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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 interventions 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.
A lack of bonding behavior on the part of the mother or parents during childhood, stress on the part of the mother during childhood or psychological problems on the part of the parents increase the risk of ADHD in children, as do low socio-economic status, a low level of education or unemployment on the part 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.
3.1.1.1.1. 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
Details
With a usual prevalence of 5 to 10 % for ADHD (all subtypes), an 11.8-fold increase in risk would mean that 60 to 100 % of all crying children develop a form of ADHD.
In addition, studies have reported that (former) crying children aged 3.5 years have more frequent behavioral problems according to their mothers, but no problems with attention span, behavior regulation and sociability.6 Crying children cause considerable stress for their parents. 5.6% of all crying children bring their parents to the point of abuse and neglect, including serious bodily harm (shaking, hitting).1
This demonstrates the considerable stress that the affected baby experiences over and above the actual cause of the crying. A self-reinforcing system develops: the child’s stress causes crying, which causes stress in the parents, which in turn increases the child’s stress.
Crying is not currently regarded as a separate, initial symptom of ADHD.
Infants who were not breastfed showed an increased risk of ADHD as children, while children who were breastfed as infants showed a reduced risk of ADHD.789 Studies report an approximately 1.55-fold (OR = 1.55) to almost 3-fold ADHD risk1011
Children who were exclusively breastfed had a 23% lower risk of ADHD and a 36% lower risk of ASD compared to children who were exclusively bottle-fed. Partially breastfed children had a 9% lower risk of ADHD and an 11% lower risk of ASD. Whether complementary food was given before 6 months of age or later had no influence.12
The risk of ADHD decreases with the duration of breastfeeding.131415
One study found no ADHD-preventive effect of breastfeeding.16
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. Physical and main 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 2011.17
Studies in mice suggest that valproate administration in newborns could cause permanent damage similar to that of ASD and, in some cases, ADHD.19
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 Disorders20
This is consistent with the findings of an increased risk of ADHD if the mother has a D3 deficiency during pregnancy (see there).
Severe bacterial infections in childhood or adolescence massively increase the risk of severe mental disorders (HR):21
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
Among 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:22
In a very large study, 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 %.23
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.24 Two other studies found no increased risk of mental disorders when antibiotics were administered in the first 1 25 to 226 years of life.
A meta-study 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).27
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 later in life.28 A Korean cohort study found a 41% increased risk of ADHD as a result of general anesthesia in early childhood. In addition, the duration of general anesthesia correlated with an increased risk of ADHD.29
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 anesthetics30
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 gender, and central nervous system surgery were significant risk factors for ADHD in the future.31
Other studies have come to similar conclusions.3233
In contrast, a cohort study in Taiwan found no increased risk of ADHD due to anesthetics in the first 3 years of life.34
It remains to be seen to what extent the probability of a surgical procedure under anesthesia is already influenced by the increased likelihood of accidents in people with ADHD. 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.35
In contrast, a cohort study found no significant (+2%) increased risk of ADHD with atopic dermatitis in childhood.36
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 ADHD later in life. A disturbance of REM sleep was cited as a possible cause, which secondarily impaired brain maturation.37
3.1.2.5. Passive smoking - smokers in the environment in the first years of life (+ 42 % to + 170 %)¶
Nicotine exposure in children is associated with a 1.42-fold38 to 2.7-fold39 increase in ADHD.14 In one study, children with ADHD were twice as likely to have smokers in the family as unaffected children.40
In the case of passive smoking, a connection is made to certain MAO-A gene variants that cause a lower level of serotonin degradation.41
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 children of mothers who smoked during pregnancy. This indicates that exposure to nicotine in the first years of life alone can increase hyperactivity and behavioral problems.42
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.43 A smaller cohort study confirmed this for particulate matter, but not for nitrogen dioxide.44 Another cohort study found a 40% to 78% increased risk of ADHD due to 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.45
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 those affected, as well as their parents’ level of education and income, were not taken into account. A meta-analysis of 28 reports found similar results for the majority of the reports.46 Even at non-toxic doses, nitrogen oxides have an influence on glutamatergic, opioidergic cholinergic and dopaminergic neurotransmission in the brain.47
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.48
One study found no association between exposure to PM2.5 and NO2 at the age of 12 and ADHD at the age of 18, but with depression at the age of 18.49
A meta-study of 12 investigations found a correlation between particulate matter and ADHD in children in 9 of them.50
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.51 A Taiwanese register study came to comparable results.52
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 oxide53
A Polish study found a correlation between54
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-study 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:55
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 severe 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.56
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 allele57
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 decreased58
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%.59 Another study found similar results.60
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%)61
Emissions of nitrogen oxides in Germany fell by almost 2/3 between 1990 and 2020.62
A comprehensive Chinese study of 8,692 children aged 6 to 12 found a significant increase in the children’s risk of ADHD:63
Home renovations
Incense burning
Cooking oil vapors
Smokers in the household
3.1.2.7. Concussions and traumatic brain injuries (+ 68 %)¶
The severity of brain injury correlates with significantly higher ADHD symptomatology. Altered morphometry of the default mode network (DMN) due to brain injury predicted higher ADHD symptoms 12 months after injury, while morphometry of the salience network (SN) and central executive network (CEN) were not significant independent predictors.64
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 a learning disability was increased by 29%.65
In more severe cases of traumatic brain injury, the correlation was not statistically significant. In an analysis of cases with possible traumatic brain injury (corresponding 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 concussion66
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.
In children between 1 and 6 years of age, chlorpyrifos residues in the blood correlated with the risk of ADHD.67 Vitamin D reduced the risk.
Chlorpyrifos also significantly increases the risk of ADHD in the case of prenatal contamination of the mother during pregnancy.
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.68
Whether this is a causal cause or a consequence of altered food preferences due to the predisposition to the disorder remains to be seen.
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 sport15
One study found a 1.7-fold prevalence of ADHD in children with hyperthyroidism.69
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.70
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 cognition7172 and impair
which can lead to attention deficits and hyperactivity
Even temporary subclinical thyroid abnormalities during pregnancy can have serious consequences.75 Correction of severe maternal hypothyroidism before the 3rd semester of pregnancy appears to prevent cognitive impairments76 and premature births .77
Studies on mice with a mutated human thyroid receptor TRb 1 gene (TRbeta transgenic mice)78 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)
Perfluorooctane sulfonate (PFOS) in breast milk correlated with a 77% increased risk of ADHD per higher interquartile range.79
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 related to DA metabolism.80
According to a meta-analysis, manganese exposure during development increased the risk of ADHD by 163%.39 Early manganese exposure causes permanent attention problems via the mTOR pathway and a change in the catecholaminergic system84 as well as sensorimotor problems.85
Manganese intoxication shows a correlation with certain CYP2D6 gene variants.86 We consider it conceivable that these also have an influence on the risk of ADHD as a result 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.85
According to a meta-analysis, exposure to phthalates during development increased the risk of ADHD for girls by 212% and for boys by 254%.39
3.1.2.19. 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 adulthood87
Febrile convulsions in children increased the risk of ADHD by 28%88 to 66%.89 A premature infant status of those affected who had febrile convulsions increased the risk of ADHD by 6.4 times and the risk of ASD by 16.9 times.90
3.1.2.20. Early puberty (pubertas praecox) (+ 40 %)¶
An ADHD prevalence of 13.5% was found among girls with early puberty (onset of sexual maturation before the age of 8 for girls and before the age of 9 for boys).91
The low-dose pyrethroid pesticide deltamethrin 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 function92
According to a meta-study, pyrethroid insecticides did not significantly increase the odds ratio for ADHD (0.99)39
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.93 Older age at surgery was associated with poorer executive function.
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.94
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.
3.2. 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.9596
Massive maternal stress in the first years of childhood causes significant epigenetic changes in the children’s DNA.97
Children whose parents were unmarried or unemployed or without social security or had a “very high” economic burden due to 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.98
Early childhood stress and chronic stress (neglect, deprivation, abuse, trauma) can be involved in the development of ADHD.9996100101 20 % to 50 % of all children who experience early childhood trauma develop clinical ADHD symptoms.99102103
The number of traumas correlates with the severity of ADHD104 as well as with the risk of ADHD. The number of Adverse Childhood Experiences (ACEs) increased the risk of ADHD:105
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
The estimates for 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.106
The number of stressful life events (measured using the Traumatic Events Screen Inventory for Children) correlated with more severe ADHD.107 ADHD symptoms correlate with:108
K-SADS-PL values for post-traumatic stress disorder at the age of 14 and 15109
sexual and physical abuse before the age of 16 or 17110111
A natural disaster during early childhood increased the risk of ADHD.112
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).113
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 22114, corresponding to a prevalence of around 20%.115100 In US child welfare agencies, the prevalence of ADHD is almost quadrupled at 19%.116
Another study did not find an increased ADHD prevalence of 5.8% in homes without depriving living conditions, but a significantly increased ADHD prevalence117 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.118
The later a child was adopted from the home, the higher the prevalence of ADHD.119120121
A study of Chinese adopted girls found an ADHD rate of 16.7%, which is around three times the usual prevalence.122 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, is an open question. There would be some evidence for an influence of the latter factor if the prevalence of ADHD did not correlate with the length of the 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 have an increased risk of ADHD. Interestingly, this seems to be less the case for black children.123
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.124
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 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 and 0.52% received ADHD medication, while only 0.63% of children born in September, i.e. who were on average 11 months older, 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 ADHD rate compared to those 11 months older, but the difference was 0.08 percentage points rather than 0.21 percentage points.125
Similarly, a meta-analysis of three Brazilian cohort studies with 8 million participants and 164,000 ADHD sufferers found that those children in a class who were among the youngest by 4 months had a 34% higher risk of ADHD.126 A study of 1,042,106 English children between the ages of 4 and 15 came to similar conclusions.127 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.128 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 11.129
A Danish study (n = 418,396) found no influence of the age of the children within a school year on (more frequent / less frequent) ADHD medication. The authors attributed this to the low ADHD prevalence, clear diagnostic criteria and high requirements for prescribing ADHD medication in Denmark and referred to studies in countries with a high ADHD prevalence in which differences were found.130
A meta-study (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 there131
The results of the study are partly consistent with the fact that, according to a study in Canada, successful ice hockey players were more often than average among the older children in a class. The same was shown among Belgium’s soccer players, where the date of birth of the particularly successful players was for a long time primarily in August and September, because the cut-off date for determining the age for player selection was August 1. After this cut-off date was moved to January 1, the most successful players most frequently had their birthdays in January and February. A further study confirmed this “effect of relative age” throughout Europe.132
On the one hand, the effect is probably due to the selection criteria. However, this could only explain the differences in athletes that can arise due to different support. However, the parallel with ADHD suggests that there could also be an effect of the developmental lever of the opportunity/risk genes.
How these differences can be explained in relation to ADHD is unclear.
One hypothesis is that younger children are more likely to be pathologized by their teachers due to their naturally immature behavior.133
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.134 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-study found that younger relative age was not statistically significantly associated with persistence of ADHD at 4-year follow-up.135
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 almost 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 between 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.136 A Canadian cohort study,44 a larger study from New Zealand137 and a smaller study of children in Barcelona138 as well as a meta-study139 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.140
Green plants reduce noise. Increased street background noise levels correlate with increased behavioral and sleep problems.141 However, noise was not a risk factor in the Canadian cohort study.44
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 sport/exercise more than people in less green (urban) environments have not come to any clear conclusions.142
Sport is 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.143
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 of up to 20 %.144
A meta-study came to similar conclusions.145 Another study found a 15% increase in the risk of externalizing behaviour if there was no green space within 300 metres of the home.146
The amount of vegetation in the environment (but not the amount of water) correlates with better working memory development in children.147
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.137 The lower the proportion of vegetation in the environment, the higher the risk of ADHD.148
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.146
The data was collected in Europe from 2013 to 2016. At the times when leaded petrol was permitted, the pollution was probably significantly higher.
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.149
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 behaviour is a risk element for ADHD.150 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.151 A lack of patience on the part of parents has been cited as a risk factor for ADHD,14 whereby impatience can be an ADHD symptom and therefore also 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.97
Poor parenting behavior is already a psychosocial risk factor for ADHD.152
Inconsistency in education
Missing rules
Frequent criticism and punishments
Cold, distant, unloving treatment
Details
How much time parents can spend with their children is not the decisive factor. It is much more important that children can absolutely rely on the fact that they are accepted, welcome and loved in every situation and especially when they misbehave. This does not mean that children are allowed to do whatever they want. Good, warm parenting is able to consistently limit inappropriate behavior by evaluating undesirable behavior without devaluing the child as a person (your behavior is not ok, you are ok). A lack of rules (and even worse: rules that only sometimes apply) are almost unbearable for children because they take away all security. The question of a mandatory “parenting license” is the subject of legal and ethical discussions.152
Figures
10.5 million households in Germany have dogs.153(Stand 2014)
8.1 million families in Germany have underage children (as of 2014).
A Google search for parenting course OR parenting courses finds 169,000 results. (20.10.2015)
A Google search for dog school finds 1,240,000 results. (20.10.2015)
Borderline disorder, which is typically caused by intense stress-induced attachment disorders to the attachment figures in early childhood (first 2 years) due to physical, sexual or psychological abuse, has a significant comorbidity with ADHD.154
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 regulation155
Stress experienced by 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.156
Single-parent families increase the risk of ADHD.15915896
Single parents naturally have a higher risk of not being able to give their children enough loving care and security. There are indeed 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 the disorder.
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.15915896
Family conflicts and ADHD
“Chronic family conflicts, reduced family cohesion and confrontation with parental psychopathology (especially on the mother’s side) are found more frequently in families with ADHD sufferers compared to control families”.162
The risk of children developing ADHD (odds ratio) increases with the level of psychosocial stress (Rutter indicator, RI). With an RI of 1, the odds ratio is 7, with an RI of 4 it is 41.7 (68). Odds ratios > 1 indicate an increased risk.163
Progression studies do not find complete persistence even during childhood and adolescence and confirm a frequent coincidence with family problems and parental problems.164 Conversely, a high level of family cohesion and social support has a protective effect against ADHD.165
Children whose mother does not have ADHD have a 14% higher risk of ADHD if one parent is younger than 20.
Children whose mother has ADHD have a 92% increased risk of ADHD if one parent is younger than 20.166 Another study also reported that younger fathers were more likely to have children with ADHD than older fathers.167 One study reported a 32% lower risk of ADHD for every 10 years increase in maternal age. However, the correlation was attenuated by other factors. These were:168
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 mothers169
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).170
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.171
One study found no correlation between the age of the mother and the risk of ADHD in the offspring.16
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 ADHD172158160 and are more likely to receive ADH)S medication.17396
Children from lower social classes have about twice the risk of ADHD as children from higher social classes (in a 3-tier model).174
Cramped living conditions also increase the risk of ADHD in children.158 Poor family finances correlated with a 2.12-fold increase in the risk of ADHD at kindergarten age in the USA.175
Details
The overall prevalence of ADHD in children and adolescents was found to be 2.2% in the 2007 Bella study176 (which we consider to be too low). A Bella sub-study with n= 2500 subjects between the ages of 7 and 17177 puts the prevalence in the parents’ assessment at around 5%. Both studies confirm a strong divergence in prevalence according to social class. According to the Bella Study 2007, the middle class has the average prevalence, while the lower social class has a prevalence of 3.9%, four times as high as the upper class.178 The Bella sub-study reports a prevalence of ADHD in the lower social class (at 7.2%) that is around 2.3 times higher than in the upper class at 2.8% (with 3 strata).177
In a cohort study in Denmark, low parental income correlated with a 2.3% increased risk of ADHD in children.179 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. The fact that this pattern is not limited to ADHD, but is found identically in other mental disorders, e.g. anxiety, depression or social behavior disorders, is seen by us as a strong indication of confirmation of the thesis of stress as the cause of mental disorders. Like ADHD, these other mental disorders are also based on a multigenetic disposition (see 2.1.3. and 2.1.4.), which is epigenetically manifested by stress exposure in early childhood.180181182
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.183
We suspect that it is not so much the socio-economic status or the size of the home itself that are relevant factors, but that these circumstances unfortunately often correlate with inappropriate parenting methods and the parents’ own problems (whereby the latter influence the socio-economic status of the parents on the one hand and can be hereditary on the other).
Parents of ADHD children showed elevated levels of cognitive impairment (IQ, reading tasks, verbal fluency), the highest stress levels of all parent groups compared, the most ADHD symptoms and poor reading performance.184
There is also evidence that (with regard to children 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.185 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.
Poorer financial resources also appear to correlate with increased ADHD symptoms among college students.186 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.187
3.2.2.9. Low level of education of parents (+ 3.5 % to + 4.9 %)¶
Low parental education increases the risk of ADHD in children.159
Children of parents with a low level of education had higher ADHD symptoms and an almost 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.188 Children of parents without a university degree had twice the risk of ADHD as children of parents with a university degree189
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.190
In a cohort study in Denmark, a low level of parental education correlated with a 3.5% higher risk of ADHD in children.179 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 mother11
A genetically predicted one SD higher level of education causally predicted a 70% lower risk of ADHD.187
In a cohort study in Denmark, parental unemployment correlated with a 2.1% increased risk of ADHD in children.179 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.
3.2.2.11. Parents are less able to reflect on their parental role¶
Lower parental reflective functioning correlated with ADHD in children.160 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 are mutually causal¶
A large register 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.191
Early television consumption at the ages of 1 and 3 correlates with attention problems at the age of 7.192
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.193ADHD, hyperactivity and impulsivity are presumably causal causes of problematic media consumption.194 Nevertheless, increased screen consumption in children appears to be able to impair attention.195
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 regresses after the screen consumption is reduced.196
3.3. Characteristics without increased risk of ADHD¶
p,p’-dichlorodiphenyltrichloroethane (p,p’-DDT) was associated with a 36% lower likelihood of ADHD79
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.79
Organic pollutants (OP pesticides, PCBs, pyrethroid insecticides and trichlorophenol (TCP)) did not significantly increase the odds ratio for ADHD (0.99)39
Sram RJ, Veleminsky M Jr, Veleminsky M Sr, Stejskalová J (2017): The impact of air pollution to central nervous system in children and adults. Neuro Endocrinol Lett. 2017 Dec;38(6):389-396. PMID: 29298278. METASTUDY ↥
