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1. Prenatal stressors as ADHD environmental causes


1. Prenatal stressors as ADHD environmental causes

Even before birth, the unborn child can be damaged by toxic influences or diseases.
Many toxins and diseases that increase the risk of ADHD in offspring do so by affecting the dopaminergic system. Toxins can also increase the risk of ADHD even before conception through epigenetic mediation.
Psychological and physical stress (toxins, illnesses) have a fundamentally comparable effect on the stress systems (HPA axis, autonomic nervous system and others).
The % values given for a possible ADHD risk increase are an indication of the magnitude of the influence of the respective exposure. We are not aware of any values for entries without a % figure.

The consumption of nicotine, alcohol or stronger drugs during pregnancy increases the risk of ADHD in the offspring. Nicotine even increases the risk if the parents only smoked before conception.
Another source of risk is toxins that the mother comes into contact with during pregnancy. These include pesticides such as organophosphates or pyrethroids and chemicals such as lead, cadmium, thallium, bisphenols, polychlorinated biphenyls or polycyclic aromatic hydrocarbons.

Air pollution, especially particulate matter and nitrogen oxides, can also increase the risk of ADHD.
A high salt intake by the mother during pregnancy can increase the unborn child’s sensitivity to stress.

Various health factors in the mother, such as illnesses, obesity, stress, infections and hormonal disorders, are also associated with an increased risk of ADHD in the child. Thyroid hormones in particular should be closely monitored. A higher level of omega-3 fatty acids in the newborn could reduce the risk and severity of ADHD and autism spectrum disorders. Vitamin D3 deficiency during pregnancy and after birth is associated with dopaminergic maldevelopment of the brain.
High cortisol exposure of the fetus or newborn, due to cortisol administration or maternal stress during pregnancy, can also increase the risk of ADHD.

It is well known that many medications can pose a risk to the unborn child during pregnancy. With regard to ADHD, paracetamol (acetaminophen), SSRIs (antidepressants), β-2 adrenaline receptor agonists, pregabalin, antibiotics and valproate are particularly relevant during pregnancy.

Finally, pregnancy circumstances such as first-born status or particularly short or long intervals to the previous pregnancy influence the child’s risk of ADHD.

There appear to be gender differences for some of these risk factors.

Although the following collection is extensive, a number of other circumstances are likely to be associated with an increased risk of ADHD.
The various factors each represent only parts of a multi-layered risk mosaic and do not automatically lead to ADHD.

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

1.1. Toxins before pregnancy as risks for ADHD - epigenetic inheritance

1.1.1. Nicotine consumption of one parent before conception (+ 259 %)

Children whose fathers smoked before pregnancy had a 2.59-fold risk of ADHD compared to children whose fathers never smoked.
Children of parents who were exposed to smoking or passive smoking before pregnancy had 1.96 times the risk of A(D)HS.
Children whose parents were exposed to tobacco smoke both before and during pregnancy had a 2.01-fold risk of ADHD.1

Nicotine consumption by a parent before conception: epigenetic inheritance of nicotine damage causes ADHD symptoms in offspring over several generations

Mice whose fathers or mothers were chronically exposed to nicotine before conception showed hyperactivity, impaired nicotine-induced motor sensitization and reduced dopamine and noradrenaline levels in the striatum and PFC.23

Nicotine consumption by the father or mother before conception causes epigenetic changes in the offspring

  • Of the dopamine D2 receptor.4
  • Of the dopamine transporter (DAT) m striatum and mPFC5
    • Through downregulation of DAT expression due to increased methylation of the DAT gene.6 Increased DRD4 and 5-HT DNA methylation correlates with ADHD.7
  • Altered expression and dysfunction of nicotinic acetylcholine receptors (nAChRs)5
  • Hypersensitivity to nicotine-induced nAChR-mediated dopamine release5

The children of the first and second generation showed typical ADHD impairments:

  1. Generation:
  • Significantly increased spontaneous locomotor activity (hyperactivity) (males and females)45
    • Reduced DAT expression causes increased dopamine levels in the striatum, resulting in dephosphorylation of AKT via activation of D2 receptors, leading to increased activation of GSK3α/β and ultimately causing hyperactivity in the offspring of the mice.6
  • Risk-taking behavior5
  • Significant deficits in reversal learning (males and females)4
  • Significant attention deficits (males)4
  • Significantly reduced monoamine content in the brain (males)4
  • Reduced dopamine receptor mRNA expression (males)4
  • Increased nicotine preference5
  • Activity rhythm altered5 Note: This could be a link to the altered circadian rhythm in ADHD
  1. Generation:
  • Significant deficits in reversal learning (males)4
  • Hyperactivity5
  • Risk-taking behavior5
  • Increased nicotine preference5
  • Activity rhythm changed5

It can be assumed that the mechanisms are similar to those in humans.

1.2. Toxins and harmful effects during pregnancy (up to + 778 %)

Toxic effects on unborn babies have been proven for:

1.2.1. Alcohol during pregnancy (+ 778 %)

Around 5% of children in the USA are said to suffer from FASD, i.e. are affected by the mother’s alcohol consumption during pregnancy.8
The vast majority of studies have found that alcohol consumption by the mother during pregnancy significantly increases the likelihood of ADHD in children.910 up to 8.78 times,11 Attention problems are also increased12
A combination of alcohol and stress in the mother during pregnancy increased the likelihood of male rats developing female sexual behavior.13
47.2% of children with FAS (fetal alcohol syndrome) also had ADHD14

There is evidence that alcohol consumption by the mother during pregnancy or while breastfeeding has a significant impact on the child’s dopamine system.15161718 The regulation of the neurotransmitters serotonin , glutamate, noradrenaline, acetylcholine and histamine is also affected1920 21

Individual studies found no connection between:

  • Alcohol consumption during pregnancy and ADHD.2223
  • Binge drinking in early pregnancy and the risk of ADHD in children aged 5 to 19 years.24
    One study found a correlation between ethoxyacetic acid (one of 6 degradation products of alcohol examined) in the mother’s urine and inhibition problems in the children.25
    A meta-study found that alcohol consumption by the mother of less than 70 g/week during pregnancy did not increase the risk of ADHD.26 Boys were less at risk from alcohol during pregnancy than girls.

Neill et al. deal with the differential diagnosis of ADHD and FASD (Fetal Alcohol Spectrum Disorder).27

1.2.2. Nicotine consumption of the mother during pregnancy (+ 58 % to + 378 %)

Prenatal smoking causes an increased risk of ADHD for the offspring at the

  • 1.58-fold (increased by 58 %)28
  • 2.7-fold (increased by 170 %)29
  • 4.78-fold (increased by 378 %)11

Other studies also found significantly increased risk values.3031323333435

Children with ADHD were more likely to have mothers who had smoked during pregnancy:

Only two studies (with overlapping authors) and one meta-study came to a different conclusion3940 41 , one study found rather weak evidence.42

Most experiments with prenatal nicotine exposure show a reduction in dopamine levels in the PFC and striatum. Under certain circumstances, increased dopamine levels were also shown.43 ADHD is neurophysiologically closely linked to reduced dopamine levels in the dlPFC (impaired working memory) and striatum (impaired motivation and motor control = hyperactivity).
Smoking by those affected must be distinguished from this - this increases the dopamine levels (at least in the striatum), as it reduces the DAT, which is too pronounced in ADHD and reduces the dopamine level in the striatum. Acute smoking thus increases the dopamine level in the striatum.

Prenatal smoking in conjunction with certain gene polymorphisms increases the likelihood of ADHD more than if these genetic risks are not present:

  • If there are no genetic risks, smoking by the mother during pregnancy increases the risk of ADHD for the child by 20 to 30 %.
  • The risk genes alone (if the mother does not smoke during pregnancy) increase the risk by 20 to 40 %.
  • However, if risk genes and maternal smoking coincide during pregnancy, the child’s risk of ADHD increases many times over:
    • DAT1-9R (440 bp): by a factor of 2.6
    • DRD4-7R by a factor of 2.9
    • Both together by a factor of 94445
      Another study confirms the involvement of DRD4-7R in gene-environment interactions.46
  • Smoking by the mother during pregnancy increased the risk of hyperactivity/impulsivity symptoms in the child by 50%.47 Even passive smoking increased this risk by almost 50%, but only for boys.

Maternal smoking during pregnancy alters the glutamate NMDA receptors in the laterodorsal tegmentum of the offspring.48 Another study also found changes in glutamatergic signaling in the hippocampus due to increased glutamate receptor expression,49 which was associated with learning problems, attention problems and increased impulsivity.
ProBDNF proteolysis is impaired by an imbalance between proBDNF and BDNF and downregulation of the proBDNF processing enzyme furin. Glucocorticoid receptor activity is altered by decreased relative nuclear GR localization. The basal plasma corticosterone level is reduced. The HPA axis is disturbed. This affects the offspring themselves, but also their children, and is therefore inherited.50

In rodents, it was found that prenatal nicotine exposure reduces dopamine levels in the mPFC of the offspring.51 In ADHD, the dopamine level in the PFC is reduced.

A study on mice whose mothers were exposed to nicotine during pregnancy found evidence that nicotine causes various effects during pregnancy that persist in the grandchildren’s generation, indicating epigenetic inheritance:52

  • Deficits in the expression of corticostriatal DNA methyltransferase 3A (DNMT3A)
  • Downregulation of methyl-CpG-binding protein 2 (MeCP2) in frontal cortices and the hippocampus
  • Downregulation of histone deacetylase 2 (HDAC2) in frontal cortices and the hippocampus
  • Abnormalities in HDAC2 (Ser394) phosphorylation in frontal cortices, striatum and hippocampus
  • No change in the expression of ten-eleven translocase methylcytosine dioxygenase 2 (TET2)
  • No abnormalities in MeCP2 (Ser421) phosphorylation in frontal cortices, striatum and hippocampus

Maternal smoking increases fetal testosterone levels.53 Elevated prenatal testosterone levels are a risk factor for ADHD. More on this under Gender differences in ADHD.

Even passive smoking, i.e. passive exposure of the mother to nicotine smoke during pregnancy, tends to increase the unborn child’s risk of later ADHD symptoms.47
Similar results were found for the causation of dyspraxia (developmental coordination disorder) by passive smoking.54

Over 70 million women in the EU smoke during pregnancy.49

It is possible that the effects of nicotine consumption by the mother during pregnancy could be compensated for by breastfeeding.55

1.2.3. Drug use by the mother during pregnancy (+ 200 %)

Children who were exposed to multiple drug use by their mothers before birth and who subsequently grew up in institutions were found to be three times more likely to develop ADHD between the ages of 17 and 22.56

Several studies have associated cannabis use during pregnancy with an increased risk of ADHD in children.57

1.2.4. Polycyclic aromatic hydrocarbons (PAHs) (+ 99 to 157 %)

Prenatal exposure to polycyclic aromatic hydrocarbons appears to increase damage from early childhood stress exposure and promote later attention and memory problems.58 A meta-study found that 4 studies by one author indicated a 1.57-fold increase in the risk of ADHD due to PAHs (OR 2.57), while the total number of all studies indicated a doubled risk (OR 1.99), which was not significant59
High prenatal PAH exposure correlated with

  • Attention symptoms60 according to DSM-IV (OR = 5.06)61. dose-dependent62
  • ADHD total score according to DSM-IV (OR = 3.37)6163
  • Anxiety and depression6064

1.2.5. Exposure of the mother to non-ionizing magnetic field radiation during pregnancy (+ 100 %)

Children whose mothers were most strongly exposed to non-ionizing magnetic field radiation (“electro-smog”) during pregnancy (in a 24-hour measurement),65

  • Showed a doubled risk of ADHD (aHR 2.01)
  • Persistence of ADHD beyond age 11 was more than three times more likely to correlate with high maternal exposure than remission of ADHD by age 11 (aHR 3.38).
  • ADHD with comorbid immune-related comorbidities (asthma or neurodermatitis / atopic dermatitis) was 4.57 times more likely to be correlated with high exposure.
  • A co-occurrence of ADHD persisting beyond the age of 11 and immune-related comorbidities was 8.27 times more likely to be associated with exposure.

1.2.6. Air pollution during pregnancy (up to + 26 %)

One study found changes in the immune system of offspring due to air pollution.66
A study of around 43,000 families in Shenzen found positive correlations between ADHD from the age of 3 and exposure to67

  • Cooking vapors
  • Tobacco smoke
  • Vapors from house renovations
  • Mosquito coils (burnt mosquito pyramids; especially in combination with incense smoke)
  • Incense smoke (especially in combination with mosquito repellent smoke)

Another study found no increase in risk from air pollution in relation to ADHD.68

A meta-analysis found that more studies (without reference to pregnancy) confirmed a link between air pollution and ADHD than denied it.69 Particulate matter (+ 26 %)

A cohort study of 425,736 births on prenatal particulate matter exposure using satellite data found that an increase in PM2.5 concentration of 10 μg/m³ during the first trimester increased the risk of ADHD by 26% and that this increased further at PM2.5 concentrations above 16 μg/m³.70
Air pollution from particulate matter during pregnancy correlated in one study with a reduced volume of the corpus callosum and a tendency towards increased hyperactivity.71 Another study found a link between particulate matter and ADHD at low levels of particulate matter exposure, while higher levels caused more severe brain damage.63

In rats, inhaled printer particles led to a 5-fold increase in dopamine levels, probably due to increased synthesis rather than decreased degradation.72

Diesel exhaust particles led to functional impairment of dopamine neurons in laboratory tests. Prenatal ingestion with the air we breathe had the same effect in mice:73

  • In the striatum
    • Reduced dopamine metabolism
    • Reduced levels of dopamine metabolites
  • In the amygdala
    • Increased dopamine levels
    • Increased dopamine metabolite levels
  • In the nucleus accumbens
    • Increased dopamine levels

Traffic ultrafine particulate matter in the air breathed after birth had the following effects on female mice:73

  • In the hippocampus
    • Increased dopamine turnover

Pre- and postnatally, particulate matter and gaseous pollutants reduced the expression of oxytocin receptors in the hippocampus74 and hypothalamus in rodents, with reduced maternal care behavior.75 Oxytocin and vasopressin communication appears to be disrupted by endocrine disrupting chemicals76, many of which are present in outdoor air.73

Studies found an association between PM2.5 and hyperactivity/attention symptoms (OR = 1.12)77, hyperactivity78, ADHD symptoms79 and between PM2.5 in the first trimester and a tendency towards attention problems and hyperactivity.80

Other studies found no link between PM2.5 and ADHD818283 Nitrogen oxides (nitrogen oxides)

Several studies have found a correlation between exposure to nitric oxide during pregnancy and ADHD.58

  • NOx correlated with hyperactivity, with a stronger correlation between ADHD and NO than between ADHD and NO2. (NO: aOR = 1.26)83
  • NO2 exposure during pregnancy was strongly correlated with ADHD symptoms, such as
    • Impulsiveness
      • Interrupting others79
      • Inability to wait your turn when playing79
    • Attention problems
      • Carelessness when crossing the road79
      • Attention impaired at the age of 4-5 years84
    • Hyperactivity78
    • Oppositional behavior (not an original ADHD symptom)
      • Lies79
      • Public disturbance79

Other studies found no significant or clear correlations between NOx and ADHD 81 7782
One study found a correlation with ASD in children, but not with ADHD.85

Emissions of nitrogen oxides in Germany fell by almost 2/3 between 1990 and 2020.86 Ozone

Ozone caused in rats:73

  • In the substantia nigra
    • Reduced number of dopamine neurons
  • In the hippocampus
    • Reduced expression of the serotonin receptors 5-HT1A, 5-HT1B and 5-HT4
    • Increased expression of the serotonin receptor 5-HT2C
  • In the hypothalamus
    • Reduced serotonin levels

No correlation with ADHD has yet been found in humans.7858

1.2.7. Polychlorinated biphenyls / polychlorinated biphenyl ethers (+ 23 %)

A long-term study found no correlation between exposure to perflouralkyl during pregnancy and ADHD. There were weak - positive and negative - correlations with working memory functions in childhood.87 A meta-study also found no significant correlation between maternal PFAS exposure and the prevalence rate of early childhood ADHD. Nevertheless, the odds ratio was partially increased:88

  • Perfluorooctanoic acid (PFOA): 1.00
  • Perfluorooctane sulfonate (PFOS): 1.01
  • Perfluorohexane sulfonate (PFHxS): 1.08
  • Perfluorononanoic acid (PFNA): 1.13
  • Perfluorodecanoic acid (PFDA): 1.23

The PFOS concentration in the children’s blood and the PFNA concentration in the mothers’ blood correlated with the prevalence of early childhood ADHD.

Another study found a correlation of perfluorooctanoic acid (PFOA) and AD(H)DS, but not of perfluorooctane sulfonate (PFOS) with ADHD or ASD.89 Another study found an increased risk of ADHD in school children with low to moderate exposure to PFAS at the age of 2 years.90

Polychlorinated biphenyls inhibit dopamine synthesis as well as the storage of dopamine in the vesicles and its release, thereby causing dopamine levels to be too low. Polychlorinated biphenyls cause hyperactivity and impulsivity (in rats even at sub-toxic doses).91 Polychlorinated biphenyls can act directly on dopaminergic processes to disrupt the dopamine system and produce Parkinson’s-like symptoms.92 Further studies also found dopamine-reducing effects of PFAs.9394 as well as influences on the acetylcholine, serotonin and glutamate neurotransmitter balance.95

1.2.8. Cadmium during pregnancy (+ 22 % for girls)

Exposure to cadmium during pregnancy increased the risk of ADHD for 6-year-old girls, but not for boys. Doubling the mother’s exposure to cadmium during pregnancy increased the risk of ADHD for girls by 22.3%.96#### 1.2.5. Lead exposure during pregnancy

Lead exposure during pregnancy9798 99 affects the mesocorticolimbic circulation and increases the offspring’s risk of ADHD.100
Rat mothers were exposed to acute stress and lead during pregnancy. The effect on the offspring differed between lead exposure alone or lead exposure plus stress exposure. Male rat pups showed increased corticosterone levels and decreased dopamine levels in the PFC only when exposed to lead alone, female rat pups only when exposed to lead and stress in combination. Even short-term lead exposure of the dams caused this effect.101 In female rat pups, lead exposure and maternal stress contributed as cumulative factors to learning difficulties during pregnancy. These were neurophysiologically mediated by the glucocorticoid system to the mesocorticolimbic system.102

Further studies also found evidence that lead exposure as well as stress during pregnancy affect the mesocorticolimbic dopamine/glutamate system of female offspring (less so in males) and mutually increase their effects.103 Under similar conditions, male rat pups showed a tendency towards serotonergic disturbances of the mesocorticolimbic system and altered delay discounting.104
Even a lead content in drinking water below the limit values is said to be problematic.98
In principle, lead water pipes are not very dangerous in areas with calcareous water, as limescale forms a reliable protective layer in the pipes. However, a descaling system for the drinking water must not be installed. Nevertheless, it is generally advisable to replace lead-containing water pipes during modernization work.

It is possible that the metabolism of cobalt, copper, lead, zinc and vanadium is altered in ADHD. Reduced cycle stability (determinism), duration (mean diagonal length) and complexity (entropy) of the exposure profiles were found.105

Lead is a divalent cation that mimics Ca2+ and activates PKC signaling.106

Arnsten107 describes lead as a poison that causes symptoms that can be confused with ADHD.

Lead appears to have a number of harmful neurophysiological effects, including on the dopaminergic system:

  • Impairment of the mesocorticolimbic dopaminergic system108
  • Impairment of dopamine receptors108
  • Impairment of attention regulation in the PFC109
  • Apoptosis110
  • Excitotoxicity110
  • Reduced cellular energy metabolism110
  • Impaired heme biosynthesis and anemia110
  • Oxidative stress110
  • Lipid peroxidation110
  • Changed activity of the second messenger system110
  • Altered neurotransmitter release110
  • Altered neurotransmitter receptor density110
  • Impaired neuropsychological functioning110
  • Impaired development and function of oligodendrocytes110
  • Abnormal myelin formation110
  • Abnormal neurotrophic factor expression110
  • Abnormal dendritic branching patterns110
  • Disruption of the blood-brain barrier110
  • Disruption of thyroid hormone transport into the brain110
  • Altered regulation of gene transcription110
  • Reduction of gray matter in the PFC, especially in the ACC111

Lead also appears to trigger the following behaviors:

  • Impulsiveness109
  • Sociopathic behavior112113
  • Irresponsible behavior112113
  • Criminal behavior112113
  • Lower IQ110
  • Impaired academic performance110

Lead poisoning correlates strongly with the crime rate and out-of-wedlock pregnancies in the USA.112113

Children with elevated blood lead levels are said to be particularly susceptible to other toxins in early childhood.114 In particular, warnings have been issued about lead in wall paints. During pregnancy, lead can be transferred from the mother to the child through the placenta.

1.2.9. Thallium during pregnancy

High exposure to thallium in the second trimester of pregnancy increased the risk of ADHD for 3-year-old boys, but not for girls.115

1.2.10. High salt consumption during pregnancy

A high salt intake from food during pregnancy could increase the unborn child’s sensitivity to stress.116

1.2.11. Pesticides during pregnancy Contact with organochlorine compounds during pregnancy

Organochlorine compounds (dichlorodiphenyltrichloroethanes (DDT), dieldrin, heptachlor, endosulfan) showed an effect on neuronal development in prenatal exposure, which (in rodents), e.g:117

  • DAT increased
  • Increased dopamine reuptake
  • Loss of dopaminergic cells
  • Alterations at the presynapse in key dopaminergic proteins in response to OC pesticides in striatum or substantia nigra
  • Noradrenaline increased
  • Increased serotonin
  • GABA receptors reduced
  • NMDA receptors reduced
  • MGluR5 receptors altered
  • Altered GABAergic, glutamatergic and dopaminergic response to endosulfan in PFC
  • Altered dopaminergic responses to heptachlor exposure identified

with impairments from, among others:

  • Attention processes
  • Cognitive performance
  • Memory
  • Social development
  • Mental and psychomotor development
  • Fine motor skills
  • Reflexes
  • Visual processing

Organochlorine compounds were nevertheless primarily associated with ASA. Organophosphate contact during pregnancy

The organophosphates chlorpyrifos and diazinon showed significant effects on neonatal brain development, including on the dopaminergic system.118 Prenatal exposure to the common pesticide chlorpyrifos impaired IQ and working memory in children aged 7119120 and executive functions.121

Organophosphates inhibit acetylcholinesterase (= the enzyme that breaks down acetylcholine).117 The organophosphate diisopropyl fluorophosphate (DFP) has been reported to increase dopamine and GABA receptors in addition to the known downregulation of cholinergic receptors. A single dose of 1 mg/kg DFP caused increased dopamine levels, a single toxic dose of 2 mg/kg DFP caused increased dopamine degradation. The levels returned to normal after 6 hours. Chronic administration of 1 mg/kg DFP resulted in decreased dopamine levels after 1 and 2 weeks, which returned to normal with continued administration. A single administration of DFP increased dopamine turnover in the striatum of rats, while chronic administration reduced it. The authors hypothesized that the changes in dopamine and GABA could be consequences of the downregulation of cholinergic receptors.122

Chlorpyrifos disrupts the serotonin system. Contact during pregnancy can trigger tremor in children and impair cognitive and neurobehavioral development.13

A measurement based on prenatal urinary dialkyl phosphate metabolites (diethyl phosphate and dimethyl phosphate) and an analysis of the maternal PON1 gene variants Q192R and L55M found no correlation between organophosphate contact of the mother during pregnancy and later ADHD in the child.123

A Norwegian cohort study found an increased risk of ADHD in the offspring if ADHD was detected in the mother’s blood during pregnancy:124

  • Di-n-butyl phosphate (DnBP)
  • Bis(1,3-dichloro-2-propyl)phosphate (BDCIPP)
  • Bis(2-butoxyethyl) phosphate (BBOEP)
    • only in boys. In girls, the risk decreases with increasing exposure.

Another Norwegian registry study found no evidence of an increased risk of ADHD in the offspring if the mother was exposed to organophosphates during the 17th week of pregnancy.125 Pyrethroid contact before or during pregnancy

Pyrethroids are widely used as insecticides and pesticides.

Each doubling of the pyrethroid metabolite 3-phenoxybenzoic acid (3-PBA) in the mother’s urine at 28 weeks’ gestation increased the risk of ADHD in the offspring by 3% and the risk of ADHD occurring among the 10% of the most severe ADHD cases by 13%.126

The pyrethroid deltamethrin apparently impairs the dopaminergic system in mice after early exposure:127

  • DAT reduced
  • D1 receptor reduced
  • Apoptosis

Furthermore, there were (with prenatal, but not with postnatal exposure)128 permanent changes in behavior with regard to:127

  • Movement activity
  • Acoustic startle reflex
  • Learning
  • Memory

3-PBA and chlorpyrifos mutually reinforce their effect on ADHD.126

Each measurement of trans-3-(2,2-dichlorovinyl)-2,2-dimethylcyclopropane-1-carboxylic acid (trans-DCCA), a metabolite of permethrin, cypermethrin and cyfluthri (trans-isomers of pyrethroids), in urine increased the risk of ADHD in offspring by 76%.126 Glyphosate contact during pregnancy

Glyphosate (e.g. Roundup) is a broad-spectrum herbicide from the group of phosphonic acids.
In rats, oral exposure of the mother to glyphosate (0.5 and 50 mg/kg body weight/day) during pregnancy and lactation (especially) affected the (female) offspring:129

  • Symptoms of depression
  • Anxiety symptoms
  • social deficits
  • reduced expression and hypermethylation of the tryptophan hydroxylase 2 gene in the hippocampus
    • Tryptophan hydroxylase is involved in serotonin synthesis in the brain
  • altered intestinal microbiota of the female offspring
    • reduced abundance of Akkermansia
    • increased abundance of Alistipes and Blautia
      (Bacteria involved in tryptophan metabolism and associated with depression and anxiety-like disorders)

This indicates that glyphosate is involved in depression and anxiety disorders. A link to ADHD has not yet been established.

1.2.12. Bisphenols during pregnancy

Bisphenol-A (BPA) is a glucocorticoid receptor agonist and is associated with changes in the HPA axis response. In female rats, prenatal BPA correlated with increased basal corticosterone levels and decreased glucocorticoid receptor expression in the hypothalamus. In response to stress, these female rats showed anxious coping behavior and a dampened corticosterone response with a lack of downregulation of glucocorticoid receptor expression in the hypothalamus. In contrast, BPA-exposed male rats showed no altered basal HPA axis function, but were unable to upregulate CRH-1 receptor expression in the pituitary gland in response to acute stress.13 The dose given to the rat mothers during pregnancy and lactation was very low at 40 micrograms/kg/day.130
5 milligrams / cubic meter in the air cause eye irritation.131 A review confirmed evidence that bishenol-A during pregnancy can increase the risk of ADHD in children, especially boys,132

BPA and BPS caused greatly increased dopamine (3 to 5-fold) and greatly decreased serotonin (by 80 %) in mouse placentas. GABA remained unchanged.133 BPA is an endocrine disruptor and mimics estrogenic activity. Thus, BPA affects various dopaminergic processes to increase mesolimbic dopamine activity, leading to hyperactivity, attention deficits and increased susceptibility to drug abuse.92

1.2.13. Phthalates during pregnancy

According to most studies, phthalic acid esters are said to increase the risk of ADHD for the unborn child,134 although the correlations are still unclear.135132 An influence on the thyroid balance is being discussed.136 Higher phthalate metabolites in the urine of pregnant women correlate with increased distractibility in preschool children.137
Prenatal di-methoxyethyl phthalate (DMEP) exposure caused abnormal brain morphology and function in mice. DMEP significantly reduced the number of neurons in the parietal cortex by impairing neurogenesis and gliogenesis during cortex development and impaired dendritic spine architecture and synaptic activity in the parietal cortex. In addition, prenatal DMEP induced hyperactivity and reduced anxiety behavior in mice.138

1.2.14. Perfluoroalkyl compounds (PFAS) in pregnancy

1.2.15. Dioxin exposure during pregnancy

Children who were exposed to dioxin during pregnancy have an increased risk of ADHD.139

1.2.16. Prenatal exposure to sulphur dioxide

Prenatal exposure to sulfur dioxide (SO2) correlated with DNA methylation and increased ADHD symptoms 140141
According to a review58, two other studies found no significant correlation.8378

1.2.17. Low urine fluoride content of the mother

One study found an inverse correlation between fluoride levels in the mother’s urine and cognitive problems in the offspring at the age of 11. The higher the fluoride content, the lower the cognitive problems.142 This was not consistent with the results of other studies, which found an increased risk of ADHD with increased urinary fluoride levels in the children themselves.143144

1.3. Illnesses of the mother/parents (up to + 310 %)

Children with ADHD were more likely to have mothers who had health problems during pregnancy:36

  • Maternal illnesses during pregnancy:
    In 34.4% of children with ADHD, the mother had an illness during pregnancy, compared to 14.4% of unaffected children.
    • Children with ADHD: 34.7%
      Diseases of the mother during pregnancy were in the following trimester:
      • 1st/2nd trimester only: 56.4 %
      • 3rd trimester only: 12.7 %
      • Entire pregnancy: 30.9 %
    • Non-affected children: 14.4 %
      Diseases of the mother during pregnancy were in the following trimester:
      • 1st/2nd trimester only: 0 %
      • 3rd trimester only: 33.3 %
      • Entire pregnancy: 66.7 %
  • Other pregnancy problems:
    • Children with ADHD: 14.5%
    • Non-affected children: 3.8 %

1.3.1. Increased or decreased thyroxine levels in the mother (up to + 310 %)

One study found a 7% increased risk of ADHD in children with untreated mild thyroxine deficiency in the mother during early pregnancy.145 In another study, reduced or untreated normal thyroxine levels in the mother showed no influence on ADHD in the children. In contrast, thyroxine treatment of the mother, especially with excessive thyroxine levels due to overdosing, appears to increase the risk of ADHD in the children.146 Another study also found evidence of thyroxine as a possible cause of ADHD,147 another study found no influence of the mother’s thyroxine levels during pregnancy.148

In male mice, a study found a significantly reduced dopamine and serotonin turnover in the striatum, nucleus accumbens, hypothalamus and hippocampus as a result of prenatal thyroxine deficiency.149 Dopamine deficiency in the striatum / nucleus accumbens is responsible for hyperactive symptoms in ADHD. Reduced and increased TSH values in newborns (+ 14 % in boys to + 310 % in girls)

A cohort study from Norway found an increased risk of ADHD later in life in newborns with low or high TSH levels, but only in girls. TSH values in the lowest 20% group increased the risk of ADHD in girls 3.1-fold, in boys by only 14%.150
Another Norwegian cohort study found a 2.27-fold risk of ADHD for thyroid hormone T3 levels in the mother at 17 weeks’ gestation within the top 1/5 compared to the lowest 1/5. For free T4, both increased and decreased levels increased the risk: the top 1/5 as well as the lowest 1/5 showed a 1.6-fold risk of ADHD in the offspring.151

1.3.2. Severe maternal obesity before or during pregnancy (+ 14% to 280%)

Massive maternal obesity during pregnancy increased the risk of later ADHD in the child by 2.8 times in one study.152
Even an excessive BMI of the mother before pregnancy increased the risk of ADHD in the offspring.153 A BMI of 25 to 30 increased the child’s risk of ADHD by 14%, a BMI of 30 to 35 by 96% and a BMI of more than 35 by 82%.154
Other fluctuations in the mother’s weight before and at the end of pregnancy do not appear to influence the risk of ADHD.30
A Norwegian registry study found only slight evidence of an influence of the parents’ BMI on the child’s ADHD risk, whereby the mother’s pre-pregnancy BMI was the object of investigation here.155 In contrast, another study found that maternal pre-pregnancy obesity increased the mother’s risk of ADHD-C by 62%.([Sanchez CE, Barry C, Sabhlok A, Russell K, Majors A, Kollins SH, Fuemmeler BF (2018): Maternal pre-pregnancy obesity and child neurodevelopmental outcomes: a meta-analysis. Obes Rev. 2018 Apr;19(4):464-484. doi: 10.1111/obr.12643. PMID: 29164765; PMCID: PMC6059608.]

1.3.3. Pre-eclampsia (gestosis) during pregnancy (+ 30 % to + 188 %)

Problems during pregnancy that impair the oxygen supply to the foetus increase the risk of ADHD in the child by 30 to 188%.156 A cohort study found a 43% increase in the risk of ADHD due to gestational gestosis.157 Several reviews confirm an increased risk of ADHD due to pre-eclampsia during pregnancy.158159

Pre-eclampsia is associated with changes in the adenosine system, including adenosine transporters and adenosine receptors. SHR are born in a pre-eclampsia-like situation due to maternal hypertension. Caffeine (an adenosine antagonist) in 7-day-old SHR prevented the negative consequences of preeclampsia (hyperactivity, worsened social interaction, worsened contextual fear conditioning), while it enhanced these symptoms in Wistar rats160
Hypoxia (lack of oxygen) increases adenosine. Adenosine antagonists can prevent or remedy the negative consequences of hypoxia. More on this under ⇒ Adenosine In the chapter Neurological aspects.

High levels of the (weak) adenosine antagonist theobromine correlated negatively with pre-eclampsia161

1.3.4. Mental stress of the mother during pregnancy (+ 72 % to + 100 %; with 5HTTLPR + 800 %)

Stress of the mother during pregnancy increased the risk of ADHD in the children

Persistent and severe (anxiety-induced, perceived threatening = cortisolergic) stress significantly increases the risk of screaming children164 (see also, anxiety disorders and ADHD.165166167168
Persistent stress (here: financial problems) is more harmful than short-term stress (here: loss of a loved one).169
High anxiety/threatening perceived stress also significantly increases the risk of borderline in children.

Children with ADHD were more likely to have mothers who experienced stress or emotional problems during pregnancy:36

  • Children with ADHD: 53.8%
    If stress/emotional problems occurred, they were in the following trimester:
    • 1st/2nd trimester only: 36.0 %
    • 3rd trimester only: 6.7 %
    • Entire pregnancy: 57.3 %
  • Non-affected children: 27.6 %
    If stress/emotional problems occurred, they were in the following trimester:
    • 1st/2nd trimester only: 28.6 %
    • 3rd trimester only: 24.9 %
    • Entire pregnancy: 28.6 %

Hair cortisol levels of mothers and their children showed a transmission of psychological stress experiences from mothers to their children.170
A study found no increased psychiatric disorders at the age of 9 years in children of women who were exposed to one month of repeated rocket fire on the civilian population during the 2006 Lebanon war.171 It is possible that one month of repeated stress is not a sufficiently intense stressor.

The cortisol released by the mother during anxiety/threatening stress is absorbed by the unborn child and leads to permanent damage to the HPA axis, which regulates stress reactions by means of cortisol.172173

Severe maternal anxiety in pregnancy during the 12th to 22nd week after the last menstrual period significantly increased the risk of ADHD, while severe anxiety in the 32nd to 40th week did not increase the risk.174 Elevated maternal cortisol levels in the 3rd trimester of pregnancy increased the offspring’s risk of ASD symptoms only in boys at 3 years of age, but were no longer significant at 5 years of age. ADHD symptoms were neither increased at the age of 3 nor at the age of 5.175
So it seems to depend very much on the time of the stress experience.

Strong anxiety of the mother during pregnancy increased the ADHD risk of the unborn child depending on its COMT gene variant (gene-environment interaction).176
In mothers with the ADGRL3 (latrophilin 3, LPHN3) gene variants (SNPs)

  • rs6551665
  • rs1947274
  • rs6858066 or
  • rs2345039

even low levels of stress during pregnancy resulted in a significantly increased risk of ADHD for the child.177

A combination of the 5HTTLPR L/L genotype and stress during pregnancy resulted in an eight times higher risk of ADHD-C or ADHD-HI.178

Early prenatal stress increases levels of immune response genes, including the proinflammatory cytokines IL-6 and IL-1β, particularly in male placentas. Male infants show stress-induced locomotor hyperactivity, a hallmark of dopaminergic dysregulation, which was ameliorated by maternal treatment with nonsterioid anti-inflammatory drugs. In addition, the expression of dopamine D1 and D2 receptors was altered by early prenatal stress in male offspring.179 This emphasizes the effect of early stress on the dopaminergic system.

High cortisol exposure of the fetus or newborn can cause methylation of the GAD1 / GAD67 gene, which encodes the key enzyme for glutamate-to-GABA synthesis, glutamate decarboxylase 1, and lead to increased glutamate levels. This epigenetic mechanism may increase the risk of ADHD in children.180 Exposure to glucocorticoids during hippocampal development in pregnancy influences the starting point of the stress response through epigenetic changes via mRNA and methylation.181 Another study reports that the maternal psychological stress-mediated risk increase for the unborn child for developmental disorders such as ADHD may be mediated by mRNA expression of glucocorticoid pathway genes in the placenta.182
Another study also describes epigenetic changes in the unborn child due to the mother’s psychological stress during pregnancy.183
One study found no significant increase in the risk of mental disorders up to the age of 10 years due to increased glucocorticoid exposure in the unborn child.184
Exposure of the mother to a natural disaster during pregnancy increased the risk of ADHD.185

In primates, the stress hormone cortisol is converted into its inactive form by the enzyme hydroxysteroid 11-β-dehydrogenase 2 (HSD11B2). This conversion in the placenta also protects the fetus.186187 However, chronic maternal stress (as well as malnutrition or hypoxia) reduces HSD11B2 expression in the placenta.187 Fetuses of chronically stressed mothers are therefore exposed to high cortisol concentrations, which triggers developmental delays and neurodevelopmental disorders such as ADHD.188189187 In rodents, the expression of Hsd11b1, which encodes an enzyme that regulates the activity of stress-related hormones in the neocortex, is reduced instead.190

1.3.5. Polycystic ovary syndrome (PCOS) in pregnancy (+ 31 to + 95 % in boys)

Children of women with polycystic ovary syndrome (PCOS) appear to have an increased risk of ADHD.191

It is possible that a connection could result from the fact that one treatment method is the use of dopamine agonists.192193 Another connection could be that PCOS is associated with hyperandrogenemia. Elevated prenatal testosterone levels are a risk factor for ADHD. More on this under Gender differences in ADHD.

One study found a 95% increased risk of ADHD in 3-year-old boys born to mothers with PCOS, while this was not increased in 3-year-old girls.194 This also points to a connection with sex hormones, although increased testosterone levels during pregnancy also cause increased ADHD symptoms in female offspring. More on this at Gender differences in ADHD. It is also known that ADHD appears later in girls than in boys.
A Chinese study found a 31% increased risk of ADHD in boys aged 3 to 6 (only).195 As ADHD can often only be diagnosed from the age of 6, we suspect a higher rate at school age.

Women with PCOS themselves had an increased risk of ADHD, although no link was found between testosterone and ADHD symptoms196

1.3.6. Unhealthy diet of the mother during pregnancy (+ 60 %)

An unhealthy or “Western” dietary intake by the mother during pregnancy increased the children’s likelihood of ADHD by more than 60%.197
Since stress increases the preference for “convenient food”, we believe that the correlation could possibly also be an indirect reflection of an increased stress load on the mother during pregnancy, since stress changes food preferences in the direction of quickly digestible foods and convenient food.

1.3.7. Fever of the mother during pregnancy (+ 31 % to + 164 %)

A cohort study of 114,000 children showed that fever in the first trimester of pregnancy increases the risk of ADHD by 31%, and multiple fevers by 164%. However, fever only increased inattention, not hyperactivity/impulsivity - this also applied to the second trimester. The results were independent of whether the mother took paracetamol (acetaminophen) or not.198

1.3.8. Reduced C-reactive protein (CRP) (+ 92 %)

Children of mothers whose CRP values were in the lowest third of the subject group had an almost doubled risk of ASD and ADHD compared to children of mothers from the middle third of CRP.199

1.3.9. Systemic lupus erythematosus (SLE) (+ 60 %)

Children of mothers who suffered from systemic lupus erythematosus (SLE) were found to have a 60% higher risk of ADHD.200

1.3.10. Parental asthma during and outside pregnancy (+ 13% to + 41%)

Asthma in the mother during pregnancy increases the risk of ADHD and ASD in the offspring.201 A cohort study of 961,202 children showed a 41% increased risk of ADHD if the mother had asthma and a 13% increased risk if the father had asthma. An asthma episode in the mother during pregnancy increased the risk of ADHD by 21%, and an asthma episode after pregnancy by 25%.202 Another study also found an increased risk of ADHD in the offspring of mothers with asthma, particularly for girls.203

1.3.11. Diabetes of one parent; diabetes during pregnancy (+ 40 %)

A cohort study of over 5 million people found an increased risk of ADHD in children if one parent had diabetes.204

Diabetes in the mother before or during pregnancy increases the risk of ADHD and ASD in the offspring.205206207
Diabetes mellitus or type 1 diabetes mellitus in the mother before pregnancy increased the children’s risk of ADHD by 40 %, type 1 diabetes mellitus in the father by 20 %.
Another study found a 2.4-fold ADHD risk in children of mothers with diabetes mellitus and a 3.7-fold ADHD risk in male offspring of mothers with diabetes mellitus. No differences were found between gestational diabetes and other diabetes.208
Children of non-insulin-treated severely obese mothers with type 2 diabetes were 2 times more likely to have psychiatric disorders than offspring of normal-weight mothers. Children of insulin-treated severely obese mothers with pregestational diabetes were 2.7 times more likely to have psychiatric disorders than offspring of normal-weight mothers.209

1.3.12. Anemia of the mother during pregnancy (+ 31 %)

A cohort study of 532,232 children over 23 years of age showed that maternal anemia in the first 30 weeks of pregnancy increased the risk of ADHD by 31%, while anemia in later weeks of pregnancy hardly increased the risk at all (by 1.4%). 210

1.3.13. Infections of the mother during pregnancy Infections in general (+ 30 %)

A meta-study found a 30% increase in the risk of ADHD in the offspring due to infections in the mother during pregnancy.211 Viral infections

A viral infection of the mother during pregnancy can affect the development of the unborn child’s dopaminergic system, e.g:212

  • Measles
  • Varicella
  • Rubella
    • Subclinical rubella infection of the mother during pregnancy also increases the child’s risk at the age of 8 to 9 years for213
      • ASS
      • ADHD
      • Developmental disorders
  • Enterovirus 71
  • Herpes virus 6
  • Influenza A

A connection seems less certain for

  • Streptococcal infection
  • Inflammation of the middle ear (otitis media)

1.3.14. Fetal inflammatory response syndrome (FIRS) (+ 27 %)

Children born to a mother with fetal inflammatory response syndrome (FIRS, an inflammation of the placenta during pregnancy) had an increased risk of:214

  • diagnosed with neuropsychiatric disorders (OR = 1.21)
  • ASS (OR = 1.35)
  • ADHS (OR = 1.27)
  • Conduct disoder (OR = 1.50)
  • PTBS (OR = 2.46)

1.3.15. Insatiable nausea (hyperemesis gravidarum) (+ 16 %)

Insatiable nausea and vomiting of the mother during pregnancy led to an increased risk of ADHD in the offspring by 16% (in 2 cohort studies) to 287%215

1.3.16. Mineral and vitamin deficiency during pregnancy

Find out more at Vitamins, minerals, dietary supplements for ADHD And Nutrition and diet for ADHD in the chapter Treatment and therapy. D3 deficiency during pregnancy

Vitamin D3 deficiency during pregnancy and after birth causes permanent maldevelopment of the brain, particularly the dopaminergic system.216217218219 In a meta-study, studies with larger sample sizes and stricter definitions of vitamin D deficiency showed positive associations for ADHD and schizophrenia.220
The incidence of ADHD-like symptoms in children decreased by 11% for every 10 ng/ml increase in maternal 25(OH)D levels.221 Another study also found that a reletively low maternal 25(OH)D level at 24 weeks gestation increased the risk of ADHD and ASD and ASD severity. High D3 supplementation (2,800 iU/day) during pregnancy did not increase ADHD risk or ASD risk.222 In our opinion, this could indicate that D3 levels, especially before 24 weeks of gestation, influence ASD and ADHD risk.
The severity of the offspring’s ADHD symptoms correlated with the level of maternal 25(OH)D deficiency.223
D3 deficiency during pregnancy reduces dopamine turnover in the offspring’s brain224 by reducing COMT.225
Reduced vitamin D3 serum levels in the mother in the 30th week of pregnancy correlated significantly with depression in the offspring up to the age of 22, but not with ADHD.226 It remains to be seen whether D3 deficiency has different effects in other weeks of pregnancy, as later mental disorders are particularly related to those regions of the brain that are experiencing a developmental boost in the respective week of pregnancy. More on this at Exposure to stress at different stages of brain development In the chapter Stress damage - effects of early / prolonged stress.

An extensive long-term study in Spain on vitamin D3 deficiency during pregnancy found no correlation between low D3 blood levels in the mother during pregnancy and ADHD in children aged 5 to 18 years.227
A study in Finland, on the other hand, found a clear correlation between a reduced D3 level in the mother during pregnancy and ADHD in the children. The risk increase reached over 50 %.228
It is possible that the difference could result from the fact that sunlight intensity in Spain is high enough to produce D3 almost all year round (so that the Spanish participants with relatively low levels still had sufficient levels), whereas in Germany, and even more so in more northern countries, sunlight intensity is too low in the winter months to mediate D3 production.

Rodents whose mothers had a vitamin D deficiency showed typical ADHD symptoms:229

  • Hyperactivity
  • Impulsiveness
  • Reduced social behavior
  • Changed frequency of ultrasound vocalization
  • More frequent self-pollution
  • Reduced grooming of puppies
  • Reduced growth factors NGF and GDNF
  • Thinner cortical layers and larger lateral ventricles
  • Smaller size of the hippocampus and smaller lateral ventricles Omega-3 fatty acid levels In the newborn

A meta-study found evidence that a higher omega-3 fatty acid level in newborns can reduce the risk and severity of ADHD and autism spectrum disorders. It is possible that an adequate supply of omega-3 fatty acids in the last trimester of pregnancy could counteract this230 During pregnancy

Another study found a 13% increased risk of ADHD in offspring at the age of 7 due to an increased omega 6 to omega 3 ratio (high omega 6 and low omega 3 values).231

1.3.17. Depression of the mother during pregnancy

In boys in particular, the severity of the mother’s depression during pregnancy and higher cyclothymic, irritable and anxious temperament levels in the mother appear to be relevant risk factors for the development of ADHD.232
A large-scale study found no causal influence of maternal depression, anxiety disorder or infection during pregnancy on the risk of neurodevelopmental disorders (ASD, ADHD, mental retardation, cerebral palsy or epilepsy) in the child.233

1.3.18. High blood pressure during pregnancy

High blood pressure during pregnancy significantly increases the risk of ADHD in the offspring.159
High blood pressure is associated with genetically inherited ADHD risks. It will therefore be necessary to differentiate whether high blood pressure during pregnancy causally increases the risk of ADHD or whether elevated blood pressure during pregnancy is an expression of the underlying genetic burden that mediates ADHD.

1.3.19. Lack of sleep during pregnancy

Girls of mothers with a sleep duration of less than 8 hours in the last trimester of pregnancy showed more frequent hyperactivity, inattention and ADHD total scores.234
Sleep problems during pregnancy correlated with an increased risk of neurodevelopmental disorders and sleep problems in early childhood.235, in particular

  • reduced and poorer sleep in the second trimester of pregnancy correlated with ADHD
  • major sleep problems in the first trimester correlated with ADHD
  • Sleep problems in the third trimester correlated with the child’s sleep problems

1.3.20. Testosterone during pregnancy

Prenatal testosterone exposure was significantly correlated with inattention and hyperactivity/impulsivity in the offspring.236

1.3.21. Inflammation during pregnancy

Perinatal inflammation correlates with increased ADHD symptom scores in children aged 8-9 years and increases the genetic predisposition to ADHD (the Polygenic Risc Score).237238

1.4. Medication taken by the mother during pregnancy as ADHD risk (up to + 250 %)

Children with ADHD were more likely to have mothers who took medication during pregnancy:36

Medication taken by the mother during pregnancy:

  • ADHD: 43.5 %
    If stress/emotional problems occurred, they were in the following trimester:
    • 1st/2nd trimester only: 36.2 %
    • 3rd trimester only: 14.5 %
    • Entire pregnancy: 49.3 %
  • Not affected: 31.4 %
    If stress/emotional problems occurred, they were in the following trimester:
    • 1st/2nd trimester only: 31.1 %
    • 3rd trimester only: 46.9 %
    • Entire pregnancy: 21.9 %

The following list is only exemplary and by no means complete.

1.4.1. Paracetamol (acetaminophen) in pregnancy (+ 37 % to + 250 %)

50% of all women use paracetamol during pregnancy.239
Taking paracetamol (in North America and Iran: acetaminophen) during pregnancy increased the risk of ADHD by up to 37%. Even short-term use is harmful according to two very comprehensive studies with a total of over 110,000 participants.240241 Further studies confirm this.242243244 Critically, Gilman et al. While the previous studies were based on the mothers’ reports of intake, a study based on blood levels found a 2.3 to 3.5-fold ADHD risk and a 1.6 to 4.1-fold ASA risk in the children if taken in the second or third trimester of pregnancy.245246

The risk of ADHD from paracetamol (acetaminophen) increases when taken247

  • By 19 % in the second trimester of pregnancy
  • By 28 % in the first and second trimester
  • By 20 % in the first to third trimester

A cohort study of 116,000 children showed that fever in the first trimester of pregnancy increases the risk of ADHD by 31%, and multiple fevers by 164%. However, fever only increased inattention, not hyperactivity/impulsivity - this also applied to the second trimester. The results were independent of whether the mother took paracetamol (acetaminophen) or not.198
A meta-study confirms the increased risk of ADHD and ASD in the offspring when taking paracetamol during pregnancy248

One study questions the previous critical results by focusing on parents’ ADHD diagnoses that have not been taken into account to date.249 Damkier is also doubtful.250 A meta-analysis of 22 studies with n = 367,775 participants found an increased risk of ADHD due to paracetamol during pregnancy, which remained unchanged by other factors (such as parental diagnoses)251

A long-term study analyzed paracetamol, methionine, serine, glycine and glutamate in umbilical cord plasma and found that increased paracetamol levels increased the risk of ADHD in parallel with the increase in 8-hydroxy-deoxyguanosine levels in umbilical cord blood. An increase in the levels of methionine, glycine, serine and 8-hydroxy-deoxyguanosine in the umbilical cord blood correlated with a significantly higher probability of ADHD in childhood. Methionine and glycine each mediated 22% of the association between elevated paracetamol levels and later ADHD.252
The damage to the development of the offspring caused by paracetamol during pregnancy appears to be mediated by changes in the endocannabinoid pathway253

Ibuprofen, on the other hand, is not thought to cause an ADHD risk for the unborn child.

1.4.2. SSRI, antidepressants during pregnancy (0 % to + 63 %)

According to two meta-analyses of 18 studies, SSRIs during pregnancy correlate with a significantly increased risk of ADHD (OR = 1.26 = approx. + 26 %) and ASD (OR = 1.42 = approx. + 42 %) in children. It is not clear whether this results from the SSRIs or from an inheritance of psychological problems of the mother for which she was treated with SSRIs, as the risk of ADHD (OR = 1.63 = approx. + 63 %) and ASD (OR = 1.39 = approx. + 39 %) was also increased in children if the mother took SSRIs or SNRIs before pregnancy but not during pregnancy.254255 a caring SSRI should be used with extreme caution during pregnancy.
A meta-study found no increased risk of ADHD in children in 7 out of 8 studies on SSRIs during pregnancy.256 The same applies to another study.257 According to one study, antidepressants during pregnancy increased the likelihood of later ADHD in the child by 1.81 times.258

1.4.3. β-2-Adrenaline receptor agonists in pregnancy (+ 30 %)

Taking β-2 adrenaline receptor agonists during pregnancy increases the risk of ADHD for the child by up to 30%.259

1.4.4. Pregabalin during pregnancy (+ 29 %)

Prenatal exposure to pregabalin increased the risk of ADHD by 29%, but this was attenuated when active comparators were taken into account.260

1.4.5. Antibiotics during pregnancy (+ 14 %)

Several meta-studies found a 14% increased risk of ADHD due to the mother taking antibiotics during pregnancy.261262

1.4.6. Valproate during pregnancy (+ 12 %)

Valproate during pregnancy is said to increase the risk of ADHD for the unborn child.263
Valproates are the salts of valproic acid.

A cohort study found an increased risk of neurodevelopmental disorders in children up to the age of 6 (which is still too early for the diagnosis of all ADHD sufferers) when taking antiepileptic drugs during pregnancy:

  • Sodium valproate together with other antipsychotics: 15 %
  • Sodium valproate as monotherapy: 12 %
  • Lamotrigine 6.3 % (no statistically significant increase due to the small number of participants in this group)
  • Carbamazepine 2% (no significant increase)
  • Children who were not exposed to any of these drugs during pregnancy: 1.8%

ASD was the most common diagnosis. 2 % of the children of medicated mothers were diagnosed with ADHD by the age of 6, 1.5 % with dyspraxia. None of the children in the controls had an ADHD diagnosis.264

1.4.7. Corticoids during pregnancy

Cortisol administration during pregnancy leads to long-term changes in the unborn child’s brain and increases the risk of ADHD.265 The children suffer a lifelong alteration of the dopaminergic system and the HPA axis, apparently caused by changes in the expression and ratio of MR and GR receptors.266 In our opinion, the ADHD symptoms described in these children could possibly be the result of an HPA axis alteration.
Corticosteroid receptor hypothesis of depression

High cortisol exposure of the fetus or newborn can cause methylation of the GAD1 / GAD67 gene, which encodes the key enzyme glutamate-to-GABA-synthesizing glutamate decarboxylase 1 and leads to increased glutamate levels. This epigenetic mechanism can increase the risk of ADHD in children.180

Exposure to betamethasone during pregnancy only marginally increased the risk of ADHD in the offspring.267

Dexamethasone during pregnancy in mice increased spontaneous activity in female offspring, while reducing it in males. Dexamethasone during pregnancy downregulated dopamine signaling and upregulated glutamate and GABA signaling in females.268

1.4.8. Valproic acid during pregnancy

Offspring of mice that received valproic acid during pregnancy showed significantly increased hyperactivity and changes in the dentate gyrus.269270 In addition, there are indications of changes in the histaminergic system and social behavior.271
Valproic acid during pregnancy increases the risk of ADHD, ASD, reduced cognitive abilities and speech disorders in the offspring.272 In addition, it causes congenital malformations such as neural tube defects, cardiac anomalies, urogenital malformations (e.g. hypospadias, skeletal malformations and orofacial clefts) in 10 % of children, depending on the dose, especially at more than 600 mg/day. High doses of folic acid before and during pregnancy could reduce the risk. The concentration of valproin in breast milk appears to be low, which is why breastfeeding does not pose a risk.

1.4.9. No increase in risk due to NSAIDs, normal caffeine consumption, benzodiazepines

A cohort study found no ADHD risk increase with non-steroidal anti-inflammatory drugs (NSAIDs) during pregnancy.273

Caffeine consumption during pregnancy below 10 cups a day did not increase the risk of ADHD.274

Benzodiazepines during pregnancy appear to increase the risk of internalizing problems in children (anxiety, emotional reactivity, somatic complaints), but not externalizing problems (hyperactivity, aggressiveness).275 A cohort study comparing siblings with and without benzodiazepine use by the mother during pregnancy found no significant increase in the risk of ADHD or ASD due to benzodiazepines; the authors rather suspect a connection with a genetic disposition of the mother.276 A meta-study also came to the conclusion that no relevant increase in the risk of ADHD in the offspring has been found for benzodiazepines during pregnancy, even though one study indicated a slight increase with benzodiazepine monotherapy in the last trimester of pregnancy.277 One study found a slight increase of 15% in the risk of ADHD when taking benzodiazepines during pregnancy.278

This list of maternal medication during pregnancy as a risk for ADHD is only an example and is by no means complete.

1.5. Other pregnancy circumstances (up to + 30 %)

1.5.1. First-born status

A large Swedish cohort study found that first-born children have a higher risk of depression and ADHD in childhood and of endocrine disorders after the age of 50.279

1.5.2. Particularly short or long intervals to the previous pregnancy (+ 25 % to + 30 %)

Particularly short or particularly long intervals between pregnancy with the preceding sibling increased the risk of ADHD by 30 % (less than 6 months) or 12 % (60 - 119 months) to 25 % (120 months and more).280

1.5.3. Protein deficiency during pregnancy and after birth

Rats whose mothers received a low-protein diet 15 days before conception and then continued to do so during lactation were significantly more susceptible to early childhood stressors (intraperitoneal injection of deltamethrin, lipopolysaccharide, or both) to develop ADHD symptoms such as hyperactivity, attention problems, and decreased anxiety.281

1.6. Pregnancy circumstances without influence on ADHD

No influence on the ADHD risk of the unborn child was found for the following factors:

  • Iodine/creatinine ratio in the mother’s urine during pregnancy
    • A large study of 3 cohorts found no effect on ADHD or ASD risk282
  • Migration of the mother
    • A meta-study found no evidence of an increased risk of ADHD due to maternal migration, but this was not the case with ASD.283
  • Iron level of the mother
    • One study found no influence of the mother’s iron level during pregnancy on the child’s risk of ADHD at the age of 7 years284
  • Artificial insemination by intracytoplasmic sperm injection (ICSI)285

1.7 Preventive factors

1.7.1. Fiber intake of the mother during pregnancy

A high-fiber diet for the mother during pregnancy reduced the risk of ADHD in the offspring by up to 20 %.286
This was independent of genetic predisposition to ADHD, unhealthy diet and socio-demographic factors.

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