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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 manifesting ADHD

A genetic disposition for ADHD does not necessarily lead to ADHD. If there are no stressful experiences in early childhood, this significantly increases the chances of not developing ADHD.
No stress experience does not mean that children have to be spoiled - that would be a serious misunderstanding.

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

Example:
If a child has injured themselves while playing (e.g. banged their knee), it is dysfunctional to scold the child or make an issue of the injury when they are very upset - because this would increase the significance of the injury and thus also the perception of pain. Fear and pain perception are learned in the same way as other skills. Appropriate care for the injury and positive, calm comfort, which above all provides emotional security, are the most important elements of a good bond.
A child needs the security of knowing that it is allowed to make mistakes. If the child learns that the parents trust them, that they do not want to make mistakes and therefore do not dramatize mistakes, but at the same time the parents naturally expect the child to learn from their mistakes and support them in doing so, they have no reason to use mistakes to provoke attention.

As the mechanism that early childhood stress increases the risk of acquiring mental disorders is universal, this does not only apply to ADHD. The model differs with regard to various mental disorders only in that different mental disorders can develop depending on the type of genetic predispositions and the type and timing of stress.
Therefore, the fact that a secure attachment reduces the risk of an existing genetic predisposition to a mental disorder manifesting itself is also universal.

2. Secure attachment contributes to the prevention of ADHD manifestation

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

Animal studies show that the positive effect of secure attachment and social behavior of the surrogate mother clearly outweighs the negative influence of the genes inherited from the biological mother.

  • Rats that descended from low-attachment mothers and were entrusted to high-attachment mothers for rearing had little tendency toward disorganized attachment behavior or ADHD; conversely, rats that descended physically from high-attachment mothers and were reared by low-attachment mothers had significant tendencies toward disorganized attachment behavior or ADHD.1

  • Early life stress in mice alters stress coping behavior in adult animals and in 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 reduced in sperm of exposed males in adulthood. If animals with genetic exposure grow up without early childhood stress in a safe environment with many opportunities for social contact (enriched environment), no adverse behavioral changes are observed. Rather, the aforementioned changes in GR gene expression and DNA methylation in the hippocampus of the male offspring were reversed.2

  • Caring brood care in rat pups in 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, only different brood care showed a different expression of the stress systems:

    • Rat pups that received little grooming and physical attention from their mothers developed lower levels of the transcription factor NGFI-A (also known as EGR1) in the hippocampus. This resulted in increased methylation and thus 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
      • Increased basal glucocorticoid level (in mice: corticosterone, in humans: cortisol)
      • Excessive cortisol stress response
      • More anxious behavior
      • In females: less brood care of their own children
    • Rat pups that received a lot of grooming and physical care from their mother developed a higher level of the transcription factor NGFI-A (EGR1) in the hippocampus. This results in reduced methylation and thus higher expression of the glucocorticoid receptor gene (GR gene) in the hippocampus.4
      A higher GR expression level in the hippocampus correlates in adulthood with4
      • Lower basal glucocorticoid level (in mice: corticosterone, in humans: cortisol)
      • Lower glucocorticoid stress response
      • Less anxious behavior
      • In females: increased brood care of their own children
  • Similarly, it is reported that all monkey children who were born to aggressive mothers and raised by caring mothers were able to give their children a caring bond, while 50 to 60% of the biological children of caring mothers who were raised by violent mothers also showed this violence towards their own children.5

  • High oxytocin receptor density in the nucleus accumbens increased newborns’ resistance to neglect through 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 influences attachment style.
    For the influence of attachment style on the likelihood of later mental disorders, see ADHD - Prevention and screening - What parents can do. Touch increases the release of oxytocin 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 provided a high level of care as adults9

    • More benzodiazepine receptors in the amygdala (central, lateral, basolateral) and locus coeruleus
    • More alpha2-adrenoreceptors in the locus coeruleus
    • Fewer CRH receptors in the locus coeruleus
    • A significantly lower level of anxiety in response to new stimuli
      Anxiety and fear are moderated, among other things, by
      • 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 care during infancy serves to “program” behavioral responses to stress in the offspring by altering the development of the neural systems that mediate anxiety.910

Studies on humans confirm these results as a universal pattern.11
Secure attachment behavior on the part of parents can have a massive influence on children’s behavior and thus prevent the manifestation of a genetic predisposition to a mental disorder.

2.1. Attachment style of parents to child particularly important for opportunity/risk genes

A number of studies have shown that the influence of attachment style is not the same for all children, but is much stronger for children with certain genetic dispositions (“opportunity/risk genes”). For these children, the attachment style has particularly serious effects, both negative and positive.121314
Fundamental to this is Belsky’s differential susceptibility hypothesis.15 It is striking that all genes named by Belsky as chance-risk genes were named as candidate genes for ADHD. Candidate genes for ADHD

So far, only a few genes have been described as specific opportunity/risk genes.

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

DRD4-7R, causes a less sensitive dopamine D4 receptor, which requires three times the amount of dopamine to react. This has the effect of an apparently reduced dopamine level. More on this, including evidence, at Dopamine receptor D4 gene, DRD4 (chromosome 11p15.5 exon III, VTNR) (x) In the article Candidate genes for 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, whereby we assume that the high sensitivity mediated by DRD4-7R is not a consequence that would only arise 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 those affected particularly susceptible to external influences and thus mediates a particularly positive and particularly negative development (opportunity-risk).

In children with the DRD4-7R gene variant (also relevant for ADHD), the parenting and attachment style has a serious influence. Poor attachment behavior is 6 times more likely to trigger high levels of aggression (risk: plus 600%). At the same time, a good attachment style, even if it was subsequently trained, results in above-average empathy (and non-aggressiveness), i.e. above and beyond 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 carriers, while a negative, controlling style leads to pronounced 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 speaks in favor of the assumed link between the DRD4-7R gene form and high sensitivity.

Conversely, only children with DRD4-7R benefited from therapeutic support for maternal sensitivity in child handling.20

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

In children with ADHD and the ADHD risk gene disposition DRD-4-7R, training parents in dealing with their children brought about an improvement of 27% on a symptom scale, while children with ADHD without this gene disposition achieved an improvement of only 12% from the same training of their parents.22

It was also observed that children with a DRD-4-7R disposition developed a particularly sociable nature (compared to non-ADHD children) if their parents had 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 secure parental attachment were those who donated the most, while those with the DRD4-7R gene who had grown up with 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 in order to receive a higher reward at the end, while those with DRD4-7R who had grown up with an insecure attachment had a significantly higher delay aversion than the control group.24

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

2.1.2. 5-HTTLPR short - Depression chance/risk gene polymorphism

People with the (short) risk variant of the serotonin transporter gene SLC6A4, the 5-HTTLPR short polymorphism,27 have a higher risk of depression. However, the increased risk of depression only exists 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
Around 20% of all Western Europeans have the 5-HTTLPR gene polymorphism 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, pronounced externalizing or internalizing behavior is associated with the cumulative presence of both gene variants (DRD4-7R and 5-HTTLPR short).32

Further studies confirm that those genes that cause a particular vulnerability to early stress experiences are also opportunity genes for special support during this time.333435

The stress response in newborns 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 - opportunity/risk gene

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

COMT-Met-158-Met carriers are more suitable than COMT-Val-158-Val carriers

  • Mentally more powerful (more efficient, not more intelligent)373839
  • More sensitive to stress (high dopamine level (only) in the PFC even at rest, significant increase in dopamine (only) in the PFC even under mild stress)
  • More anxious
  • More sensitive to pain.404142

Another study confirms the leverage effect of the COMT gene for the effect of parental behavior on ADHD symptoms (gene-environment interaction).43
Severe anxiety in the mother during pregnancy increases the unborn child’s risk of ADHD 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 overall more sensitive 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 only have major behavioral problems if they have suffered maltreatment. Without maltreatment, they were less aggressive than boys with the non-risk variant of MAO-A.1847 An MAO-A variant that breaks down dopamine particularly efficiently prevented antisocial behavior in maltreated children.48

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

The response to stress in newborns with the MAOA-L allele was associated with higher scores for Negative Emotionality, lower scores for Orientation/Regulation and a lower decrease in cortisol after acute stress.36

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

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

2.1.6. Increased sensitivity due to opportunity-risk genes DRD4-7R / 5-HTTLPR

The 5-HTTLPR short gene polymorphism 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. With increasing intensity (loudness) of an acoustic stimulus, the amplitude increases faster in 5-HTTLPR short than in the l/l genotype. (Decrease via electrode Cz = vertex of the head).50
We understand this to mean that people with 5-HTTLPR short are more sensitive to acoustic stimuli.

Details on serotonin transporters:51

High (5HTTLPR long/long) and low (5HTTLPR short/short) serotonin activity caused by 5-HTTLPR indicates ADHD symptoms in the presence of psychosocial stress, but not medium (5HTTLPR long/short) serotonin activity.52

2.1.7. Stress sensitivity as a risk with opportunity/risk genes

A study of preschool children revealed a particularly intense stress reaction (heart rate and cortisol levels) in some of them. These children who reacted more intensively were more aggressive than the others in the event of problems at home (money problems, marital problems, strict parenting, caregiver depression). Without these problems, on the other hand, the stress-sensitive children behaved more socially than the stress-resistant children, acted out less often and were more involved in school53 5455

Children who had a “difficult” temperament at 6 months of age showed more behavioral problems at the age of 10 than children with an “easy” temperament at that time if they were poorly cared for by their caregivers. With good and loving care, they developed better social skills and had fewer problems than the “easy” children.
The same applied to thinking skills and academic performance.
The different susceptibility to external influences remained with those affected at least until early puberty, but probably throughout their lives.56

There are several other studies on this topic.57585459

From our point of view, this answers the question of whether discipline and harshness or empathy and warmth are the best way to make children strong. In any case, harsh, strict parenting destroys sensitive children. However, clear rules that don’t just apply sometimes are helpful for all children.

2.1.8. Conclusions on opportunity/risk genes

It is assumed that 15 to 20 % of all people are equipped with the opportunity/risk genes described.60
This prevalence of chance/risk genes in people of 15 to 20 % coincides (by chance?) with the prevalence figures assumed for high sensitivity: 15 to 20 %61 or 15 to 25 %.62

The wealth of results indicates that certain genetic variants increase the “sensitivity” or “intensity” of people, with these having an equal impact as both a risk and an opportunity. The only difference is that as children, those affected are helplessly at the mercy of whether their genetic disposition will turn out to be an opportunity or a risk due to the lack of influence on their parents’ attachment behavior.
The results can be interpreted to mean that a higher level of sensitivity means greater vulnerability on the one hand and greater development potential on the other. This is in line with our understanding of the connection between giftedness and high sensitivity. Giftedness and ADHD

A basic pattern emerges:
Gene variants can cause changes in the brain, as can early childhood experiences. If the 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 in which the healthy balance (the optimal level for neurotransmitters) is abandoned. This often leads to (psychological) problems. A gene variant that breaks down dopamine particularly well would, without a simultaneous environmental effect that increases dopamine by other means, result in a dopamine level that is 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 early childhood stress in the first generation, which led to 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 expression in newborns can show which modes of handling can bring about psychologically healthy development. (This expressly does not include a statement as to whether this is ethically justifiable. This must be discussed elsewhere)

2.2. 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 levels of depression and anxiety. Anxious attachment style correlated with higher psychological distress in adults with ADHD, and secure attachment style did not correlate with ADHD, anxiety and depression, which the authors interpret as a resilience factor against psychological distress in ADHD sufferers.63

3. Frequency of maltreatment and ADHD development

The prevalence of sexual abuse in children is 1.6 %,64 for physical abuse at 8 %64 and for psychological abuse between 0.3 and 36.3 %.65 Psychological abuse has the same fatal consequences in terms of genetic manifestation of predispositions, brain developmental delays and long-term stress dysregulation as physical or sexual abuse.66
The wide range of 0.3% to 36.3% for psychological abuse is probably due to different scales.
Further 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 behavioral disorders.67
According to another study, of n = 9336 traumatized children, 48 % developed behavioral problems, 41 % school problems and 37 % behavioral problems in school/kindergarten etc., each of which is associated with ADHD. 31 % of the children developed attachment disorders, 11 % suicidal tendencies and 24 % PTSD.68

4. Social support

Social support reduces long-term consequences of ADHD.69


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