3. Stressful physical or emotional childhood experiences as the cause of ADHD

Author: Ulrich Brennecke
Review: Dipl.-Psych. Waldemar Zdero

Stressful physical or psychological childhood experiences can be a contributory cause of ADHD.

For infants:
Bottle feeding increases the risk of ADHD, while breastfeeding reduces the risk. Crying babies, feeding and sleeping problems in infants, subependymal pseudocysts and antihistamines in the first years of life increase the risk of ADHD.

For infants and children:
Exposure to passive smoking, air pollution (especially particulate matter and nitrogen oxides) and various pollutants such as lead, manganese or phthalates are associated with an increased risk of ADHD.
Surgical procedures under anesthesia, neurodermatitis, bacterial infections, concussions are ADHD risk factors, as are stressful psychological childhood experiences such as trauma, chronic stress or growing up in a home.
Poor bonding behavior of the mother or parents in childhood, stress of the mother in childhood or mental health problems of the parents increase the risk of ADHD in children, as do low socio-economic status, a low level of education or unemployment of the parents.
Earlier school entry and the young age of a child within a class are further risk factors.

During puberty:
A high level of stress during puberty is considered a risk factor for the persistence of ADHD into adulthood.

The % values indicate the possible ADHD risk increase due to the respective cause.

• 3.1. Stressful physical childhood experiences as a (co-)cause of ADHD
  • 3.1.1. Newborns, infants
    • 3.1.1.1. Screaming children (+ 30 to + 1181 %)
      • 3.1.1.1.1. Factors that increase the risk of crying children
      • 3.1.1.1.2. Increased risk of ADHD in crying children
    • 3.1.1.2. Bottle feeding increases (up to + 270 %), breastfeeding reduces ADHD risk (- 23 % to -74 %)
    • 3.1.1.3. Feeding problems with infants
    • 3.1.1.4. Sleep problems in infants
    • 3.1.1.5. Subependymal pseudocysts
    • 3.1.1.6. Valproic acid
    • 3.1.1.7. D-3 insufficiency in the first 12 months
  • 3.1.2. Children
    • 3.1.2.1. Bacterial infections (+ 693 %)
      • 3.1.2.1.1. Bacterial meningitis (inflammation of the meninges) (+ 150 % to + 280 %)
    • 3.1.2.2. D-3 insufficiency (+157 %)
    • 3.1.2.3. Surgical procedures under anesthesia (+ 39 %)
    • 3.1.2.4. Neurodermatitis / atopic eczema / atopic dermatitis in childhood
    • 3.1.2.4. Antihistamines in the first years of life
    • 3.1.2.5. Passive smoking - smokers in the environment in the first years of life (+ 42 % to + 170 %)
    • 3.1.2.6. Air pollution in childhood
      • 3.1.2.6.1. Particulate matter and nitrogen oxides (+ 78 %)
      • 3.1.2.6.2. Renovation fumes, incense, cooking oil vapors
    • 3.1.2.7. Concussions and traumatic brain injuries (+ 68 %)
    • 3.1.2.8. Chlorpyrifos
    • 3.1.2.9. Sugar consumption
    • 3.1.2.10. Ozone exposure
    • 3.1.2.11. Hyperthyroidism / hyperthyroidism (+ 70 %)
    • 3.1.2.12. Abnormal thyroid hormone levels during pregnancy
    • 3.1.2.13. Perfluorooctane sulfonate (PFOS) (+ 77 %)
    • 3.1.2.14. β-Hexachlorocyclohexane (β-HCH) (+ 75 %)
    • 3.1.2.15. Lead (+ 160 % to + 306 %)
    • 3.1.2.16. Mercury (+ 168 %)
    • 3.1.2.17. Manganese (+ 163 %)
    • 3.1.2.18. Arsenic
    • 3.1.2.19. Phthalates (+ 212 % (girls) to + 254 % (boys) )
    • 3.1.2.20. Febrile convulsions (+ 28 % to + 66 %; + 640 % in premature babies)
    • 3.1.2.20. Early puberty (pubertas praecox) (+ 40 %)
    • 3.1.2.21. Pyrethroid pesticides
    • 3.1.2.21. Metopic synostosis (+ 500 %)
    • 3.1.2.22. Organophosphates
    • 3.1.2.23. Polychlorinated biphenyls (PCBs)
    • 3.1.2.24. Lack of sleep
    • 3.1.2.26. Craniosynostosis
    • 3.1.2.27. Acne vulgaris
• 3.2. Stressful psychological childhood experiences as a (co-)cause of ADHD
  • 3.2.1. Stress
    • 3.2.1.1. Early massive stress experiences
    • 3.2.1.2. Stressful experiences in childhood and early adolescence cause persistent ADHD in adulthood
    • 3.2.1.3. Growing up in a home
    • 3.2.1.4. Growing up in adoption
    • 3.2.1.5. Growing up in a dysfunctional neighborhood
    • 3.2.1.6. Relatively earlier school enrollment / older classmates
    • 3.2.1.7. Little green growth in the vicinity of kindergarten / school / home (+ 20 %)
    • 3.2.1.8. Car traffic density on nearest road (+ 10 %)
    • 3.2.1.9. Noise from roads and neighbors
  • 3.2.2. Parents
    • 3.2.2.1. Poor bonding behavior of the mother/parents in the (first) years of childhood
    • 3.2.2.2. Emotionally withdrawn father behavior in infancy
    • 3.2.2.3. Stress in the mother during childhood
    • 3.2.2.4. Psychological problems of the parents
      • 3.2.2.4.1. Depression (+ 42 to 125 %)
      • 3.2.2.4.2. Bipolar Disorder ( + 100 %)
      • 3.2.2.4.3. Antisocial personality disorder of the father
      • 3.2.2.4.4. Alcohol problems of the father
    • 3.2.2.5. Incomplete families
    • 3.2.2.6. Family instability, constant arguments between the parents
    • 3.2.2.7. Young age of parents (+ 14 % to + 92 %)
    • 3.2.2.8. Low socio-economic status of the family of origin (+ 50 % to + 130 %)
    • 3.2.2.9. Low level of education of parents (+ 3.5 % to + 4.9 %)
    • 3.2.2.10. Unemployment of parents (+ 2.1 %)
    • 3.2.2.11. Parents are less able to reflect on their parental role
    • 3.2.2.12. Low educational attainment and ADHD mutually causal
  • 3.2.3. Media
    • 3.2.3.1. Early television consumption
    • 3.2.3.2. Amount of media consumption does not cause ADHD, media consumption addiction correlates with ADHD
• 3.3. Characteristics without increased risk of ADHD
• 3.4. Characteristics with risk reduction of ADHD

3.1. Stressful physical childhood experiences as a (co-)cause of ADHD¶

3.1.1. Newborns, infants¶

3.1.1.1. Screaming children (+ 30 to + 1181 %)¶

3.1.1.1.1. Factors that increase the risk of crying children¶

If the parents are heavy smokers, or if the mother smokes during pregnancy, the risk of a crying child increases by 30 to 150% (several studies); the largest study on this (n = 5845) states a 69% increased risk.¹
In addition, there are several other possible causes that should be systematically ruled out.²

3.1.1.1.2. Increased risk of ADHD in crying children¶

Cry babies have a significantly increased risk of ADHD.³⁴ Another study reports an 11.8 times higher risk of developing hyperactivity at the age of 8 to 10 years (plus 1181%), behavioral problems and a negative emotional orientation were reported twice as often as in those not affected.⁵

3.1.1.2. Bottle feeding increases (up to + 270 %), breastfeeding reduces ADHD risk (- 23 % to -74 %)¶

Infants who were not breastfed showed an increased risk of ADHD as children, while children who were breastfed as infants showed a decreased risk of ADHD ^{7 8 910}

• 3.71-fold ADHD risk (OR = 3.71). (Meta-analysis of k = 11 studies).¹¹
• almost 3 times the risk of ADHD¹²
• approx. 1.55-fold ADHD risk (OR = 1.55)¹³

Children with ADHD were 1.51 times more likely to be exclusively breastfed for less than 3 months and 52% less likely to be exclusively breastfed for more than 3 months. Children with ADHD had a significantly (2.44 months) shorter duration of breastfeeding (SMD: Hedges’ g = - 0.36) (meta-analysis of k = 11 studies). ¹¹

Children who were exclusively breastfed had a lower risk of breastfeeding compared to children who were exclusively bottle-fed

• aDHD risk reduced by 23¹⁴
• a 36% reduction in the risk of ASA¹⁴
• aDHD risk reduced by 38% with exclusive breastfeeding for at least 6 months, after adjustment for potential confounding factors¹⁵
• Each additional month of breastfeeding reduced the risk of ADHD by 8%¹⁵
• Each additional month of exclusive breastfeeding reduced the risk of ADHD by approx. 8% (but not statistically significant)¹⁵

Partially breastfed children had a

• aDHD risk reduced by 9 %¹⁴

• aSS risk reduced by 11 % ¹⁴

• Whether complementary food was given before 6 months of age or later had no influence¹⁴¹⁵

• In a small Lebanese correlational study (n = 119), breastfeeding reduced the risk of ADHD by 74% (OR = 0.263).¹⁶

The risk of ADHD decreases with the duration of breastfeeding.¹⁷¹⁸¹⁹

One study found no ADHD-preventive effect of breastfeeding.²⁰

Breast milk contains many substances that are essential for the development of babies, such as polyunsaturated fatty acids.⁹

It is unclear what influence breastfeeding through the breast or the food itself has on this. Body and skin contact has a considerable influence on the well-being and positive development of children.
It is known that bisphenol A increases the risk of ADHD. Bisphenol A was still much more common in baby bottles in 2007 than in 2011, which could explain why a study found a five-fold increase in the risk of ADHD in children fed with bottles in 2007, but no increase in risk in children fed with bottles in 2011.²¹

3.1.1.3. Feeding problems with infants¶

Feeding problems in infants correlate with ADHD in adolescence and adulthood.⁴

3.1.1.4. Sleep problems in infants¶

Sleep problems in infants correlate with ADHD in adolescence and adulthood.⁴

3.1.1.5. Subependymal pseudocysts¶

Subependymal pseudocysts in newborns increase the risk of ADHD and autism.²²

3.1.1.6. Valproic acid¶

Studies in mice suggest that valproate administration in newborns could cause permanent damage similar to that caused by ASA and, in some cases, ADHD.²³

3.1.1.7. D-3 insufficiency in the first 12 months¶

A vitamin D3 level of less than 25 ng/ml in the first 12 months of life was dose-dependently associated with an increased risk of ADHD in childhood. This also applied to ASD and Emotional Behavioral Disorders²⁴
This is consistent with the findings of an increased risk of ADHD if the mother has a D3 deficiency during pregnancy (see there).

3.1.2. Children¶

3.1.2.1. Bacterial infections (+ 693 %)¶

Severe bacterial infections in childhood or adolescence massively increase the risk of severe mental disorders (HR):²⁵

• ASS: 13,80
• ADHD: 6.93
  • ADHD medication use: 11.81
• Tic Disorder: 6.19
• OCD: 3.93
• Bipolar Disorder: 2.50
• Depressive disorders: 1.93
  • Antidepressant intake: 2.96
  • Mood stabilizer intake: 4.51
  • Atypical antipsychotic use: 4.23

Of the bacterial species examined (streptococci, staphylococci, pseudomonas, klebsiella, haemophilus, mycoplasma, tuberculosis, meningococci, escherichia, chlamydia and scrub typhus), streptococci were associated with the most disorders. ADHD was associated with eight bacterial pathogen infections.

The prevalence of Streptococcus agalactiae infection (Group B Streptococcus, GBS) in infants was 0.07%.
GBS has brought about:²⁶

• increased infant mortality (19.41-fold)
• long-term neurological developmental disorders (3.49-fold)

GBS meningitis increased the risk of²⁶

• ADHD
• cerebral palsy
• Epilepsy
• Hearing impairment
• profound and specific developmental disorders

Antibiotic administration in the second year of life increased the risk of ADHD by 20 to 33% and of sleep problems by 24 to 50% in a very large study.²⁷ An even larger study from Korea found a 10% dose-dependent increase in the risk of ADHD, with prenatal and early childhood administration together further increasing the risk²⁸
A smaller study found more frequent behavioral difficulties and depressive symptoms in 3 1/2 year old children who had received antibiotics in the first year of life.²⁹ Two other studies found no increased risk of mental disorders when antibiotics were given in the first 1 ³⁰ to 2³¹ years of life.

3.1.2.1.1. Bacterial meningitis (inflammation of the meninges) (+ 150 % to + 280 %)¶

Consequences, children with bacterial meningitis (but not enteroviral meningitis) had an increased risk of ADHD or ADHD medication use:³²

• Meningitis in the first 90 days of life;
  • ADHD risk 2.8-fold (aHR 2.8)
  • ADHD medication intake 2.2-fold
  • ASS risk 1.9-fold
  • Behavioral and emotional disorders 2-fold
  • Learning and intellectual development disorders 4.2-fold
• Meningitis between day 90 and 18 years:
  • ADHD risk 1.4-fold
  • ADHD medication intake 1.5-fold
  • Learning and intellectual development disorders 1.5-fold

3.1.2.2. D-3 insufficiency (+157 %)¶

A meta-analysis of 10,334 children and adolescents found a 2.57-fold risk of ADHD with a D3 insufficiency (between 10 and 30 mg/nl in blood plasma).³³

3.1.2.3. Surgical procedures under anesthesia (+ 39 %)¶

Children who underwent a single surgical procedure under anesthesia up to the age of 5 were 37% more likely to take ADHD medication in later years.³⁴ A Korean cohort study found a 41% increased risk of ADHD as a consequence of general anesthesia in early childhood. In addition, the duration of general anesthesia correlated with an increased risk of ADHD.³⁵
One study found a 37% increase in the risk of ADHD with a single anesthetic during an operation at the age of up to 5 years, and a 75% increase with multiple anesthetics³⁶
A cohort study of n = 15,072 children, half of whom had received anesthetics between the ages of 0-3 years, found a 39% increased risk of ADHD.Frequency of anesthetic exposure, duration of exposure, male sex, and central nervous system surgery were significant risk factors for ADHD in the future.³⁷
Other studies have come to similar conclusions.³⁸³⁹
A meta-analysis found a 25% increase in the later risk of ADHD due to general anesthesia in childhood (RR = 1.26).⁴⁰

• 38 % (RR = 1.38) due to single general anesthesia of max. 60 minutes in children
• 55 % (RR = 1.55) by single general anesthesia of max. 61 to 120 minutes or more than 120 minutes in children
• 61 % (RR = 1.61) after several general anesthetics

In contrast, a cohort study in Taiwan found no increased risk of ADHD due to anesthetics in the first 3 years of life.⁴¹

The extent to which the likelihood of a surgical procedure under anesthesia is already influenced by the increased likelihood of accidents among people with ADHD remains to be seen. For more information, see ⇒ Consequences of ADHD.

3.1.2.4. Neurodermatitis / atopic eczema / atopic dermatitis in childhood¶

Neurodermatitis / atopic eczema / atopic dermatitis in childhood correlates with an increased risk of ADHD.⁴²
In contrast, a cohort study found no significant (+2%) increased risk of ADHD in childhood atopic dermatitis.⁴³
A cohort study of n = 69,732,807 people found an increased risk of learning difficulties (OR = 1.77) and memory problems (OR = 1.69) with atopic dermatitis.
The increase in risk was unevenly distributed: In children with neurodevelopmental disorders such as ADHD, the risk of memory or learning difficulties was increased 2 to 3-fold. In contrast, atopic dermatitis did not change the risk of learning or memory difficulties in children without neurodevelopmental disorders.⁴⁴

One study found evidence that susceptibility to atopic dermatitis causally increased the risk of ADHD (+ 11.6 %) and ASD (+ 13.1 %). Conversely, susceptibility to ADHD (+ 11.2 %) and anorexia nervosa (+ 10 %) caused an increased risk of atopic dermatitis. Only the causal relationship between AD and ASD was independent of the reverse effect bias.⁴⁵

In low birth weight infants, a history of T2 inflammatory diseases such as asthma and atopic dermatitis increased the risk of:⁴⁶

• mental disability by 35 %
• ASS by 47 %
• ADHD by 81 %
• Learning disability by 74 %

3.1.2.4. Antihistamines in the first years of life¶

A large cohort study found that taking antihistamines (especially first-generation antihistamines) in the first years of life significantly increased the risk of later ADHD. Disorder of REM sleep was cited as a possible cause, which secondarily impaired brain maturation.⁴⁷

3.1.2.5. Passive smoking - smokers in the environment in the first years of life (+ 42 % to + 170 %)¶

Passive nicotine exposure increases the risk of ADHD.⁴⁸ Nicotine exposure in children is associated with a 1.42-fold⁴⁹ to 2.7-fold⁵⁰ increase in ADHD.¹⁸ In one study, children with ADHD were twice as likely to have smokers in the family as children who were not affected.⁵¹
In the case of passive smoking, a connection is made to certain MAO-A gene variants that cause a lower level of serotonin degradation.⁵²

In children, a linear association was found between salivary cotinine (a nicotine breakdown product) and hyperactivity and behavioral problems. This association remained significant after adjusting for family poverty, parental education, a history of ADHD, hostility, depression, caregiver IQ, and obstetric complications, and also after excluding from the calculation children of mothers who had smoked during pregnancy. This indicates that exposure to nicotine in the first years of life alone can increase hyperactivity and behavioral problems.⁵³

3.1.2.6. Air pollution in childhood¶

3.1.2.6.1. Particulate matter and nitrogen oxides (+ 78 %)¶

A large cohort study found a statistically significant association between nitrogen oxides and particulate matter (<2.5 pm) in childhood and the development of ADHD.⁵⁴ A smaller cohort study confirmed this for particulate matter, but not for nitrogen dioxide.⁵⁵ Another cohort study found a 40% to 78% increased risk of ADHD from PM2.5 exposure in the first to third year of life. The risk was associated with PM2.5 >16 μg/m3 and increased sharply with PM2.5 > 50 μg/m3. There was no gender-dependent association.⁵⁶
In another study, the risk of ADHD increased by 38% for every 10 μg/m3 increase in nitrogen oxide and by 51% for every 5 μg/m3 increase in particulate matter PM2.5. When both factors were considered together, the influence of nitrogen oxide predominated. The age and gender of the persons with ADHD as well as the parents’ level of education and income were excluded. A meta-analysis of 28 reports found similar results for the majority of the reports.⁵⁷ Even at non-toxic doses, nitrogen oxides have an influence on glutamatergic, opioidergic cholinergic and dopaminergic neurotransmission in the brain.⁵⁸
One study found a 97% increase in the risk of ADHD in children due to a 10 μg/m3 increase in PM10 and a 32% increase in nitrogen oxide due to a 10 μg/m3 increase.⁵⁹
One study found no association between exposure to PM2.5 and NO2 at age 12 and ADHD at age 18, but with depression at age 18.⁶⁰

A meta-analysis of 12 studies found a correlation between particulate matter and ADHD in children in 9 of them.⁶¹
A Korean cohort study found a 44% increase in the risk of ADHD in children and adolescents for every 10 µg/m3 increase in PM10, with a tendency towards dose-dependent symptom severity.⁶² A Taiwanese register study came to comparable results.⁶³
A longitudinal study of 2,750 children found an increased risk of ADHD and ASD from particulate matter PM2.5 and PM10, but not from ambient noise, ozone, sulfur dioxide, soot, nitrogen dioxide, or nitrogen oxide⁶⁴
A Polish study found a correlation between⁶⁵

• long-term NO2 and PM10 exposure with poorer visual attention in children with ADHD
• short-term NO2 exposure with less efficient executive attention and higher impulsivity in TD children and more errors in children with ADHD
• short-term PM10 exposure with fewer omission errors in the CPT in TD children

A meta-analysis examined the effects of traffic-related air pollution on the neurological development of children in several countries using PM2.5 (particulate matter <2.5 µm), PM10, elemental carbon (EC), black carbon (BC), NO2 and NOx:⁶⁶
Increased traffic-related air pollution correlated with an increase in ADHD, autism and impaired cognitive development.
PM2.5 reduced the expression of BDNF in the placenta.
Elevated PM2.5 concentrations impaired the cognitive development of adults (episodic memory) and increased major depressive disorders.
Elevated NO2 concentrations correlated with dementia, NOx with Parkinson’s disease.

In one study, inhaled printer particles led to a 5-fold increase in dopamine levels in rats, although this was probably due to increased synthesis and not reduced degradation.⁶⁷

Individual differences in susceptibility to air pollution appear to be related to the ε4 allele of the apolipoprotein E gene (APOE), which is the most important genetic risk factor for Alzheimer’s disease. PAH, EC and NO2 correlated significantly only in carriers of the APOEε4 allele⁶⁸

• Behavioral problems,
• a smaller decrease in inattention over time
• a smaller caudate volume

Elevated levels of NO2 and particulate matter in schools appear to impair the development of working memory. For each interquartile range increase in exposure, the annual development of working memory decreased⁶⁹

• by 20 % for NO2 outdoors
• by 19.9 % for ultrafine particulate matter indoors

Children in schools with higher levels of chronic traffic-related air pollution (elemental carbon, nitrogen dioxide and ultrafine particulate matter [10-700 nm]) in the schoolyard and classroom showed slower cognitive development. The improvement in working memory was only 7.4 % (compared to 11.5 %). Growth was reduced in all cognitive measures. Moving from the first to the fourth quartile of indoor elemental carbon levels reduced the gain in working memory by 13.0%.⁷⁰ Another study found similar results.⁷¹

One study found an increase in ADHD-related hospital admissions in adolescents after short-term exposure to nitrogen oxide (+68%), short-term exposure to sulphur dioxide (+29%) and short-term exposure to PM10 (+17%)⁷²

Exposure to nitrogen dioxide, ozone and sulfur dioxide has been linked to behavioral and developmental disorders, anxiety to particulate matter (PM10), ozone and sulfur dioxide, and overall pollution to ADHD and eating disorders⁷³

Emissions of nitrogen oxides in Germany fell by almost 2/3 between 1990 and 2020.⁷⁴

PM2.5 exposure⁷⁵

• reduced viability and increased apoptosis in hippocampal neurons
• disrupted synaptic ultrastructure and synapse-related protein expression

PKA/CREB/BDNF mediates the damaging effects of PM2.5 The neuronal and synaptic damage induced by PM2.5⁷⁵

• were aggravated by reduction of PKA/CREB/BDNF
• were improved by increasing KA/CREB/BDNF

3.1.2.6.2. Renovation fumes, incense, cooking oil vapors¶

A large Chinese study of 8,692 children aged 6 to 12 found a significant increase in the children’s risk of ADHD due to:⁷⁶

• Home renovations
• Incense burning
• Cooking oil vapors
• Smokers in the household

3.1.2.7. Concussions and traumatic brain injuries (+ 68 %)¶

Brain injury severity correlates with significantly higher ADHD symptomatology. Brain injury-altered default mode network (DMN) morphometry predicted higher ADHD symptomatology 12 months after injury, while salience network (SN) and central executive network (CEN) morphometry were not significant independent predictors.⁷⁷

One study examined mild (concussion) and severe traumatic brain injuries before the age of 10. The incidence was 1,156 per 100,000 person-years. At the age of 19, the risk of ADHD was increased by 68% and the risk of learning disability was increased by 29%.⁷⁸
In more severe cases of traumatic brain injury, the correlation was not statistically significant. In an analysis of cases with possible traumatic brain injury (equivalent to a concussion), the result was significant (risk of ADHD increased by 105%, risk of learning disability increased by 42%). The risk in adulthood was particularly increased in children with the least severe injuries.

Among 1,709 ice hockey players aged 11 to 17, the rate of concussions correlated with higher self-reported and parent-reported scores for attention problems. Only self-reported hyperactivity, not parent-reported hyperactivity, also correlated significantly with concussion. A T-score ≥ 60 combining attention problems and hyperactivity scores (an estimate of probable attention deficit hyperactivity disorder) was not significantly associated with incidence of injury or concussion⁷⁹

This is consistent with the known increased risk of accidents and injuries due to ADHD. The question therefore arises as to whether concussions and traumatic brain injuries are a cause or rather a consequence of ADHD.

3.1.2.8. Chlorpyrifos¶

In children between 1 and 6 years of age, chlorpyrifos residues in the blood correlated with the risk of ADHD.⁸⁰ Vitamin D reduced the risk.
Chlorpyrifos also significantly increases the risk of ADHD in the case of prenatal contamination of the mother during pregnancy.

3.1.2.9. Sugar consumption¶

One study found a correlation between sugar intake at 30 months and the risk of ADHD, sleep disorders and anxiety. No correlation was found at the age of 12 months.⁸¹
Whether this is a causal cause or a consequence of changed food preferences due to the disorder predisposition is an open question.

3.1.2.10. Ozone exposure¶

Children between the ages of 3 and 12 in China who were exposed to higher concentrations of ozone showed an increased risk of ADHD. This was further increased by sports¹⁹

3.1.2.11. Hyperthyroidism / hyperthyroidism (+ 70 %)¶

One study found a 1.7-fold prevalence of ADHD in children with hyperthyroidism.⁸²

Hyperthyroidism can cause ADHD-like symptoms, including anxiety, nervousness, irritability and physical hyperactivity. One study found a correlation between elevated TSH levels and hyperactivity in ADHD.⁸³

3.1.2.12. Abnormal thyroid hormone levels during pregnancy¶

Abnormal thyroid hormone levels during pregnancy can have profound effects on the development of the child’s brain and cognition⁸⁴⁸⁵ and impair

• Neurodevelopmental processes⁸⁶
  • Cell differentiation
  • Neurite growth
  • Synaptogenesis
  • Myelination
• Neurotransmitter systems⁸⁷
  • monoaminergic system
  • cholinergic system
  • which can lead to attention deficits and hyperactivity

Even transient subclinical thyroid abnormalities during pregnancy can have serious consequences.⁸⁸ Correcting severe maternal hypothyroidism before the 3rd semester of pregnancy appears to prevent cognitive impairments⁸⁹ and premature births .⁹⁰

Studies on mice with a mutated human thyroid receptor TRb 1 gene (TRbeta transgenic mice)⁹¹ found that these

• normal thyroid hormone levels of triiodothyronine (T3) and thyroxine (T4) (euthyroid) except for a short period during postnatal development
• into adulthood
  • Changes in the dopaminergic system (increased dopamine turnover)
  • ADHD symptoms
    • Hyperactivity
    • Inattention
  • ADHD symptoms are reduced by MPH

3.1.2.13. Perfluorooctane sulfonate (PFOS) (+ 77 %)¶

Perfluorooctane sulfonate (PFOS) in breast milk correlated with a 77% increased risk of ADHD per higher interquartile range.⁹²
PFOS caused ADHD symptoms (hyperactivity, cognitive problems) in zebrafish, decreased dopamine levels and the number of dopaminergic neurons, and disrupted the transcriptional profiles of genes related to the dopaminergic system. MPH alleviated the ADHD symptoms induced by PFOS and restored DA levels, the number of dopaminergic neurons and the expression of genes associated with DA metabolism.⁹³

3.1.2.14. β-Hexachlorocyclohexane (β-HCH) (+ 75 %)¶

Peβ-hexachlorocyclohexane (β-HCH) in breast milk correlated with a 75% increased risk of ADHD per higher interquartile range.⁹²

3.1.2.15. Lead (+ 160 % to + 306 %)¶

According to several meta-analyses, lead exposure during development increased the risk of ADHD by

• 239 to 306 %⁹⁴
• 160 to 260 %⁹⁵
• 95 %⁹⁶

3.1.2.16. Mercury (+ 168 %)¶

According to a meta-analysis, exposure to methylmercury during development increased the risk of ADHD by 168%.⁵⁰ A review describes the causality.⁹⁷⁹⁵
A meta-analysis found no significant increase in risk from mercury.⁹⁶

3.1.2.17. Manganese (+ 163 %)¶

According to a meta-analysis, exposure to manganese during development increased the risk of ADHD by

• 163 %⁵⁰
• 79 %⁹⁶
• Early exposure to manganese causes permanent attention problems via the mTOR pathway and an alteration of the catecholaminergic system⁹⁸ as well as sensorimotor problems.⁹⁹
  Manganese intoxication shows a correlation with certain CYP2D6 gene variants.¹⁰⁰ We consider it conceivable that these also have an influence on the risk of ADHD as a consequence of manganese exposure.

MPH reduced the attention problems and sensorimotor problems caused by early manganese exposure in rats. 0.5 mg/kg/d completely improved the attention problems, but only after prolonged treatment, 3.0 mg/kg/d improved the sensorimotor deficits immediately. Selective antagonization of D1, D2 or α2A receptors did not affect Mn-induced attention problems or their improvement by MPH. D2R antagonists reduced the sensorimotor deficits of Mn. D1 antagonists reduced the efficacy of MPH on sensorimotor deficits.⁹⁹

In people with ADHD, elevated manganese levels were only found in the hair, but not in blood levels.¹⁰¹
A doubling of the manganese content in teeth from both the prenatal and postnatal period increased the risk of attention problems and ADHD symptoms in the school years by 5%. Manganese from childhood showed no influence.¹⁰²
An animal model with developmental manganese exposure showed that manganese can cause permanent attention and sensorimotor deficits resembling ADHD-I. Oral methylphenidate was able to fully compensate for the deficits caused by early manganese exposure.¹⁰³

3.1.2.18. Arsenic¶

According to a meta-analysis, exposure to arsenic during development increased the risk of ADHD by

• 53 %⁹⁶

3.1.2.19. Phthalates (+ 212 % (girls) to + 254 % (boys) )¶

According to a meta-analysis, exposure to phthalates during development increased the risk of ADHD by 212% for girls and 254% for boys.⁵⁰
Another study found that phthalate exposure in early childhood only increased ADHD symptoms by 10% in children with ASD, primarily in the direction of externalizing behaviors.¹⁰⁴

3.1.2.20. Febrile convulsions (+ 28 % to + 66 %; + 640 % in premature babies)¶

According to clinical and animal studies, febrile convulsions have harmful effects on neurodevelopment, which can lead to ADHD, increased susceptibility to epilepsy, hippocampal sclerosis and cognitive decline in adulthood¹⁰⁵
Febrile convulsions in children increased the risk of ADHD by 28%¹⁰⁶ to 66%.¹⁰⁷ Prematurity of persons with ADHD who had febrile convulsions increased the risk of ADHD 6.4-fold and the risk of ASD 16.9-fold.¹⁰⁸

3.1.2.20. Early puberty (pubertas praecox) (+ 40 %)¶

Among girls with early puberty (onset of sexual maturation before the age of 8 for girls and before the age of 9 for boys), the prevalence of ADHD was found to be 13.5%.¹⁰⁹

3.1.2.21. Pyrethroid pesticides¶

The pyrethroid pesticide deltamethrin at low doses causes changes in ADHD- and NDD-related behaviors and in the striatal dopamine system during development in male mice.

Deltamethrin during development caused a multimodal biophenotype in the brain relevant to ADHD. Mouse mothers received deltamethrin (3 mg/kg or vehicle every 3 days) during gestation and lactation, which is well below the limits set by the EPA. Male offspring showed alterations in several canonical clock genes. Kinome analysis revealed alterations in the activity of several kinases involved in synaptic plasticity, including mitogen-activated protein kinase (MAP) ERK. Multiomics integration revealed a dysregulated protein-protein interaction network with primary clusters for MAP kinase cascades, regulation of apoptosis and synaptic function¹¹⁰

According to a meta-analysis, pyrethroid insecticides did not significantly increase the odds ratio for ADHD (0.99)⁵⁰

3.1.2.21. Metopic synostosis (+ 500 %)¶

Around one in two children who had surgery for metopic synostosis (trigonocephaly or metopic suture craniosynostosis) at 9.5 (± 7.9) months of age showed at least borderline hyperactivity and inattention scores at 10.3 (± 3.5) years of age.¹¹¹ Older age at surgery was associated with poorer executive functions.

3.1.2.22. Organophosphates¶

Exposure to organophosphates in childhood correlated with an increased risk of ADHD.⁹⁵

3.1.2.23. Polychlorinated biphenyls (PCBs)¶

Exposure to polychlorinated biphenyls (PCBs) in childhood correlated with an increased risk of ADHD.⁹⁵

3.1.2.24. Lack of sleep¶

Short sleep correlated with increased risk of anxiety, attention deficit hyperactivity disorder and activity-limiting emotional and psychological states after adjusting for ethnicity, deprivation, age and gender.¹¹²
Ethnicity and socioeconomic disadvantage in the neighborhood were independently correlated with short sleep and snoring/noisy breathing during sleep.
Long sleep correlated independently with an increased risk of depression.

3.1.2.26. Craniosynostosis¶

Craniosynostosis is a premature ossification of cranial sutures. Maternal smoking during pregnancy significantly increases the risk of craniosynostosis. In one study, the majority of children with craniosynostosis also showed symptoms of ADHD.¹¹³

3.1.2.27. Acne vulgaris¶

One study found moderately elevated levels in adolescents (12 to 17 years) with acne vulgaris for¹¹⁴

• Hyperactivity
• Hyperactivity/impulsivity
• Inattention
• ADHD total score

Both acne vulgaris and ADHD are thought to be partly caused by increased androgen hormone levels in the womb.

3.2. Stressful psychological childhood experiences as a (co-)cause of ADHD¶

Traumatizing experiences, but also stressful experiences that already cause considerable stress below the threshold of trauma, are risk factors for ADHD. Social risk factors increase the risk of ADHD.¹¹⁵¹¹⁶
Massive maternal stress in the first years of childhood causes significant epigenetic changes in the children’s DNA.¹¹⁷

Children whose parents were unmarried or unemployed or without social security or had a “very high” economic burden of childcare or where at least one parent had a disability certificate had a 21% increased risk of ADHD, a 36% increased risk of learning disability and an 80% increased risk of ASD at the age of 5.5 years. This affected 10.8% of the 19,185 children.¹¹⁸

3.2.1. Stress¶

3.2.1.1. Early massive stress experiences¶

Early childhood stress and chronic stress (neglect, deprivation, abuse, trauma) can be involved in the development of ADHD.^{119116 120 121} 20% to 50% of all children who experience early childhood trauma develop clinical ADHD symptoms.^119122123
The number of traumas correlates with the severity of ADHD¹²⁴ as well as with the risk of ADHD. The number of Adverse Childhood Experiences (ACEs) increased the risk of ADHD:¹²⁵

• 1 ACE: 2.1 times the risk of ADHD
• 2 ACEs: 4.5 times the risk of ADHD
• 3 and more ACEs: 5.2 times the risk of ADHD
• Estimates of ADHD symptoms were higher for sexual abuse, emotional and physical neglect, and bullying.

The stress caused by early separation from the mother triggered hyperactivity and inattention in rats, which could be eliminated by MPH.¹²⁶
The number of stressful life events (as measured by the Traumatic Events Screen Inventory for Children) correlated with more severe ADHD.¹²⁷
ADHD symptoms correlate with:¹²⁸

• K-SADS-PL values for post-traumatic stress disorder at the age of 14 and 15¹²⁹
• sexual and physical abuse before the age of 16 or 17¹³⁰¹³¹

A natural disaster during early childhood increased the risk of ADHD.¹³²

See in detail at ⇒ Trauma as a cause of ADHD

3.2.1.2. Stressful experiences in childhood and early adolescence cause persistent ADHD in adulthood¶

A study of stress levels in children with ADHD found that severe stress levels in childhood and adolescence were associated with severe ADHD-HI or ADHD-I progression into adulthood, while children with low stress levels in childhood and adolescence often showed remitting ADHD (ADHD-HI as well as ADHD-I).¹³³

3.2.1.3. Growing up in a home¶

Children who were exposed to multiple drug use by their mothers before birth and who subsequently grew up in institutions were found to be three times more likely to have ADHD between the ages of 17 and 22¹³⁴, corresponding to a prevalence of around 20%.¹³⁵¹²⁰ In US child welfare agencies, the prevalence of ADHD is almost quadrupled at 19%.¹³⁶

Another study did not find an increased ADHD prevalence of 5.8% in homes without depriving living conditions, but a significantly increased ADHD prevalence¹³⁷ of almost 4 to 7 times (19% to 29.3%) in children who had grown up for six months or longer in the harsh living conditions of Romanian orphanages.¹³⁸
The later the adoption from the home, the higher the prevalence of ADHD.^139140141

3.2.1.4. Growing up in adoption¶

A study of Chinese adopted girls found an ADHD rate of 16.7%, which is around three times the usual prevalence.¹⁴² It remains to be seen whether this is a consequence of the adoption or the problems of the birth parents, which were then also the cause of the adoption approval. There would be some evidence for an influence of the latter factor if the prevalence of ADHD did not correlate with the length of stay in the home before the adoption (see previous section).

3.2.1.5. Growing up in a dysfunctional neighborhood¶

Children who grow up in a dysfunctional neighborhood / dysfunctional urban environment are at increased risk for ADHD. Interestingly, this seems to be less the case for black children.¹⁴³

Higher neighborhood poverty correlated with higher parent-reported ADHD and lower parent-reported medication use in the bivariate analysis. Poverty no longer correlated with ADHD in the multivariate analysis, but medication use still correlated negatively with ADHD.¹⁴⁴

3.2.1.6. Relatively earlier school enrollment / older classmates¶

The youngest children in a class who start school have a 30% higher risk of ADHD than the oldest children in a class. A study of over 400,000 children in the USA showed that in states where school enrollment was determined by a fixed age on September 1, 0.85% of children born in August, i.e. those who reached school age immediately before the cut-off date, had an ADHD diagnosis and 0.52% received ADHD medication, while of children born in September, i.e. those who were on average 11 months older, only 0.63% had an ADHD diagnosis and 0.4% received ADHD medication. In the states where school enrollment was not fixed by age on a cut-off date, those born in August still had a slightly higher rate of ADHD compared to those 11 months older, but the difference was 0.08 percentage points instead of 0.21 percentage points.¹⁴⁵
Similarly, a meta-analysis of three Brazilian cohort studies with 8 million participants and 164,000 people with ADHD found that those children in a class who were among the youngest by 4 months had a 34% increased risk of ADHD.¹⁴⁶ A study of 1,042,106 English children between the ages of 4 and 15 came to similar conclusions.¹⁴⁷ The risk of depression and intellectual impairment increased in parallel with that of ADHD.
A French registry study (n = 58 million) found that the youngest children and adolescents in a class were more likely to be diagnosed with ADHD and prescribed methylphenidate.¹⁴⁸ Delaying (pre-)school entry by one year dramatically reduced inattention/hyperactivity in the following year (effect size = -0.73). The effect was primarily found in girls and lasted until the age of 11.¹⁴⁹
A Danish study (n = 418,396) found no influence of the age of children within a school grade on (more frequent / less frequent) ADHD medication. The authors attributed this to, among other things, the low ADHD prevalence, clear diagnostic criteria and high requirements for prescribing ADHD medication in Denmark and referred to studies in countries with high ADHD prevalence in which differences were found¹⁵⁰
A meta-analysis (19 studies from 13 countries with n = 15.4 million children) confirmed that the relatively youngest children in a class have an increased risk of ADHD (17 of 19 studies) and suspected the reason for the lack of effect in Denmark to be the later school enrollment of children with developmental deficits practiced there¹⁵¹

It is unclear how these differences can be explained in relation to ADHD.

One hypothesis is that younger children are more likely to be pathologized by their teachers due to their naturally immature behavior.¹⁵³

Another hypothesis interprets behavioral problems less as a social consequence of the relatively young age within a class than as an absolute consequence of early school entry in general. In this study, however, no difference was found for ADHD.¹⁵⁴ In our opinion, it is also likely that younger children start school earlier than older children. The extent of this influence on ADHD remains to be seen.
A meta-analysis found that younger relative age was not statistically significantly associated with persistence of ADHD at 4-year follow-up.¹⁵⁵

Our hypothesis is that being among the youngest (and therefore the weakest) in a class could also be a psychological burden. It is well known that low social rank is a significant stressor. We are not yet aware of any studies on whether or to what extent this influences ADHD diagnoses in schoolchildren.

3.2.1.7. Little green growth in the vicinity of kindergarten / school / home (+ 20 %)¶

A very comprehensive study of nearly 60,000 children (4.4% of whom were diagnosed with ADHD) between the ages of 2 and 17 in 93 kindergartens/schools in Northeast China found a strong negative correlation of the amount of greenery (amount of plant life) in the kindergarten/school environment of children with ADHD. The less greenery there was, the higher the ADHD rate.¹⁵⁶ A Canadian cohort study,⁵⁵ a larger study from New Zealand¹⁵⁷ and a smaller study of children in Barcelona¹⁵⁸ and a meta-analysis¹⁵⁹ came to similar conclusions.

The conclusions drawn from this are controversially discussed by the authors of the Chinese study:

• It is conceivable that green plants have a general calming effect. As humans were still nomadic until 10,000 years ago, a green environment encoded the calming signal of food for millions of years. Humans could not survive for long in regions without green growth. This corresponds to the biophilia hypothesis.¹⁶⁰
• Green plants reduce noise. Increased street background noise levels correlate with increased behavioral and sleep problems.¹⁶¹ However, noise was not a risk factor in the Canadian cohort study.⁵⁵
• Green growth serves as a filter for air pollutants and thus reduces particulate matter and nitrogen oxides. Particulate matter and nitrogen oxides are discussed as ADHD risk factors (see there).
• Studies on whether people in green regions do more sports / exercise more than people in less green (urban) environments do not come to any clear results.¹⁶²
  Sports are a significant factor in preventing / reducing ADHD symptoms.
• Poorer immune regulation can have adverse effects on brain development and behavior. Failure of immune regulation correlates with reduced exposure to macroorganisms and microorganisms. Green growth can enrich the microbial inputs from the environment that induce immune regulation.¹⁶³

A very large Danish cohort study also came to the conclusion that fewer green plants in the living environment correlate with an increased risk of ADHD by up to 20 %.¹⁶⁴
A meta-analysis came to similar conclusions.¹⁶⁵ Another study found a 15% increase in the risk of externalizing behaviour if there was no green space within 300 metres of the home.¹⁶⁶
The amount of vegetation in the environment (but not the amount of water) correlates with better working memory development in children.¹⁶⁷

According to a cohort study, children who grew up in a rural environment from the age of 3 had a one-third lower risk of ADHD.¹⁵⁷ The lower the proportion of vegetation in the environment, the higher the risk of ADHD.¹⁶⁸

Green plants indoors could possibly also have a positive influence on stress levels and mental health.¹⁶⁹

3.2.1.8. Car traffic density on nearest road (+ 10 %)¶

The density of car traffic on the nearest road correlated with a 7% increase in externalizing symptoms and a 10% increase in the ADHD index.¹⁶⁶
The data was collected in Europe from 2013 to 2016. At the times when leaded petrol was permitted, the pollution was probably significantly higher.

Living in the city was most strongly associated with autism+ADHD and least strongly associated with ADHD only compared to other environmental causes. Maternal smoking was associated with ADHD only, but not with autism only. Parental psychiatric history showed similar associations with all subgroups.¹⁷⁰

3.2.1.9. Noise from roads and neighbors¶

In 9-year-old children, street noise and noise from neighbors correlated with ADHD.¹⁷¹ The result was independent of sleep problems.

3.2.2. Parents¶

3.2.2.1. Poor bonding behavior of the mother/parents in the (first) years of childhood¶

A child’s lack of secure attachment to the mother, like social and emotional deprivation, has extensive negative effects on the child’s mental health, even in later life.¹⁷²

The security of the infant’s bond with the mother or the central caregiver determines the level of the stress hormone cortisol in the baby’s brain.

Disorganized attachment behavior is a risk element for ADHD.¹⁷³ Attachment disorders in children in the first years of life lead to activation of the DRD4 gene, which is also frequently involved in ADHD, if there is a corresponding genetic disposition.¹⁷⁴ A lack of parental persistence has been cited as a risk factor for ADHD,¹⁸ whereby persistence is an ADHD symptom and can therefore also be an expression of ADHD in the parents and thus of genetic transmission.

Massive maternal stress in the first years of childhood causes significant epigenetic changes in the children’s DNA.¹¹⁷

Poor parenting behavior is already a psychosocial risk factor for ADHD.¹⁷⁵

• Inconsistency in education
• Missing rules
• Frequent criticism and punishments
• Cold, distant, unloving treatment

Borderline, which typically results from intense stress-inducing attachment disorders with attachment figures in early childhood (first 2 years) due to physical, sexual or psychological abuse, has a significant comorbidity with ADHD.¹⁷⁷

3.2.2.2. Emotionally withdrawn father behavior in infancy¶

One study observed father-baby behavior and its influence on children’s emotion regulation in infancy and ADHD symptoms in middle childhood.
Fathers’ emotional withdrawal in infancy and minimizing responses to children’s anxiety in toddlerhood predicted the development of ADHD symptoms in middle childhood. Fathers’ parenting performance at 8 and 24 months of children’s age significantly influenced ADHD risk at age 7 years through toddlers’ difficulties with emotion regulation¹⁷⁸

3.2.2.3. Stress in the mother during childhood¶

Stress in the mothers of 5- to 13-year-old boys with ADHD tended to increase their ADHD symptoms 12 months later and significantly worsened the children’s quality of life.¹⁷⁹. Parental stress generally correlated with increased ADHD symptoms in children.¹⁸⁰

3.2.2.4. Psychological problems of the parents¶

Parental mental health problems increase the risk of ADHD in children.¹⁸¹¹¹⁶
Psychological problems of the parents could act as an environmental and/or genetic influence.

3.2.2.4.1. Depression (+ 42 to 125 %)¶

Depressive symptoms in the father or mother increase the children’s risk of ADHD¹⁸²

• by 66 %¹⁸³
• by 42 % to 125 %:¹⁸⁴
  • before pregnancy
    • Depression of a parent:
      • ADHD + 92 %
      • ASS + 63 %
    • Depression of the mother:
      • ADHD + 125 %
      • ASS + 101 %
  • during the birth
    • Depression of a parent:
      • ADHD + 72 %
      • ASS + 88 %
    • Depression of the mother:
      • ADHD + 75 %
      • ASS + 58 %
  • in the first year of the child’s life
    • Depression of a parent:
      • ADHD + 71 %
      • ASS + 110 %
    • Depression of the mother:
      • ADHD + 55 %
      • ASS + 59 %
  • in the 2nd to 4th year of the child’s life
    • Depression of a parent:
      • ADHD + 52 %
      • ASS + 101 %
    • Depression of the mother:
      • ADHD + 55 %
      • ASS + 64 %
  • from the age of 4 of the child
    • Depression of a parent:
      • ADHD + 42 %
      • ASS + 85 %
    • Depression of the mother:
      • ADHD + 43 %
      • ASS + 65 %
• maternal depression increases the risk of ADHD and ASD in offspring more than paternal depression¹⁸⁵

3.2.2.4.2. Bipolar Disorder ( + 100 %)¶

• Bipolar Disorder in a parent doubles the risk of ADHD¹⁸⁶

3.2.2.4.3. Antisocial personality disorder of the father¶

Antisocial Disorder in a parent is a huge (and usually violent) risk for ADHD in the offspring.¹⁸⁷

3.2.2.4.4. Alcohol problems of the father¶

Alcohol problems in the father increase the risk of ADHD in the offspring.¹⁸⁸

3.2.2.5. Incomplete families¶

Single-parent families increase the risk of ADHD.^188187116180

Single parents naturally have a higher risk of not being able to give their children enough loving care and security. However, there are single parents who are very good at this. The decisive factor is not the amount of time that (part-time/working) parents can spend (less) with their children, but whether the children have the constant and secure feeling that they are accepted and loved at all times, just as they are.

People with ADHD suffer more frequent break-ups in their relationships (even in adulthood) than people without ADHD.

3.2.2.6. Family instability, constant arguments between the parents¶

A high level of stress in the primary family increases the risk of ADHD.^188187116180

Progression studies do not find complete persistence even during childhood and adolescence and confirm a frequent coincidence with family problems and parental problems.¹⁹¹ Conversely, a high level of family cohesion and social support has a protective effect against ADHD.¹⁹²

3.2.2.7. Young age of parents (+ 14 % to + 92 %)¶

Children whose mother does not have ADHD have a 14% increased risk of ADHD if one parent is younger than 20 years old. Children whose mother has ADHD have a 92% increased risk of ADHD if one parent is younger than 20.¹⁹³¹⁹⁴ Another study also reported that younger fathers were more likely to have children with ADHD than older fathers.¹⁹⁵ One study reported a 32% reduced risk of ADHD for every 10 years increase in maternal age. However, the correlation was attenuated by other factors. These were:¹⁹⁶

• Family income
• Training of the caregiver
• Polygenic ADHD risk score
• Duration of breastfeeding
• Prenatal alcohol exposure
• Prenatal tobacco exposure

In a cohort study, children with ADHD also had younger than average mothers¹⁹⁷
under 24 years: 1.66 times
25 to 29 years: 0.92 times
30 to 34 years: 0.66 times
over 35 years: 0.58 times

Another study also reports this, supplemented by an increase in learning problems among particularly young (20 to 24 years) and particularly old mothers (35 to 39 years).¹⁹⁸

In a larger study, almost 2 out of 3 young mothers reported at least one mental health problem. Almost 40% had more than one. Young mothers were two to four times more likely to have an anxiety disorder (generalized anxiety disorder, separation anxiety disorder, social phobia and specific phobia), attention-deficit/hyperactivity disorder, oppositional defiant disorder or conduct disorder than older comparison mothers or women aged 15-17, and two to four times more likely to have more than one psychiatric problem.¹⁹⁹

One study found no correlation between the age of the mother and the offspring’s risk of ADHD.²⁰

3.2.2.8. Low socio-economic status of the family of origin (+ 50 % to + 130 %)¶

Children from “lower class” families have an increased correlation with ADHD^{200187 182} and are more likely to receive ADH)S medication.²⁰¹¹¹⁶
Children from lower classes have about twice the risk of ADHD as children from higher classes (in a 3-tier model).²⁰²

Cramped living conditions also increase the risk of ADHD in children.¹⁸⁷ Poor family finances correlated with a 2.12-fold increased risk of ADHD at kindergarten age in the USA.²⁰³

Interestingly, in one study, families with a high socioeconomic status did not benefit from behavioral therapy in addition to drug treatment. Only families with a low socioeconomic status benefited more from a combination therapy of medication treatment and behavioral therapy than from medication treatment alone.²¹¹

We suspect that the decisive factors are not so much socio-economic status (income or the size of the home itself), but that these circumstances correlate more frequently with inappropriate parenting methods and parents’ own problems (the latter influencing the socio-economic status of the parents on the one hand and being hereditary on the other).
Pure behavioral therapy has a clear focus on symptom reduction. It is conceivable that families with a high socioeconomic status have a greater ability to adapt their behavior to given circumstances. Such a higher ability to adapt behavior would already have a behavior-correcting effect per se and would anticipate the behavioral adaptations through behavioral therapy.

Parents of ADHD children showed elevated scores of cognitive weaknesses (IQ, reading tasks, verbal fluency), the highest stress scores of all parent groups compared, the most ADHD symptoms, and poor reading performance.²¹²

There is also evidence that (with regard to people with ADHD) environment-centered psychotherapies (interventions in the family, with parents, in kindergarten or at school) are more effective than patient-centered behavioral therapies. In some cases, patient-centered behavioral therapies have been denied effectiveness.²¹³ This is likely to be particularly true for younger children (up to 6 or 8 years).
This could indicate that external factors are a significant cause of ADHD in children.

Among college students, poorer financial resources also appear to correlate with increased ADHD symptomatology.²¹⁴ There was no correlation with (self-induced) student debt.

A genetically predicted one SD lower socioeconomic status causally predicted a 5.3-fold ADHD risk, while conversely ADHD only very slightly causally caused socioeconomic status. A genetically predicted one SD higher family income causally predicted a 65% lower ADHD risk. Again, the reverse effect was small.²¹⁵

3.2.2.9. Low level of education of parents (+ 3.5 % to + 4.9 %)¶

Low education of the mother¹⁰ or the parents¹⁸⁸ increases the children’s risk of ADHD.
Children of parents with low levels of education had higher ADHD symptoms and a nearly doubled risk of severe ADHD symptoms. The association was independent of genetic and family environmental factors. The transfer of this model to depression was weaker and could be fully explained by common genetic factors.²¹⁶ Children of parents without a university degree had twice the risk of ADHD as children of parents with a university degree²¹⁷
A lower level of education of the mother is said to correlate with an increased screen consumption of the children, which in turn correlates with behavioral problems.²¹⁸
In a cohort study in Denmark, a low level of parental education correlated with a 3.5% increased risk of ADHD in children.²⁰⁷ Children of parents who were unemployed and had a low income and a low level of education were found to have a 4.9% higher risk of ADHD.
An Ethiopian study found an approximately tripled risk of ADHD in children due to illiteracy of the mother¹²

A genetically predicted one SD higher educational attainment causally predicted a 70% lower risk of ADHD.²¹⁵

3.2.2.10. Unemployment of parents (+ 2.1 %)¶

In a cohort study in Denmark, parental unemployment correlated with a 2.1% increased risk of ADHD in children.²⁰⁷ Children of parents who were unemployed and had a low income and a low level of education were found to have a 4.9% higher risk of ADHD. Unemployment or occupational problems of the parents increased the ADHD symptoms in children.¹⁸⁰

3.2.2.11. Parents are less able to reflect on their parental role¶

Lower parental reflective functioning correlated with ADHD in children.¹⁸² Parental reflective functioning is defined as the parents’ ability to reflect on their own and their child’s inner mental experiences.

3.2.2.12. Low educational attainment and ADHD mutually causal¶

A large registry study in the Netherlands (n = 1.7 million) found evidence that low educational attainment is a causal factor in the development of ADHD and that ADHD is a causal factor in low educational attainment.²¹⁹

3.2.3. Media¶

3.2.3.1. Early television consumption¶

Early television consumption at the ages of 1 and 3 correlates with attention problems at the age of 7.²²⁰

It must be questioned whether high television consumption by children at an early age is a causal cause of attention problems or whether parents with a lack of ability to pay attention due to their own psychological problems often leave children to their own devices and park them in front of the television. In the latter case, television consumption could also be merely a correlation and not necessarily a causal cause of ADHD. This is because - as will be described below - there are countless studies that prove that a caring, warm and secure attachment style can prevent ADHD even in the presence of a genetic disposition.
So while it is certain that intensive parental attention is a good protection against ADHD, no studies are known on this side that television deprivation prevents ADHD.
The fact that intensive television consumption as a substitute for personal attention correlates with a lack of personal attention is the more conclusive link from this point of view. The fact that television and internet consumption with age-inappropriate content can cause further damage is also likely to be certain.

3.2.3.2. Amount of media consumption does not cause ADHD, media consumption addiction correlates with ADHD¶

The amount of social media use has no influence on ADHD. Only media consumption addiction is associated with increased ADHD levels.²²¹ Presumably, ADHD, hyperactivity and impulsivity are causal factors in problematic media consumption.²²² Nevertheless, increased screen consumption in children appears to be able to impair attention.²²³

It has also been reported that screen consumption of more than 4 hours can cause “virtual autism” in children under the age of 6. However, this disappears again once screen consumption is reduced.²²⁴

3.3. Characteristics without increased risk of ADHD¶

• p,p’-dichlorodiphenyltrichloroethane (p,p’-DDT) was associated with a 36% lower likelihood of ADHD⁹²
• Hexachlorobenzene (HCB) showed a non-linear relationship with ADHD, with an increasing risk in the low exposure range, which turned into a decreasing risk at concentrations above 8 ng/g lipid.⁹²
• Organic pollutants (OP pesticides, PCBs, pyrethroid insecticides and trichlorophenol (TCP)) did not significantly increase the odds ratio for ADHD (0.99)⁵⁰
• The prevalence of microcytic anemia was found to be 14% lower in children with ADHD (OR: 0.86)²²⁵
• Growing up bilingual did not increase the risk of ADHD²²⁶
• According to a meta-analysis, exposure to cadmium during development did not significantly increase the risk of ADHD⁹⁶

3.4. Characteristics with risk reduction of ADHD¶

Immigrant status of parents causes a reduced risk of ADHD²²⁷ within the first 2 generations.²²⁸