.1002/ajmg.b.32556.

  46. Abraham, Scott, Blair (2020): Catechol-O-methyltransferase Val158Met Genotype and Early-Life Family Adversity Interactively Affect Attention-Deficit Hyperactivity Symptoms Across Childhood. Front Genet. 2020 Jul 10;11:724. doi: 10.3389/fgene.2020.00724. PMID: 32765586; PMCID: PMC7381281. n = 1.292 Kinder und Familien über 11 Jahre

  47. Kim-Cohen, Caspi, Taylor, Williams, Newcombe, Craig, Moffitt (2006): MAOA, maltreatment, and gene-environment interaction predicting children’s mental health: new evidence and a meta-analysis. Mol Psychiatry. 2006 Oct;11(10):903-13.

  48. Caspi, McClay, Moffitt, Mill, Martin, Craig, Taylor, Poulton (2002): Role of Genotype in the Cycle of Violence in Maltreated Children. Science 02 Aug 2002: Vol. 297, Issue 5582, pp. 851-854 DOI: 10.1126/science.1072290

  49. Berndt (2013): Resilienz

  50. Becker (2007): Zusammenhang zwischen der Lautstärkeabhängigkeit akustisch evozierter Potentiale und dem 5-HTTLPR, Dissertation, Seite 44

  51. http://user.medunigraz.at/helmut.hinghofer-szalkay/II.2.htm#kat

  52. Nikolas, Friderici, Waldman, Jernigan, Nigg (2010): Gene × environment interactions for ADHD: synergistic effect of 5HTTLPR genotype and youth appraisals of inter-parental conflict; Behavioral and Brain Functions20106:23; DOI: 10.1186/1744-9081-6-23

  53. Obradović, Bush, Stamperdahl, Adler, Boyce (2010): Biological Sensitivity to Context: The Interactive Effects of Stress Reactivity and Family Adversity on Socio-Emotional Behavior and School Readiness; Child Dev. 2010 Jan-Feb; 81(1): 270–289. doi: 10.1111/j.1467-8624.2009.01394.x, n = 334, zitiert auch in Glomp (2011): GLÜCKSFALL PROBLEMKIND, Bild der Wissenschaft, 11/2011, Seite 84 – Kultur & Gesellschaft

  54. Bush, Obradović, Adler, Boyce (2011): Kindergarten stressors and cumulative adrenocortical activation: the “first straws” of allostatic load?; Dev Psychopathol. 2011 Nov;23(4):1089-106. doi: 10.1017/S0954579411000514.

  55. Berndt (2013): Resilienz, Seite 140

  56. Langzeitstudie des amerikanischen National Institute of Child Health and Human Development in Bethesda, Maryland, Start 1991, n > 1000, zitiert nach Glomp (2011): GLÜCKSFALL PROBLEMKIND, Bild der Wissenschaft, 11/2011, Seite 84 – Kultur & Gesellschaft

  57. Obradović, Bush, Boyce (2011): The interactive effect of marital conflict and stress reactivity on externalizing and internalizing symptoms: the role of laboratory stressors. Dev Psychopathol. 2011 Feb;23(1):101-14. doi: 10.1017/S0954579410000672.

  58. Essex, Boyce, Hertzman, Lam, Armstrong, Neumann, Kobor (2013): Epigenetic Vestiges of Early Developmental Adversity: Childhood Stress Exposure and DNA Methylation in Adolescence; Child Dev. 2013 Jan; 84(1): 58–75. doi: 10.1111/j.1467-8624.2011.01641.x

  59. Boyce, Bick, Zhu, Stamoulis, Fox, Zeanah, Nelson (2015): Effect of Early Institutionalization and Foster Care on Long-term White Matter Development: A Randomized Clinical Trial; JAMA. 2015;313(15):1564-1565. doi:10.1001/jama.2015.34. n = 64

  60. Kordahji, Ben-David, Elkana (2021): Attachment Anxiety Moderates the Association Between ADHD and Psychological Distress. Psychiatr Q. 2021 Jul 10. doi: 10.1007/s11126-021-09919-6. PMID: 34245401. n = 99

  61. Angabe der WHO, zitiert aus Weber, Ohrfeigen für die Seele, Süddeutsche Zeitung 15.10.2015, Seite 16

  62. Stoltenborgh (2012), Journal of Aggression, Maltreatment & Trauma, Metaanalyse von 29 Studien, n = 7.082.279

  63. Vachon, Kruger, Rogosch, Cicchetti (2015): Assessment of the Harmful Psychiatric and Behavioral Effects of Different Forms of Child Maltreatment; doi:10.1001/jamapsychiatry.2015.1792, Langzeitstudie, n = 2300

  64. Ackerman, Newton, McPherson, Jones, Dykman (1998): Prevalence of post traumatic stress disorder and other psychiatric diagnoses in three greoups of abused children (sexual, physical and both). Clid Abuse & Neglect, 22: 759-774, zitiert von Krüger (2014): Vortrag Trauma und Traumafolgestörung bei Kindern und Jugendlichen, Seite 6

  65. Pynoos, Fairbank, Steinberg, Amaya-Jackson, Gerrity, Mount, Maze (2008): The National Child Traumatic Stress Network: Collaborating to improve the standard of care. Professional Psychology: Research and Practice, Vol 39(4), Aug 2008, 389-395. http://dx.doi.org/10.1037/a0012551, zitiert nach Krüger (2014): Vortrag Trauma und Traumafolgestörung bei Kindern und Jugendlichen, Seite 8

  66. Glomp (2011): GLÜCKSFALL PROBLEMKIND, Bild der Wissenschaft, 11/2011, Seite 84 – Kultur & Gesellschaft mit Verweis auf Tom Boyce und Bruce Ellis, University of Arizona

  67. Tews (2010): Hochsensibilität – Der schmale Grat zwischen Krankheit und Fähigkeit

  68. Trappmann-Korr (2008/2010), Das Phänomen Hochsensivität und der Zusammenhang mit AD(H)S, Seite 10