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. Febrile convulsions in premature babies (+ 640 %)
    • 3.1.1.3. Bottle feeding increases (up to + 270 %), breastfeeding reduces ADHD risk (- 23 % to -74 %)
    • 3.1.1.4. First-born status (+ 31 to + 35 %)
    • 3.1.1.5. Feeding problems with infants
    • 3.1.1.6. Sleep problems in infants
    • 3.1.1.7. Subependymal pseudocysts
    • 3.1.1.8. Valproic acid
    • 3.1.1.9. D-3 insufficiency in the first 12 months
  • 3.1.2. Children
    • 3.1.2.1. Bacterial infections (+ 593 %)
      • 3.1.2.1.1. Bacterial meningitis (meningitis) (+ 40 % to + 180 %)
      • 3.1.2.1.2. Antibiotics in the first years of life (+ 10 to 20 %)
    • 3.1.2.2. Craniosynostosis (+ 500 %)
    • 3.1.2.3. Lead (+ 160 % to + 310 %)
    • 3.1.2.4. Phthalates (+ 212 % for girls to + 254 % for boys)
    • 3.1.2.5. Passive smoking - smokers in the environment in the first years of life (+ 42 % to + 170 %)
    • 3.1.2.6. Mercury (+ 168 % ?)
    • 3.1.2.7. Manganese (+ 163 % to + 257 %)
    • 3.1.2.8. D-3 insufficiency (+ 157 %)
    • 3.1.2.9. Air pollution in childhood
      • 3.1.2.9.1. Particulate matter and nitrogen oxides (+ 78 %)
      • 3.1.2.9.2. Renovation fumes, incense, cooking oil vapors
    • 3.1.2.10. Perfluorooctane sulfonate (PFOS) (+ 77 %)
    • 3.1.2.11. β-Hexachlorocyclohexane (β-HCH) (+ 75 %)
    • 3.1.2.12. Hyperthyroidism / hyperthyroidism (+ 70 %)
    • 3.1.2.13. Concussions and traumatic brain injuries (+ 68 %)
    • 3.1.2.14. Febrile convulsions (+ 28 % to + 66 %)
    • 3.1.2.15. Chlorinated kerosenes (+ 57 % / quartile)
    • 3.1.2.16. Diet high in sugar (+ 41 %)
    • 3.1.2.17. Early puberty (pubertas praecox) (+ 40 %)
    • 3.1.2.18. Surgical procedures under anesthesia (+ 25 to 39 %)
    • 3.1.2.19. Neurodermatitis / atopic eczema / atopic dermatitis in childhood
    • 3.1.2.20. Antihistamines in the first years of life
    • 3.1.2.21. Chlorpyrifos
    • 3.1.2.22. Ozone exposure
    • 3.1.2.23. Arsenic
    • 3.1.2.24. Pyrethroid pesticides
    • 3.1.2.25. Organophosphates
    • 3.1.2.26. Polychlorinated biphenyls (PCBs)
    • 3.1.2.27. Lack of sleep
    • 3.1.2.28. Acne vulgaris
    • 3.1.2.29. Spray disinfectant
    • 3.1.2.30. Pets
    • 3.1.2.31. Cadmium (?)
    • 3.1.2.32. Copper
    • 3.1.2.33. Antimony
    • 3.1.2.34. Zinc
    • 3.1.2.35. Printing ink on food paper
    • 3.1.2.36. Commercially packaged pasta
    • 3.1.2.37. Unpackaged flour
• 3.2. Stressful psychological childhood experiences as a (co-)cause of ADHD
  • 3.2.1. Stress
    • 3.2.1.1. Early massive stress experiences (up to + 420 %)
    • 3.2.1.2. Growing up in a home (+ 200 %)
  • 3.2.2. Growing up in adoption ( + 200 %)
  • 3.2.3. Parents and family
    • 3.2.3.1. Low socio-economic status of the family of origin (+ 50 % to + 130 %)
    • 3.2.3.2. Psychological problems of the parents
      • 3.2.3.2.1. Depression (+ 42 to 125 %)
      • 3.2.3.2.2. Bipolar Disorder ( + 100 %)
      • 3.2.3.2.3. Antisocial personality disorder of the father
      • 3.2.3.2.4. Alcohol problems of the father
      • 3.2.3.2.5. ADHD of the parents
    • 3.2.3.3. Young age of parents (+ 14 % to + 92 %)
    • 3.2.3.4. Injuries to a parent
    • 3.2.3.5. Low level of education of parents (+ 3.5 % to + 4.9 %)
    • 3.2.3.6. Unemployment of parents (+ 2.1 %)
    • 3.2.3.7. Poor bonding behavior of the mother/parents in the (first) years of childhood
    • 3.2.3.8. Emotionally withdrawn father behavior in infancy
    • 3.2.3.9. Stress in the mother during childhood
    • 3.2.3.10. Thyroid problems in the mother
    • 3.2.3.11. Incomplete families
    • 3.2.3.12. Family instability, constant arguments between the parents
    • 3.2.3.13. Parents are less able to reflect on their parental role
  • 3.2.4. Relatively earlier school enrollment / older classmates (+ 34 %)
  • 3.2.5. Urban environment
    • 3.2.5.1. Little green growth in the vicinity of kindergarten / school / home (+ 20 %)
    • 3.2.5.2. Car traffic density on nearest road (+ 10 %)
    • 3.2.5.3. Noise from roads and neighbors
  • 3.2.6. Growing up in a dysfunctional neighborhood
  • 3.2.7. Class size
  • 3.2.8. Low educational attainment and ADHD mutually causal
  • 3.2.9. Only child
  • 3.2.10. Media
    • 3.2.10.1. Early television consumption
    • 3.2.10.2. 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,.{Schmid, Wolke (2014): Preschool regulatory problems and attention-deficit/hyperactivity and cognitive deficits at school age in children born at risk: different phenotypes of dysregulation? Early Hum Dev. 2014 Aug;90(8):399-405. doi: 10.1016/j.earlhumdev.2014.05.001. n = 1120}}³ The risk of developing hyperactivity at 8 to 10 years of age was 11.8 times higher (plus 1181%), and behavioral problems and negative emotional adjustment were reported twice as often as in unaffected individuals.⁴

3.1.1.2. Febrile convulsions in premature babies (+ 640 %)¶

Febrile convulsions increased the risk of ADHD in premature infants 6.4-fold and the risk of ASD 16.9-fold.⁶

3.1.1.3. 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 % reduced 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
• Prebiotics²¹
  • Oligosaccharides
  • which promote the growth and activity of beneficial microorganisms

The substances contained in breast milk promote²¹
- antimicrobial active ingredients
- bacterial growth
- secreted IgA for a regulatory immune system

Stilen in the first three months of life influences the intestinal microbiotics:²¹

• increases the frequency of
  • Lactobacillus (Bacillota strain)
  • Bifidobacterium
  • Enterococcus
  • Corynebacterium
  • Propiobacterium
  • Streptococcus
  • Sneathia
• reduces the frequency of
  • Bacteroides (strain Bacteroidota)
  • Staphylococcus

Bottle-fed infants show a different gut microbiome:²¹

• increased frequency of
  • Atopobium (strain Actinomycetota)
  • Bacteroides (strain Bacteroidota)
  • Bilophila (strain Thermodesulfobacteriota)
  • Enterobacter (strain Pseudomonadota)
  • Escherichia (strain Pseudomonadota)
  • Citrobacter (strain Pseudomonadota)
  • Clostridium (Bacillota strain)
  • Enterococcus (Bacillota strain)
  • Lactobacillus (Bacillota strain)
  • Granulicatella (strain Bacillota)

More on the influence of the gut-brain axis on ADHD at Gut-brain axis and ADHD

Bisphenol A is known to increase the risk of ADHD. Exposure to PAHs, particularly bisphenol A (BPA), is associated with ADHD symptoms in primary school children and a significant reduction in the volume of the caudate nucleus²²²³ Bisphenol A was 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 by bottle in 2007, but no increase in risk in children fed by bottle in 2011.²⁴

After all, breastfeeding has its own influence on the well-being and positive development of children, independent of food intake.
Maternal care is the infant’s first social experience and has a decisive influence on its survival, proper development and social skills throughout life.
Infants and puppies do not yet have a high inherent value for their respective mothers at birth.²⁵. Breastfeeding in humans and suckling puppies in animals are rewarding and reinforcing stimuli that promote maternal behavior and bonding. Suckling puppies activates the mesocorticolimbic dopamine system in mothers, which reinforces bonding and nurturing behavior. The extracellular dopamine levels in the nucleus accumbens (the reward center of the brain) increase and correlate with the time spent caring for the offspring.

3.1.1.4. First-born status (+ 31 to + 35 %)¶

A study of Ethiopian students found a significant ADHD risk increase for first-time mothers²⁶ and explained this conclusively by increased perinatal risk factors and birth-related complications, which are a major contributor to ADHD and are so much more common in first-time mothers that they have been labeled high-risk patients:²⁷

• low birth weight 57% more frequently (evidence that this increases the risk of ADHD)
• Emergency caesarean sections 57 % more frequent
• pregnancy-induced high blood pressure 15.38 % more frequently
• intrauterine growth retardation 19.23 % more frequently
• premature labor 9.61 % more often
• fetal distress 19.23 % more frequent
• Oligohydraminos 17.30 % more frequent

It remains to be seen whether there are other risk factors.

A very large Swedish registry study found an increased risk of ADHD and depression for first-born children.²⁸
According to the German KiGGS study (n = 13,488), first-born children have a 31% increased risk of ADHD compared to last-born children and children without siblings.²⁹
A Spanish study of n = 1,104 primary school children found a 35% higher risk of ADHD for first-born children³⁰
A large Spanish registry study found a 3.0-fold risk of ADHD among firstborns compared to children with younger and older siblings.³¹
A study of Saudi Arabian medical students found a 22% increased risk of ADHD for firstborns and a 70% increased risk of ADHD if one (1) sibling was present.³²
An Indian study found a high first-born rate among people with ADHD³³
A smaller study found a nearly doubled risk of ADHD for firstborns compared to non-firstborns.³⁴
In a Chinese study of 1,855 boys with ADHD, first-born status increased the risk of severe externalizing symptoms by 28%.³⁵ An earlier study by the same research group on children with ADHD found a 45% increased risk of aggressive behavior due to first-born status. The risk was even higher if there were older siblings.³⁶
Children with ASD had a significantly reduced risk of ADHD if they had an older sibling³⁷

No influence of first-born status on the risk of ADHD found

• an Iranian study on n = 400 children³⁸,
• a study of n = 387 Iranian students.³⁹
• a study of n = 598 children and adolescents with ADHD from relatively large families (more than 47% had at least 4 siblings)⁴⁰
• two smaller studies (n = 100 and n = 32)⁴¹
• a smaller study (n = 173)⁴²

3.1.1.5. Feeding problems with infants¶

Feeding problems in infants correlate with ADHD in adolescence and adulthood.³

3.1.1.6. Sleep problems in infants¶

Sleep problems in infants correlate with ADHD in adolescence and adulthood.³

3.1.1.7. Subependymal pseudocysts¶

Subependymal pseudocysts in newborns increase the risk of ADHD and autism.⁴³

3.1.1.8. 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.⁴⁴

3.1.1.9. 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 Disorders⁴⁵
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 (+ 593 %)¶

Severe bacterial infections in childhood or adolescence massively increase the risk of severe mental disorders (HR):⁴⁶

• 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
• Schizophrenia⁴⁷

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.⁴⁶

The prevalence of Streptococcus agalactiae infection (Group B Streptococcus, GBS) in infants was 0.07%.
GBS has brought about:⁴⁸

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

GBS meningitis increased the risk of⁴⁸

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

3.1.2.1.1. Bacterial meningitis (meningitis) (+ 40 % to + 180 %)¶

Consequences, children with bacterial meningitis (but not enteroviral meningitis) had an increased risk of ADHD or ADHD medication use:⁴⁹

• 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

3.1.2.1.2. Antibiotics in the first years of life (+ 10 to 20 %)¶

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.⁵⁰ 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 risk⁵¹
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.⁵² Two other studies found no increased risk of mental disorders when antibiotics were given in the first 1 ⁵³ to 2⁵⁴ years of life.

The administration of antibiotics in the first three years of life reduces the diversity, stability and composition of the microbiome:²¹

• reduced frequency of genera
  • Bacteroides
  • Bifidobacterium
  • Lactobacillus
  • Staphylococcus
  • Sediminibacterium
• increased frequency of
  • Members of the Enterobacteriaceae family
  • of the genus Enterococcus

During the maturation of the microbiome, several processes of the central nervous system take place, such as synaptogenesis, myelination and synaptic pruning, which can be influenced by microbiome-associated metabolites.²¹

3.1.2.2. Craniosynostosis (+ 500 %)¶

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.⁵⁵

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.⁵⁶ Older age at surgery was associated with poorer executive functions.

3.1.2.3. Lead (+ 160 % to + 310 %)¶

According to several meta-analyses, lead exposure during development increased the risk of ADHD⁵⁷ by

• 433 % in the half of Spanish children (8 to 15 years) with the higher urinary lead exposure.⁵⁸
• 310 % increased) for the 20 % with the highest blood lead level compared to those with the lowest 20 %⁵⁹
• 239 to 306 %⁶⁰
• 160 to 260 %⁶¹
• 95 %⁶²
• Every doubling of blood lead levels increased the risk of ADHD in children by 35%⁶³ This was true even at very low lead levels of less than 10 mug/dl.

Mice that are chronically exposed to inorganic lead from birth show about three times more spontaneous motor activity than control mice. In addition, their behavioral responses to amphetamine, methylphenidate and phenobarbital are altered.⁶⁴
Elevated lead urine levels correlated with increased inattention and hyperactivity symptoms and reduced IQ in children.⁶⁵
Children with ADHD had significantly higher lead hair levels than children without ADHD.⁶⁶

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

According to a meta-analysis, exposure to phthalates during development increased the risk of ADHD by 212% for girls and 254% for boys.⁶⁷
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.⁶⁸

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.⁶⁹ Nicotine exposure in children is associated with a 1.42-fold⁷⁰ to 2.7-fold⁶⁷ 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.⁷¹
In the case of passive smoking, a connection is made to certain MAO-A gene variants that cause a lower level of serotonin degradation.⁷²

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.⁷³

One study found no link between smoke exposure after birth and ADHD.⁵⁹

3.1.2.6. Mercury (+ 168 % ?)¶

According to a meta-analysis, exposure to methylmercury during development increased the risk of ADHD by 168%.⁷⁴ One review found an increased risk of ADHD and ASD.⁷⁵ Two reviews describe the causality.⁷⁶⁶¹
Two meta-analyses found no significant increase in risk from mercury.⁶²⁵⁷
Mercury urine levels were not significantly elevated in children with ADHD.⁶⁵ Mercury blood levels were unchanged in children with ADHD.⁶³

3.1.2.7. Manganese (+ 163 % to + 257 %)¶

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

• 163 %⁶⁷
• 79 %⁶²
• Early exposure to manganese causes permanent attention problems via the mTOR pathway and an alteration of the catecholaminergic system⁷⁷ as well as sensorimotor problems.⁷⁸
  Manganese intoxication shows a correlation with certain CYP2D6 gene variants.⁷⁹ 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 the manganese-induced attention problems or their improvement by MPH. D2R antagonists reduced the sensorimotor deficits of manganese. D1 antagonists reduced the efficacy of MPH on sensorimotor deficits.⁷⁸

In persons with ADHD, elevated manganese levels were only found in the hair, but not in blood levels⁸⁰, another study also found elevated manganese blood levels in school children with ADHD.⁸¹ Children with ADHD had manganese hair levels twice as high as children without ADHD. High manganese hair levels increased the risk of ADHD 3.57-fold (+257%).⁶⁶

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.⁸²
An animal model of 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.⁸³

In children with ADHD, urinary manganese levels were slightly lower than in children without ADHD.⁶⁵

3.1.2.8. 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).⁸⁴

3.1.2.9. Air pollution in childhood¶

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

A review of k = 45 METASTUDY studies found a 1.82-fold risk of ADHD due to PM2.5 exposure.⁸⁵

• There is clear evidence of a link between PM2.5 and NO2 levels⁸⁶
  • in early childhood and ASD
  • in childhood and ADHD
• ADHD was found in⁸⁷
  • 11.0% of urban children living in cities who were exposed to air pollution, especially particulate matter (PM10)
  • 2.7 % in the control group
  • Risk thus + 307 %
• Children in the highest third of PM10 or NO2 exposure had a two to three times higher risk of ADHD than children in the lowest tercile⁸⁸
• Children in the highest quintile of NO2 and PM2.5 exposure had a 1.70 and 1.63 times higher risk of ADHD, respectively, than children in the lowest quintile⁸⁹
• Increasing exposure to N2O from air pollution could contribute significantly to the development of ADHD⁹⁰
• Environmentally relevant concentrations of N2O, even at trace levels, impair cognitive functions such as working memory in adult males⁹¹

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.⁸⁹ A smaller cohort study confirmed this for particulate matter, but not for nitrogen dioxide.⁹² 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.⁹³
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.⁹⁴ Even at non-toxic doses, nitrogen oxides have an influence on glutamatergic, opioidergic cholinergic and dopaminergic neurotransmission in the brain.⁹⁵
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.⁹⁶
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 18.⁹⁷

A meta-analysis of 12 studies found a correlation between particulate matter and ADHD in children in 9 of them.⁹⁸
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.⁹⁹ A Taiwanese register study came to comparable results.¹⁰⁰
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 oxide¹⁰¹
A Polish study found a correlation between¹⁰²

• 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:¹⁰³
Increased traffic-related air pollution correlated with increases 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.¹⁰⁴

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 allele¹⁰⁵

• 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 decreased¹⁰⁶

• 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%.¹⁰⁷ Another study found similar results.¹⁰⁸

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%)¹⁰⁹

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 disorders¹¹⁰

Emissions of nitrogen oxides in Germany fell by almost 2/3 between 1990 and 2020.¹¹¹

PM2.5 exposure¹¹²

• 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 PM2.5¹¹²

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

Pathways of air pollution on ADHD:⁹¹

• Inflammation
• Thyroid hormones
• Disorder of β-adrenergic, dopaminergic and glutamatergic (NMDAR) signaling pathways, resulting in disorder of G-protein/cAMP signaling, Ca2+ homeostasis and neurotransmitter pathways
• (reversible) inhibition of alpha-7-nicotinic acetylcholine receptors (α7 nAChRs) by N2O exposure
  • Oxidative stress
    • thereby, among other things, increased peripheral noradrenaline¹¹³
  • reduced central noradrenaline¹¹⁴
  • Promotion of a parasympathetically dominated state by NO¹¹⁵

3.1.2.9.2. 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:¹¹⁶

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

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

Perfluorooctane sulfonate (PFOS) in breast milk correlated with a 77% increased risk of ADHD per higher interquartile range.¹¹⁷
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.¹¹⁸

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

Peβ-hexachlorocyclohexane (β-HCH) in breast milk correlated with a 75% increased risk of ADHD per higher interquartile range.¹¹⁷

3.1.2.12. Hyperthyroidism / hyperthyroidism (+ 70 %)¶

One study found a 1.7-fold prevalence of ADHD in children with hyperthyroidism.¹¹⁹

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.¹²⁰

For the effects of abnormal thyroid hormone levels during pregnancy, see Prenatal stressors as ADHD environmental causes

3.1.2.13. 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.¹²¹

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%.¹²²
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.

Traumatic brain injuries in children correlated with a doubled likelihood of ADHD medication in the following 20 years of life¹²³

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 concussion¹²⁴

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.

3.1.2.14. Febrile convulsions (+ 28 % to + 66 %)¶

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 adulthood¹²⁵
Febrile convulsions in children increased the risk of ADHD by 28%¹²⁶ to 66%¹²⁷

3.1.2.15. Chlorinated kerosenes (+ 57 % / quartile)¶

Chlorinated kerosenes (CP) are widespread environmental and industrial pollutants.
A large study (n = 122,965, including 7,139 with ADHD) examined the ADHD risk of PM2.5, PM2.5-bound short-chain CPs (SCCPs), medium-chain CPs (MCCPs) and long-chain CPs (LCCPs). An increase in CP concentrations in the interquartile range (IQR) increased the risk of ADHD by 57% (OR = 1.57). The risk increased linearly in a dose-dependent manner and was particularly driven by SCCPs and MCCPs.¹²⁸

3.1.2.16. Diet high in sugar (+ 41 %)¶

A diet high in refined sugar and saturated fats during childhood increased the risk of ADHD by 41%, while a healthy diet reduced the risk of ADHD by 35%. (Meta-analysis, k = 14 studies)¹²⁹ Compared to a healthy diet, an unhealthy diet therefore increases the risk by 117%.

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.¹³⁰
In an Egyptian study, a child’s daily consumption of sweets correlated with a 6.82-fold risk of ADHD (+ 582 %).⁶⁶ Whether this is a causal cause or a consequence of changed food preferences due to the predisposition to the disorder remains to be seen.

3.1.2.17. 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%.¹³¹

3.1.2.18. Surgical procedures under anesthesia (+ 25 to 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.¹³² 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.¹³³
One study found a 37% increase in the risk of ADHD with a single anesthetic during surgery up to the age of 5 years, and a 75% increase with multiple anesthetics¹³⁴
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.¹³⁵
Other studies have come to similar conclusions.¹³⁶¹³⁷
A meta-analysis found a 25% increase in the later risk of ADHD due to general anesthesia in childhood (RR = 1.26).¹³⁸

• 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.¹³⁹

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.

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

Neurodermatitis / atopic eczema / atopic dermatitis in childhood correlates with an increased risk of ADHD.¹⁴⁰
In contrast, a cohort study found no significant (+2%) increased risk of ADHD in childhood atopic dermatitis.¹⁴¹
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.¹⁴²

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.¹⁴³
Urticaria increased the risk of ADHD by 9%¹⁴⁴

In low birth weight infants, a history of T2 inflammatory diseases such as asthma and atopic dermatitis increased the risk of:¹⁴⁵

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

3.1.2.20. 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.¹⁴⁶

3.1.2.21. Chlorpyrifos¶

In children between 1 and 6 years of age, chlorpyrifos residues in the blood correlated with the risk of ADHD.¹⁴⁷ Vitamin D reduced the risk.
Chlorpyrifos also significantly increases the risk of ADHD in the case of prenatal contamination of the mother during pregnancy.

3.1.2.22. 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 sports.¹⁹

3.1.2.23. Arsenic¶

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

• 53 %⁶²

3.1.2.24. 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 function¹⁴⁸

According to a meta-analysis, pyrethroid insecticides did not significantly increase the odds ratio for ADHD (0.99)⁶⁷

3.1.2.25. Organophosphates¶

Exposure to organophosphates in childhood correlated with an increased risk of ADHD.⁶¹

Pathways of action (among others): Endocannabinoid pathway¹⁴⁹

3.1.2.26. Polychlorinated biphenyls (PCBs)¶

Exposure to polychlorinated biphenyls (PCBs) in childhood correlated with an increased risk of ADHD.⁶¹
Prenatal PCB exposure slightly reduced internalizing symptoms by 17% and slightly reduced ADHD risk by 16%.¹⁵⁰
Rats that were exposed perinatally to A1221 (a PCB mixture) showed¹⁵¹

• a reduced sucrose preference (females only)
• a reduced reaction latency in the attention shifting task (males and females)
• TH+ cells in the VTA increased (males and females)
• DRD1 increased in the combined midbrain nuclei (males and females)
• Behavior correlated with number of dopaminergic cells in the VTA (in females)
• Behavior correlated with dopamine signaling genes (in males)
• Conditioned orientation and serum estradiol (E2) unchanged

3.1.2.27. 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.¹⁵²
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.

3.1.2.28. Acne vulgaris¶

One study found moderately elevated levels in adolescents (12 to 17 years) with acne vulgaris for¹⁵³

• 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.

3.1.2.29. Spray disinfectant¶

Spray disinfectants led to lung diseases in South Korea, as extreme use was widespread there.
One study found a link between spray sanitizer use, especially in early childhood or prolonged use, and ADHD.¹⁵⁴

3.1.2.30. Pets¶

Preschool children aged 3 to 6 years had a 58% to 66% increased risk of ADHD if the children grew up with pets in a large Chinese population-based study based on parental reports.¹⁵⁵

3.1.2.31. Cadmium (?)¶

The risk of ADHD was 269% higher in the half of Spanish children (8 to 15 years) with higher urinary cadmium levels.¹⁵⁶ Cadmium was also associated with increased inattention symptoms.
In a study of children with and without ADHD, children with ADHD-I had the highest urinary cadmium levels.⁶⁵ Cadmium correlated negatively with IQ.
0 %: Cadmium exposure during development did not significantly increase the risk of ADHD, according to a meta-analysis⁶²

3.1.2.32. Copper¶

The risk of ADHD was 1,546% higher in the half of Spanish children (8 to 15 years) with higher urinary copper levels.¹⁵⁶ Copper was also associated with increased inattention symptoms.

Note: If one were to assume an ADHD baseline prevalence of 6.47 % in children, this would result in a prevalence of 100 % in those 50 % children with the higher copper urine values.

3.1.2.33. Antimony¶

ADHD risk 204% higher in the half of Spanish children (8 to 15 years) with higher urinary antimony exposure.¹⁵⁶
In a study of children with and without ADHD, children with ADHD-H/I showed the highest antimony urine levels.⁶⁵ Antimony urine levels correlated with the severity of ADHD symptoms according to the teacher rating.

3.1.2.34. Zinc¶

One study found elevated zinc blood levels in school children with ADHD.⁸¹

3.1.2.35. Printing ink on food paper¶

Using newspapers to wrap food 3 or more times a week increased the risk of ADHD by 105 times in an Egyptian study.⁶⁶ It may depend on the approved printing inks.
With these figures, however, we ask ourselves whether contact with newspapers (when reading) should not already lead to a measurable increase in the risk of ADHD.

3.1.2.36. Commercially packaged pasta¶

A child’s consumption of commercially packaged pasta 3 or more times per week correlated with a 57-fold risk of ADHD.⁶⁶
Whether this is related to ingredients in commercially packaged noodles in Egypt, food preferences due to ADHD, or a consequence of low family socioeconomic status is an open question.

3.1.2.37. Unpackaged flour¶

The use of unpackaged flour in cooking correlated with a 44-fold risk of ADHD in an Egyptian study.⁶⁶

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.¹⁵⁷¹⁵⁸
Massive maternal stress in the first years of childhood causes significant epigenetic changes in the children’s DNA.¹⁵⁹

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.¹⁶⁰

3.2.1. Stress¶

3.2.1.1. Early massive stress experiences (up to + 420 %)¶

Early childhood stress and chronic stress (neglect, deprivation, abuse, trauma) can be involved in the development of ADHD.^161158162163 20% to 50% of all children who experience early childhood trauma develop clinical ADHD symptoms.^161164165
The number of traumas correlates with the severity of ADHD¹⁶⁶ as well as with the risk of ADHD. The number of Adverse Childhood Experiences (ACEs) increased the risk of ADHD:¹⁶⁷

• 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.

ACE increased¹⁶⁸

• Hyperactivity and inattention more common in women than in men
• Hyperactivity and inattention roughly equal in women
• Hyperactivity in men stronger than inattention
• Aggressiveness in women, mediated by ADHD symptoms

The stress caused by early separation from the mother triggered hyperactivity and inattention in rats, which could be eliminated by MPH.¹⁶⁹
The number of stressful life events (as measured by the Traumatic Events Screen Inventory for Children) correlated with more severe ADHD.¹⁷⁰
ADHD symptoms correlate with:¹⁷¹

• K-SADS-PL values for post-traumatic stress disorder at the age of 14 and 15¹⁷²
• sexual and physical abuse before the age of 16 or 17¹⁷³¹⁷⁴

A natural disaster during early childhood increased the risk of ADHD.¹⁷⁵

See in detail at ⇒ Trauma as a cause of ADHD

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).¹⁷⁶
Eviction as a stressful experience correlated with increased depression and anxiety, but not with increased ADHD.¹⁷⁷

3.2.1.2. Growing up in a home (+ 200 %)¶

Children who were exposed to multiple drug use by their mother 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 22¹⁷⁸, corresponding to a prevalence of around 20%.¹⁷⁹¹⁶² In US child welfare agencies, the prevalence of ADHD is almost quadrupled at 19%.¹⁸⁰

Another study did not find an increased ADHD prevalence of 5.8% in homes without depriving living conditions, but a significantly increased ADHD prevalence¹⁸¹ 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.¹⁸²
The later the adoption from the home, the higher the prevalence of ADHD.^183184185

3.2.2. Growing up in adoption ( + 200 %)¶

A study of Chinese adopted girls found an ADHD rate of 16.7%, which is around three times the usual prevalence.¹⁸⁶ 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).

3.2.3. Parents and family¶

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

Children from “lower class” families have an increased correlation with ADHD^{187188 189} and are more likely to receive ADH)S medication.¹⁹⁰¹⁵⁸
Children from lower classes have about twice the risk of ADHD as children from higher classes (in a 3-tier model).¹⁹¹

Cramped living conditions also increase the risk of ADHD in children.¹⁸⁸ Poor family finances correlated with a 2.12-fold increased risk of ADHD at kindergarten age in the USA.¹⁹²

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.²⁰⁰

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.²⁰¹

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.²⁰² 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.²⁰³ 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.²⁰⁴

3.2.3.2. Psychological problems of the parents¶

Parental mental health problems increase the risk of ADHD in children.²⁰⁵¹⁵⁸
Parental mental health problems could be an environmental and/or genetic influence.

3.2.3.2.1. Depression (+ 42 to 125 %)¶

Depressive symptoms in the father or mother increase the children’s risk of ADHD¹⁸⁹

• by 66 %²⁰⁶
• by 42 % to 125 %:²⁰⁷
  • 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 depression²⁰⁸

3.2.3.2.2. Bipolar Disorder ( + 100 %)¶

• Bipolar Disorder in a parent doubles the risk of ADHD²⁰⁹

3.2.3.2.3. Antisocial personality disorder of the father¶

Antisocial Disorder in a parent is a huge (and usually violent) risk for ADHD in the offspring.¹⁸⁸

3.2.3.2.4. Alcohol problems of the father¶

Alcohol problems in the father increase the risk of ADHD in the offspring.²¹⁰

3.2.3.2.5. ADHD of the parents¶

Parental ADHD not only increases the risk of the child inheriting ADHD genetically, but also independently represents an increased risk of being taught dysfunctional lifestyle habits. Of course, it can also be an advantage for a child with ADHD if parents have learned to cope well with their ADHD and are therefore much more aware of functional compensatory coping strategies. However, there is a not insignificant proportion of parents who are themselves affected and do not want to admit this to themselves. This often leads to additional conflicts due to a more or less conscious rejection of the behavior of the person with ADHD, for which the child is not responsible.
Furthermore, even the most committed parents - like everyone - may not always be up to date with their own theory.

Mothers with ADHD showed more problems monitoring their children’s dental care and health.²¹¹
On the other hand, children with ADHD symptoms in Spain had a higher risk of²¹²

• Caries (OR: 2.16)
• Extraction (OR: 1.42)
• Restoration (OR: 1.47)
• Bleeding gums (OR: 1.64)
  The increased caries risk persisted even when the analyses were restricted to middle/higher social class families and children with low sugar consumption, good oral hygiene habits and regular visits to the dentist.

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

A Danish coparent study (n = 943,785) found a more than doubled risk of ADHD if the parents were 20 years old or younger, compared to parents 26 to 30 years old.²¹³ 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 20.²¹⁴²¹⁵ Another study also reported that younger fathers were more likely to have children with ADHD than older fathers.²¹⁶ 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:²¹⁷

• 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 mothers²¹⁸
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).²¹⁹

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.²²⁰

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

3.2.3.4. Injuries to a parent¶

Children and adolescents (aged 5 to 17) whose parent had to receive medical treatment for an unintentional injury showed in a registry study:²²¹

• a 69% increased risk of ADHD
• a higher Washington Group Composite Disability Scores (OR 1.77)
• a 129% higher risk of personal injury
• 49% higher risk of own emergency doctor visits

It remains an open question whether the increases in risk are a psychotraumatic consequence of the parent’s injury or a consequence of the fact that the genetic heritability of ADHD is 80% and the parent’s injury was a consequence of their own ADHD, as ADHD is known to carry a higher risk of injury or emergency room visits.

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

Low education of the mother¹⁰ or the parents²¹⁰ 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.²²² Children of parents without a university degree had twice the risk of ADHD as children of parents with a university degree²²³
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.²²⁴
In a cohort study in Denmark, a low level of parental education correlated with a 3.5% increased risk of ADHD in children.¹⁹⁶ 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.²⁰⁴

3.2.3.6. Unemployment of parents (+ 2.1 %)¶

In a cohort study in Denmark, parental unemployment correlated with a 2.1% increased risk of ADHD in children.¹⁹⁶ 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.²²⁵

3.2.3.7. 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.²²⁶

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.²²⁷ 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.²²⁸ 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.¹⁵⁹

Poor parenting behavior is already a psychosocial risk factor for ADHD.²²⁹

• 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.²³¹

3.2.3.8. 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 regulation²³²

3.2.3.9. 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.²³³. Parental stress generally correlated with increased ADHD symptoms in children.²²⁵

3.2.3.10. Thyroid problems in the mother¶

However, maternal hyperthyroidism, which was first diagnosed and treated after the birth of the child, increased the risk of ADHD in the child by 23%, while hypothyroidism diagnosed in this way increased the risk of ASD by 34%.²³⁴

3.2.3.11. Incomplete families¶

Single-parent families increase the risk of ADHD.^210188158225

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.

3.2.3.12. Family instability, constant arguments between the parents¶

A high level of stress in the primary family increases the risk of ADHD.^210188158225

Progression studies do not find complete persistence even during childhood and adolescence and confirm a frequent coincidence with family problems and parental problems.²³⁷ Conversely, a high level of family cohesion and social support has a protective effect against ADHD.²³⁸

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

Lower parental reflective functioning correlated with ADHD in children.¹⁸⁹ Parental reflective functioning is defined as the parents’ ability to reflect on their own and their child’s inner mental experiences.

3.2.4. Relatively earlier school enrollment / older classmates (+ 34 %)¶

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 the states in which a fixed age on September 1 determines school enrollment, 0.85% of children born in August, i.e. who reached school age immediately before the cut-off date, had an ADHD diagnosis (+35%) and 0.52% received ADHD medication, while of children born in September, i.e. 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 rather than 0.21 percentage points.²³⁹
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.²⁴⁰ Similar results were found in a study of 1,042,106 English children between the ages of 4 and 15.²⁴¹ 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.²⁴² 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 11.²⁴³
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 there²⁴⁴

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 found²⁴⁵

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.²⁴⁷

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.²⁴⁸ 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.²⁴⁹

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.

3.2.5. Urban environment¶

Growing up in an urban environment is also associated with increased risks for other disorders:^250251252

• Schizophrenia^253254255
• Psychosis²⁵⁶²⁵⁷
• abnormal brain responses to stress in healthy subjects²⁵⁸²⁵⁹

In many studies, an urban environment improved cognitive abilities and showed preventive effectiveness against mental problems - even in older people.²⁶⁰

Growing up in an urban environment influences the dopaminergic system.²⁶¹²⁶⁰

3.2.5.1. 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.²⁶² A Canadian cohort study,⁹² a larger study from New Zealand²⁶³ and a smaller study of children in Barcelona²⁶⁴ and a meta-analysis²⁶⁵ 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.²⁶⁶
• Green plants reduce noise. Increased street background noise levels correlate with increased behavioral and sleep problems.²⁶⁷ However, noise was not a risk factor in the Canadian cohort study.⁹²
• 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.²⁶⁸
  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.²⁶⁹

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 %.²⁷⁰
A meta-analysis came to similar conclusions.²⁷¹ Another study found a 15% increase in the risk of externalizing behaviour if there was no green space within 300 metres of the home.²⁷²
The amount of vegetation in the environment (but not the amount of water) correlates with better working memory development in children.²⁷³

According to a cohort study, children who grew up in a rural environment from the age of 3 had a one-third (33%) lower risk of ADHD.²⁶³ The lower the proportion of vegetation in the environment, the higher the risk of ADHD.²⁷⁴

Green plants indoors could possibly also have a positive influence on stress levels and mental health.²⁷⁵

Urban environments also increase the risk of other mental disorders such as schizophrenia²⁷⁶
The risk of schizophrenia and ADHD is increased by inflammation. Particulate matter increases the inflammatory load on the brain. Particulate matter increases the risk of ADHD.

In Polish children aged 10 to 13, attention tended to be improved by tree cover, gardens and water areas and tended to be worsened by grass areas, in each case within 500 meters of the home address.²⁷⁷

One study found no association between green growth during pregnancy and early childhood and ADHD symptoms.²⁷⁸ In our opinion, this could be interpreted as an indication of more psychological effects.

3.2.5.2. 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.²⁷²
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.²⁷⁹

3.2.5.3. Noise from roads and neighbors¶

In 9-year-old children, street noise and noise from neighbors correlated with ADHD.²⁸⁰ The result was independent of sleep problems.

3.2.6. 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.²⁸¹

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.²⁸²

3.2.7. Class size¶

One study found that larger class sizes in Korea were associated with a reduced rate of ADHD. It was assumed that hyperactive, impulsive, inattentive or disorganized children are less noticeable in larger classes, meaning that class size does not influence the development of ADHD but rather its recognition²⁸³
In contrast, another study found that teachers in a larger class in the USA were more likely to notice indications of ADHD and therefore recognize ADHD more often than in a small class.²⁸⁴
A French article suggests that a higher level of stimulation (noise, visual distractions, large class sizes) is likely to reveal or reinforce instability, impulsivity and inattention and thus make ADHD more visible²⁸⁵
The influence of class size on the occurrence or frequency of diagnosis of ADHD is thus unclear.

3.2.8. 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.²⁸⁶

3.2.9. Only child¶

Since only children are likely to result predominantly from first births, and first-time mothers are much more likely to suffer birth complications (see under first-born status), which (certainly) increase the risk of ADHD, it would be surprising for us if only children did not have an increased risk of ADHD. It remains to be seen whether there are other risk factors.

A large Spanish registry study found a 3.1-fold risk of ADHD for only children compared to children with younger and older siblings.²⁸⁷
Preschool children aged 3 to 6 years had a 30% increased risk of ADHD if the children were only children in a large Chinese population-based study using parental data.¹⁵⁵
Children with ASD had a significantly reduced risk of ADHD if they had an older sibling³⁷

The German KiGGS study (n = 13,488) found no evidence of a link between the number of siblings and ADHD.²⁹

3.2.10. Media¶

3.2.10.1. Early television consumption¶

Early television consumption at the ages of 1 and 3 correlates with attention problems at the age of 7.²⁸⁸

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.

3.2.10.2. 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.²⁸⁹ Presumably, ADHD, hyperactivity and impulsivity are causal factors in problematic media consumption.²⁹⁰ Nevertheless, increased screen consumption in children appears to be able to impair attention.²⁹¹

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.²⁹²
Daily childhood television consumption of more than 5 hours correlated with a 63-fold risk of ADHD.⁶⁶

3.3. Characteristics without increased risk of ADHD¶

• Dichlorodiphenyldichloroethylene did not influence the risk of ADHD¹⁵⁰
• 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.¹¹⁷ Another study found no effect on ADHD.¹⁵⁰
• Organic pollutants (OP pesticides, PCBs, pyrethroid insecticides and trichlorophenol (TCP)) did not increase the odds ratio for ADHD (0.99)⁶⁷
• Bismuth urine levels were slightly lower in children with ADHD than in children without ADHD.⁶⁵
• Aluminum blood levels were unchanged in children with ADHD.⁶³
• The prevalence of microcytic anemia was found to be 14% lower in children with ADHD (OR: 0.86)²⁹³
• Growing up bilingual did not increase the risk of ADHD²⁹⁴
• Autoimmune diseases showed no evidence of causality of autoimmune diseases for ADHD. The study examined²⁹⁵
  • Lupus erythematosus
  • Crohn’s disease
  • Ulcerative colitis
  • Type 1 diabetes
  • rheumatoid arthritis
  • Psoriasis
  • Ankylosing spondylitis
  • Multiple sclerosis

3.4. Characteristics with risk reduction of ADHD¶

• Immigrant status of parents causes a reduced risk of ADHD²⁹⁶ within the first 2 generations.²⁹⁷
• p,p’-dichlorodiphenyltrichloroethane (p,p’-DDT) was associated with a 36% lower likelihood of ADHD¹¹⁷