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4. Age-independent physical stress as an environmental cause of ADHD

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4. Age-independent physical stress as an environmental cause of ADHD

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Certain physical illnesses, toxins or food intolerances seem to increase the risk of ADHD (or other mental disorders) throughout life.
The % values indicate the possible ADHD risk increase due to the respective cause. They refer to individual known, but rather selective stress factors. However, they are nevertheless helpful as an indication of the magnitude of the possible increase in risk.

4.1. Toxins

4.1.1. Phthalates (+ 200 % to + 900 %)

Higher phthalate metabolites in the urine of children correlated with an increased probability of ADHD by a factor of 3 to 9.1

4.1.2. Fluoridated drinking water (+ 510 % if 1 mg/L too high)

In Canada, a study found that a 1 mg/liter increase in fluoride levels in drinking water above acceptable limits increased the risk of ADHD in 6- to 17-year-olds by 6.1 times. In 14-year-olds living in areas where fluoride was added to drinking water, there was a 2.8-fold risk of an ADHD diagnosis compared to 14-year-olds in areas without fluoridated drinking water. Older children responded with a higher risk.2 Fluorine urine levels, on the other hand, did not correlate with ADHD (1,877 test subjects).
A study in Mexico found a link between increased prenatal fluoride exposure and inattention and ADHD, but not hyperactivity3 and cognitive problems.4 Another study found similar results.5 A review summarizes the results.6

In Germany, 90% of drinking water has a fluoride content of 0.3 mg/liter. Drinking water is not fluoridated in Germany.7

A study found an inverse correlation between fluoride levels in the mother’s urine during pregnancy and cognitive problems in the offspring at the age of 11. The higher the pregnancy urine fluoride content, the lower the cognitive problems.8 This was not consistent with the results of other studies, which found an increased risk of ADHD with increased urine fluoride levels in the children themselves.

Sodium fluoride in drinking water (20 ppm to 100 ppm) led to a dose-dependent reduction of dopamine, noradrenaline and acetylcholine in the brain of rats, while the levels of adrenaline, histamine, serotonin and glutamate increased.9

4.1.3. Lead (+133 %)

Elevated blood lead levels lead to an increased risk of ADHD.10111213 A blood lead level of ≥ 5 μg/dl was found to increase the risk of ADHD by 1.33 (OR 2.33).14

Lead influenced the dopamine balance in many studies.

  • Reduced dopamine signaling
    • caused cognitive deficits with delayed spatial alternation, which could be corrected by L-dopa and without L-dopa only ended 8 years after the 2-year lead exposure15
    • in the nucleus accumbens16
  • Increased dopamine signaling
    • in mesolimbic pathways (nucleus accumbens)17
    • Lead increases dopaminergic activity and has been linked to attention deficits, Alzheimer’s disease and increased drug sensitivity.18

A connection between ADHD and lead is said to be promoted by the DRD2 gene variant rs1800497r.19 A connection to certain MAO-A gene variants is also mentioned, which causes lower serotonin degradation.20 A study in rats indicates interactions between lead exposure and early stress on the dopaminergic system.21 A long-term study found no directly increased risk of ADHD in people with previous lead exposure, but increased externalizing behaviours and increased risk of addiction22

In one study, lead altered neostriatal serotonin and norepinephrine levels, increased anxiety and decreased open-field activity.23

Lead exposure during pregnancy can increase the risk of ADHD. See there.
Even a lead content in drinking water below the limit values is said to be problematic.24
Increased lead absorption can occur from old water pipes. In principle, lead water pipes are not very dangerous in areas with calcareous water, as lime forms a reliable protective layer in the pipes. However, if a water softening system is installed, this protective lime layer can be lost. If old lead pipes are still present, this can lead to increased lead absorption.
Lead is hardly relevant as a toxin in Central Europe. In less developed countries, however, lead can be a serious problem.

In children who have been exposed to lead, succimer chelation can produce lasting cognitive benefits if chelation sufficiently reduces the lead concentration in the brain. At the same time, succimer treatment without lead exposure leads to permanent cognitive dysfunction.25

4.1.4. Inorganic arsenic (+ 102 %)

Those children who were among the 20% with the highest arsenic levels in their urine were found to have double the risk of ADHD (OR 2.02).14

4.1.5. Benzene, toluene, ethylbenzene, xylene/xylene (BTEX) (+ 54 %)

Higher exposure to these substances in the air correlated with a 1.54-fold increase in the risk of ADHD at kindergarten age.26

4.1.6. Smoking by parents (+ 30 %)

Postnatal smoking by parents correlates with a 1.3-fold risk (increased by 30%)27 of ADHD in the offspring.
This could be related to genetic factors, as ADHD sufferers are significantly more likely to smoke. The co-morbidity between smoking and ADHD is 40%.28 In contrast, around 25 % fewer of the total population smoke, namely 26.9 % of women and 32.6 % of men.29

4.1.7. Polychlorinated biphenyls (PCBs) / polychlorinated biphenyl ethers (+ 26 % to + 92 %)

Polychlorinated biphenyls and polychlorinated biphenyl ethers are suspected of causing ADHD.
PCBs are banned in many countries, in Germany since 1989. PCBs were used in particular as lubricants and coolants in electrical appliances and as building materials. Due to their chemical stability, many areas around the world are still contaminated with PCBs. Contaminated food, especially seafood from contaminated rivers and lakes, is the most common source of contamination today.3031

Even low levels of PCB exposure during development impair neurobiological, cognitive and behavioral functions.31
One study found a 26% to 92% increased risk of ADHD.32 Individual studies found contradictory or weak impairments,3334 however, the vast majority show evidence of relevance in ADHD.2735

Polychlorinated biphenyls affect the dopamine system.36 PCBs inhibit dopamine synthesis as well as the storage of dopamine in the vesicles and its release, thereby causing low dopamine levels3712 in the basal ganglia and PFC3839 37 40 41 42 , as well as reduced DAT in the striatum43, which overall corresponds quite closely to the picture of ADHD.

Prenatal exposure to PCBs has an adverse effect:

  • Hyperactivity (in rats even at subtoxic doses)3712
  • IQ, memory, attention 44
  • Memory, attention45
  • Impulsivity (via corpus callosum)4647 in rats even at subtoxic doses3712
  • Male and female offspring were trained as adults to perform asymptotically in a differential reinforcement of low rates (DRL) task. The PCB-exposed groups had a lower ratio of reinforced to non-reinforced responses than the control groups.36
  • no effect on sustained attention33

4.1.8. Polyvinyl chloride (PVC)

One review describes a suspected correlation between PVC exposure and ADHD.48

4.1.9. Pesticides

With regard to pesticides (especially organochlorine compounds, pyrethroids, organophosphates), there are indications of relevance to ADHD.2712

For pesticides during pregnancy and ADHD, see there.

4.1.9.1. Organochlorine compounds

With regard to organochlorine compounds, there are indications of relevance in ADHD.271249

A study of Greek schoolchildren with ADHD found no elevated blood serum levels of50

  • Dichlorodiphenyltrichloroethane (DDT) Metabolites
  • Hexachlorocyclohexane (HCH) isomers
  • Cyclodienes
  • Methoxychlorine
4.1.9.2. Organophosphates

According to a large number of studies, organophosphate pesticides have a correlation between prenatal and postnatal exposure and ADHD 3151 52 53 49 54 or a theoretically possible increase in the risk of ADHD.55 One source suggests an increased risk of ADHD due to organophosphates, especially when combined with a certain MAO-A gene variant that causes a lower serotonin degradation.20
In contrast, two larger studies found no influence 5657
With regard to hyperactivity, 2 studies found an association between organophosphates and hyperactivity, 4 studies found no association.58
One study found no correlation of chlorpyrifos with hyperactivity in rats59 while another found it in females.60
A study in rats was able to induce ADHD-like behaviors in Wystar and SHR rats with organophosphates and found strong evidence that these are mediated by reductions in fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) via the cannabinoid receptor.61
Blood values were measured in Egyptian adolescents, some of whom used pesticides, and the parents were asked about ADHD symptoms in the adolescents:62 No correlation was found with ADHD in relation to the organophosphate chlorpyrifos.

Higher vitamin D levels appear to reduce the negative effect of chlorpyrifos on the risk of ADHD.54

4.1.9.3. Pyrethroids (+ 142 %)

Various studies indicate a correlation between pyrethroid exposure in childhood and neurodevelopmental disorders such as ADHD with a 2.42-fold risk of ADHD 63 Other studies also found a link with ADHD6449 , ASD or developmental delay.31
Blood levels were measured in Egyptian adolescents, some of whom used pesticides, and the parents were asked about ADHD symptoms in the adolescents:62 A correlation to ADHD was found in relation to the pyrethroid λCH through the measured value Cis-DCCA (all those affected reported clinical ADHD symptoms).

4.1.9.4. Carbamate (-)

One review found no association between carbamates and ADHD.49

4.1.9.5. Neonicotinoids (- ?)

One review found no links between neonicotinoids and ADHD, although there were few studies on this topic.49

4.1.10. Mercury / Amalgam (Mercury)

There are weak indications (= not proven) of relevance in ADHD.271265
A large study with n = 2073 participants was unable to establish a connection between amalgam and ADHD.66
Mercury is also suspected of being a possible contributory cause of Parkinson’s disease.67 This would be a clear indication of a damaging effect on the dopamine system.

4.1.11. Manganese

There is weak evidence of relevance in ADHD, although elevated manganese levels were only found in the hair of ADHD sufferers, but not in blood levels.2768

An animal model with developmental manganese exposure showed that manganese can cause permanent attention and sensorimotor deficits resembling ADHD-I. Oral methylphenidate was able to fully compensate for the deficits caused by early manganese exposure.25

A study reports benefits of choline supplementation during pregnancy in rats to prevent manganese-induced developmental disorders in the offspring69

4.1.12. Bisphenol A

Bisphenol A is suspected of increasing the risk of ADHD.12 A connection with certain MAO-A gene variants that cause lower serotonin degradation20 and an influence on the thyroid balance is being discussed.70
A meta-study found a clear link between bisphenol exposure and ADD(H)S.71

4.1.13. Perfluoroalkyl compounds

Elevated levels of perfluoroalkyl compounds have been observed in ADHD.72

4.1.14. Synergy effects of neurotoxins

The synergistic effects of neurotoxins must be taken into account:2773

  • Formaldehyde increases the toxicity of mercury.
  • Amalgam increases the toxicity of PCBs and formaldehyde.
  • Mercury and PCBs potentiate each other’s effects.

4.2. Interrupted breathing during sleep

Breathing interruptions in children’s sleep can trigger cognitive stress, causing symptoms that resemble ADHD.74

It remains to be seen whether breathing interruptions during sleep can represent such a stress load that they can contribute to ADHD through epigenetic changes, or whether they merely cause symptoms that are similar to those of ADHD. In the latter case, people who did not previously have ADHD and who developed ADHD (similar) symptoms as a result of breathing interruptions during sleep should see these symptoms disappear completely once the breathing interruptions during sleep have been eliminated. We are not yet aware of any studies on this.

4.3. Food intolerances, allergies

It is certain that ADHD is not caused by individual, specific foods, phosphates or additives.

However, individual food intolerances or allergies are just as much stressors as illnesses, toxins or psychological stress and can therefore worsen the stress situation of those affected to such an extent that symptoms develop. This is not a finding specific to ADHD. For example, in a group of children with schizophrenia problems, dietary treatment of an existing gluten intolerance eliminated the schizophrenia symptoms in the affected children.7576 The same was observed in patients with non-affective psychosis.77

Food additives (here: Sun yellow, carmoisine, tartrazine, ponceau 4R; quinoline yellow, allura red, sodium benzoate) can cause histamine release from circulating basophils. This is not allergic, i.e. not dependent on immunoglobulin E. The increased release of histamine can increase ADHD symptoms in carriers of certain gene variants of the genes that encode histamine-degrading enzymes78

To identify rare food intolerances (which, unlike allergies, cannot be detected by blood tests), an elimination diet can be helpful. However, such a diet is very difficult to implement and adhere to and is particularly difficult to adhere to in younger children. In particular, any benefits must be weighed against the sometimes serious social consequences.

In other cases, such a diet can help to alleviate the symptoms of existing intolerances.

When assessing the effectiveness of diets (and other “desirable” therapies), parents’ assessments are often far higher than what tests or teacher evaluations can confirm.

More information at ⇒ Nutrition and diet for ADHD.

4.4. Gut bacteria, gut-brain axis (gut-brain axis)

The gut and brain are connected via 3 pathways:79

  • Nerve pathways: Vagus nerve
  • Immune system: circulating cytokines
  • Metabolic pathway: Chemical signals (GABA, serotonin, dopamine, noradrenaline, short-chain fatty acids (SCFAs))

Treatment options include probiotics and fecal transplants.

The gut-brain axis plays a role in brain development, particularly in infancy, early childhood and childhood. The mother’s microbiome, the type of birth and the environment influence the microbiome, breastfeeding and a healthy diet and provide the child’s gut with important probiotic elements, while antibiotics can (disrupt) the gut flora.

The communication of the gut-brain axis is bidirectional. The brain influences the motor, sensory and secretory functions of the gastrointestinal tract top-down via efferent fibers of the vagus nerve. The gut influences the function of the brain bottom-up, in particular the amygdala and hypothalamus, via the afferent vagal fibers.79

Bacteria can synthesize neurotransmitters and hormones and react to them79

  • Bacillus species
    • produce noradrenaline8081
    • produce dopamine8081
  • Bifidobacterium species
  • Candida
    • produce serotonin81
  • Enterococcus
    • produce serotonin8081
  • Escherichia
    • produce noradrenaline81
    • produce dopamine8081
    • produce serotonin8182
  • Hafnia alvei (NCIMB, 11999)
    • produce serotonin83
  • Klebsiella pneumoniae (NCIMB, 673)
    • produce serotonin83
  • L. lactis subsp. lactis (IL1403)
    • produce serotonin83
  • Lactobacillus species
    • produce acetylcholine and GABA8081
    • Lactobacillus plantarum (FI8595)
      • produce serotonin83
    • Lactobacillus rhamnosus (JB-1)
      • reduced the stress-induced release of corticosterone84
      • reduced anxiety- and depression-related behavior84
      • altered the expression of GABA receptors in the brain via the vagus nerve84
      • GABA B1b receptor mRNA
        • increased in the cortex (cingulate and prelimbic)
        • reduced in hippocampus, amygdala and locus coeruleus
      • GABA-Aα2 mRNA
        • reduced in PFC and amygdala
        • increased in the hippocampus.
  • Lactococcus lactis subsp. cremoris (MG 1363)
    • produce serotonin83
  • Morganella morganii (NCIMB, 10466)
    • produce serotonin83
  • Saccharomyces
    • produce noradrenaline81
  • Serratia
    • produce dopamine81
  • Streptococcus
    • produce serotonin8081
    • Streptococcus thermophilus (NCFB2392)
      • produce serotonin83

Acetylcholine can cross the blood-brain barrier. However, dopamine, noradrenaline, serotonin and GABA do not, meaning that these latter neurotransmitters produced in the gut do not directly change the levels in the brain.

4.4.1. Gut bacteria as a possible causal cause of ADHD?

One study found evidence of a causal relationship between gut bacteria and ADHD.85 (Note: Even if causality were confirmed, it should be assumed that this is only one of many different possible ways in which ADHD can develop and would therefore not apply to all sufferers)

One study found that mice whose guts were contaminated with gut bacteria from people with ADHD showed structural changes in the brain (white matter, gray matter, hippocampus, internal capsule), reduced connectivity between motor and visual cortices on the right side of the resting state, and higher anxiety than mice in which gut bacteria from people without ADHD were used.86

A single-case study reports an improvement in ADHD symptoms in a young woman as a result of intestinal bacterial replacement related to a recurrent Clostridioides difficile infection.87

4.4.2. Microbiome and short-chain fatty acids in ADHD

The primary functions of the microbiota include88

  • Protection against pathogens by increasing mucus production and thus stabilizing the intestinal-blood barrier
  • Support for the immune system
  • Production of vitamins
  • Production of short-chain fatty acids (SCFAs) from indigestible carbohydrates

Short-chain fatty acids are:
C1:0 (no SCFA) Formic acid Methanoic acid Formates Methanoates HCOOH
C2:0 Acetic acid Ethanoic acid Acetate Ethanoate CH3COOH
C3:0 Propionic acid Propanoic acid Propionates Propanoates CH3CH2COOH
C4:0 Butyric acid Butanoic acid Butyrate Butanoate CH3(CH2)2COOH
C4:0 Isobutyric acid 2-Methylpropanoic acid Isobutyrate]] 2-Methylpropanoate (CH3)2CHCOOH
C5:0 Valeric acid Pentanoic acid Valerate Pentanoate CH3(CH2)3COOH
C5:0 Isovaleric acid 3-Methylbutanoic acid Isovalerate 3-Methylbutanoate (CH3)2CHCH2COOH
C6:0 Caproic acid Hexanoic acid Capronate Hexanoate CH3(CH2)4COOH

A study on short-chain fatty acids in the blood serum of ADHD compared to healthy family members found:89

  • Adults with ADHD
    • Formic acid reduces
    • Acetic acid reduces
    • Propionic acid reduces
    • Succinic acid reduced (C4H6O, an aliphatic dicarboxylic acid; food additive number E 363)
  • Children with ADHD
    • Formic acid lower than in adults
    • Propionic acid lower than in adults
    • Isovaleric acid lower than in adults
  • Antibiotic medication in the last 2 years caused
    • Formic acid reduces
    • Propionic acid reduces
    • Succinic acid reduces
  • current stimulant use in children caused
    • Acetic acid reduces
    • Propionic acid reduces

4.4.3. Gut microbiota in ADHD

Studies found abnormalities in the intestinal flora of children with ADHD88
ADHD correlated with leaky gut, neuroinflammation and overactivated microglial cells. The colonic microbiota exhibits a pro-inflammatory shift and harbors more gram-negative bacteria that contain immune-triggering lipopolysaccharides in their cell walls.90

Adults with ADHD had lower plasma concentrations of formic, acetic, propionic and succinic acid than their healthy family members. When ADHD patients were adjusted for SCFA-influencing factors, children had lower concentrations of formic, propionic, and isovaleric acids than adults, and those who had taken more antibiotic medications in the past two years had lower concentrations of formic, propionic, and succinic acids. After adjusting for antibiotic medication, we found that among children, those currently taking stimulant medications had lower acetic and propionic acid concentrations, and adults with ADHD had lower formic and propionic acid concentrations than adult healthy family members.

Early disruptions to the developing gut microbiota can affect neurological development and potentially lead to adverse mental health outcomes later in life.91

4.4.3.1. Reduced in ADHD
  • Bacteroides coprocola (B. coprocola)92
  • Butyricicoccus85
  • Coprococcus
    • Anti-inflammatory90
  • Desulfovibrio85
  • Dial register93
    • Dialister level increased after ADHD treatment
  • Enterococcus94
  • Eubacterium
    • anti-inflammatory90
  • Eubacterium rectale
    • anti-inflammatory90
  • Enterococcus94
  • Faecalibacterium prausnitzii94
    • anti-inflammatory90
  • Faecalibacterium959694
    • Anti-inflammatory90
  • LachnospiraceaeNC2004group85
  • Lachnospiraceae bacterium94
  • Lactobacillus
    • anti-inflammatory90
  • Oxalobacteraceae85
  • Peptostreptococcaceae85
  • Prevotella97
    • produce short-chain fatty acids (SCFAs)98
    • anti-inflammatory90
  • Romboutsia85
  • Ruminococcus gnavus 94
    • Increased against: RuminococcaceaeUCG01385
4.4.3.2. Increased in ADHD
  • Acidaminococcus99
  • Actinobacteria100
    • Collinsella100
  • Agathobacter99
    • correlated with withdrawal symptoms and depression
  • Bacillota (synonym: Firmicutes)100
    • Coprococcus100
    • Subdoligranulum100
  • Bacteroidetes100
    • Bacteroides100
      • Bacteroides uniformis (B. uniformis)92
      • Bacteroides ovatus (B. ovatus)
        • Increase correlated with ADHD symptoms92
      • Bacteroides caccae94
      • Bacteroides faecis (OR: 1.09)101
      • Bacteroides eggerthii correlated with PTSD (OR: 1.11), not with ADHD101
      • Bacteroides thetaiotaomicron correlated with PTSD (OR: 1.11), not with ADHD101
  • Bacteroidota100
    • Alistipes100
      • Pro-inflammatory90
  • Bifidobacterium
    • Anti-inflammatory90
    • Increases102
      • A slight increase in Bifidobacterium in the gut is thought to be associated with increased production of cyclohexadienyl dehydratase, which is a precursor to phenylanaline, which is a precursor to dopamine. At the same time, the increase in Bifidobacterium is thought to be associated with reduced reward anticipation, which may indicate reduced dopamine levels in the striatum. How these two seemingly contradictory pathways fit together is not yet clear to us.
      • Bifidobacterium encodes the enzyme arenate dehydratase (ADT), which is important for the production of phenylalanine. Phenylalanine can cross the blood-brain barrier and is a precursor of tyrosine, which is required for DA and NE synthesis.103 However, a small study found no systematic phenylalanine or tyrosine_abnormalities in children with ADHD.104
  • Eggerthella96
    • Pro-inflammatory90
  • Eubacteriumhalliigroup85
  • Flavonifractor
    • Pro-inflammatory90
  • Odoribacter splanchnicus94
  • Odoribacter96
    • Different a study according to which Odoribacter were reduced94
  • Paraprevotella xylaniphila94
  • Phascolarctobacterium99
  • Prevotella_2,99
  • Proteobacteria (Phylum)99
  • Roseburia8599
    • anti-inflammatory90
  • Ruminococcus gnavus99
    • correlated with rule-breaking behavior
  • Ruminococcustorquesgroup 85
    • RuminococcaceaeUCG01385
  • Sutterella stercoricanis (S. stercoricanis)
    • Increase correlated with intake of dairy products, nuts, seeds, legumes, iron, magnesium92
    • Increase correlated with ADHD symptoms92
  • Veillonella parvula94
  • Veillonellaceae94

No significant difference was found in the alpha diversity of the intestinal bacteria.9495

75 infants were randomly assigned to receive either Lactobacillus rhamnosus GG or a placebo in the first 6 months of life. After 13 years, ADHD or ASD was found in 17% of the placebo group and in none of the probiotic group. Bifidobacteria were significantly reduced in the intestinal microbiome of the affected children in the first 6 months of life.105106

A study of urine and fecal samples using 1H nuclear magnetic resonance spectroscopy and liquid chromatography-mass spectrometry found gender-specific patterns in the metabolic phenotype of ADHD107

  • Urine profile
    • Hippurate (a product of microbial host co-metabolism that can cross the blood-brain barrier)
      • increased (men only)
      • correlated negatively with IQ (in men)
      • correlated with fecal metabolites associated with microbial metabolism in the gut.
  • Fecal profile (independent of ADHD medication, age and BMI)
    • Stearoyl-linoleoyl-glycerol increased
    • 3,7-Dimethylurate increased
    • FAD increased
    • Glycerol-3-phosphate reduced
    • Thymine reduced
    • 2(1H)-quinolinone reduced
    • Aspartate reduced
    • Xanthine reduces
    • Hypoxanthine reduces
    • Orotate reduced

4.4.4. Gut microbiota similar in ADHD and ASD

The intestinal microbiota in ADHD and ASD are quite similar in both alpha and beta diversity and differ significantly from non-affected individuals.
In addition, a subgroup of ADHD and ASD cases showed an increased concentration of lipopolysaccharide-binding protein, which correlated positively with interleukin IL-8, IL-12 and IL-13, compared to unaffected children. This indicates a disturbance of the intestinal barrier and a dysregulation of the immune system in a subgroup of children with ADHD or ASD.108

4.4.5. Urinary microbiota in ADHD

An underestimation of the urinary microbiome in ADHD was found:109

  • a lower alpha diversity in the urine bacteria of the ADHD group
    • reduced Shannon and Simpson indices (p < 0.05)
  • significant differences in beta diversity
  • were common in ADHD:
    • Phyla Firmicutes
    • Actinobacteriota
    • Ralstonia (genus)
    • Afipia (genus)
  • less frequently with ADHD:
    • Phylum Proteobacteria
    • Corynebacterium (genus)
    • Peptoniphilus (genus)
  • Afipia correlated significantly with the results of the Child Behavior Checklist Attention Problems and the DSM-oriented ADHD subscale

4.5. Polycystic ovary syndrome (PCOS)

Women with polycystic ovary syndrome (PCOS) appear to have an increased risk of mental disorders, primarily anxiety disorders and depression, but also ADHD.110

4.6. (Untreated) type 1 diabetes

A study of diabetics with and without insulin pump treatment found a 2.45-fold increased risk of ADHD in non-treated type 1 diabetics, with ADHD being considered a risk factor for inconsistent diabetes treatment.111

4.7. Phenylketonuria (PKU)

Phenylketonuria (Følling disease, phenylpyruvic acid oligophrenia) is a genetically caused metabolic disorder in which the amino acid phenylalanine cannot be broken down into tyrosine due to the lack of the enzyme phenylalanine hydroxylase (PAH). Tyrosine, in turn, is required for the synthesis of dopamine, meaning that dopamine deficiency is a consequence of PKU.112 PKU has a prevalence of 1 in 8000 people.

One study found an ADHD rate of 38% in phenylketonuria despite adequate treatment.113
ADHD is also associated with dopamine deficiency.

4.8. Anabolic androgenic steroids (AAS)

Strength athletes who take anabolic androgenic steroids are significantly more likely to have ADHD than strength athletes who do not take them.114

4.9. Infections

4.9.1. Susceptibility to infection and infection burden

A higher burden of infection may have a cumulative association with psychiatric disorders that goes beyond what has been described for individual infections. Susceptibility to infections is reflected in the infection burden (the number of specific infection types or sites). An increased burden of infection correlates with an increased risk of115

  • ADHD
  • ASS
  • bipolar disorders
  • Depression
  • Schizophrenia
  • psychiatric diagnoses overall.
    A modest but significant heritability was found for the burden of infection (h2 = 0.0221) and a high degree of genetic correlation between it and the overall psychiatric diagnosis (rg = 0.4298). There was also evidence of genetic causality of the overall infection for the overall psychiatric diagnosis.

4.9.2. Viral infections

4.9.2.1. Enteroviruses in general

(Non-polio) enteroviruses cause a good half of all cases of aseptic meningitis and are therefore among the most important known causes.116 In addition to encephaltitis117, (non-polio) enteroviruses also frequently cause febrile illnesses, hand-foot-and-mouth disease, herpangina, aseptic meningitis and encephalitis, as well as sometimes serious and threatening infections such as myocarditis or neonatal sepsis.

A previous study found an increased risk of ADHD from mild enterovirus infections (16%) and severe enterovirus infections (182%)(Chou IC, Lin CC, Kao CH (2015): Enterovirus Encephalitis Increases the Risk of Attention Deficit Hyperactivity Disorder: A Taiwanese Population-based Case-control Study. Medicine (Baltimore). 2015 Apr;94(16):e707. doi: 10.1097/MD.0000000000000707. PMID: 25906098; PMCID: PMC4602682.))

4.9.2.2. Enterovirus A71 (EV-A71) (+ 200 %)

A longitudinal study of 43 adolescents between the ages of 6 and 18 who had a central nervous system infection with enterovirus A71 (EV-A71) found that 34.9% had ADHD. This more than tripled the risk of ADHD. There was also an increase in autistic symptoms. Other psychiatric diagnoses were not elevated.118119 Another study found ADHD to be particularly common when the A71 infection was accompanied by cardiopulmonary failure.120
EV-A71 often shows weakness, atrophy of the limbs, seizures, hand-foot-and-mouth disease, encephalitis and reduced intelligence.

4.9.2.3. HIV

A study of children and adolescents with HIV in a stable state of health found ADHD symptoms in 20%.121

4.9.2.4. Zoster encephalitis

In one individual case, ADHD was mentioned in connection with zoster encephalitis.122

4.9.2.5. Human endogenous retroviruses (HERV)

The topic Human endogenous retroviruses (HERV) and ADHD Is presented due to its high heritability in the chapter Development in the article Genetic and epigenetic causes of ADHD - Introduction

4.9.3. Bacterial infections

Periodontal disease is a bacterial inflammation of the gums caused by the bacterium P. gingivalis, which secretes toxins. Periodontal disease has been described as a risk factor for ADHD.123

4.9.4. Parasitic infections

A study of 100 children with ADHD and 100 healthy children found a correlation of ADHD with:124

  • Toxoplasma
  • Toxocara
  • Cryptosporidium parvum
  • Giardia lamblia
  • Entamoeba histolytica
    No difference was found with regard to Schistosoma (coccidia parasites).

4.10. Glucose-6-phosphate dehydrogenase deficiency (G6PD)

Glucose-6-phosphate dehydrogenase (G6PD) deficiency increased the risk of ADHD by 16%125

G6PD deficiency is an X-linked genetic disorder and affects around 4.9% of all people.
The enzyme glucose-6-phosphate dehydrogenase (G6PD) facilitates the synthesis of nicotinamide adenine dinucleotide phosphate (NADPH) and glutathione (GSH), which are involved in oxidation-reduction equilibrium regulation. G6PD deficiency causes reduced GSH levels and thus increased oxidative stress.

G6PD deficiency is mostly food-related (favism; hemolytic reaction to the consumption of fava beans) and sometimes genetic (more common in the Mediterranean region and the Middle East, partly in Asia and Africa).
G6PD deficiency can trigger (especially in children):

  • severe hemolysis
  • Hyperbilirubinemia
  • Jaundice
  • Hearing disorders
  • Behavioral disorders
  • lead to long-lasting neurological damage
  • increased production of reactive oxygen species (ROS)
    • resulting in activation of astrocytes and microglia, increased proinflammatory chemokines and cytokines, neuroinflammation, impaired brain development
  • Imbalance in the antioxidant system
    • this leads to impairment of astrocytes, neuronal death and DNA damage
    • oxidative cell death of leukocytes, myocytes and other immunological players.

4.11. Kawasaki syndrome

One study found an increased prevalence of ADHD in Kawasaki sufferers126, other studies found only a tendency127 or no connection.128

4.12. Factors without relevant contribution

4.12.1. High blood pressure

One study found no statistical significance for a genetic link between high blood pressure and ADHD.129

4.12.2. COVID-19 gene therapy

Gene predisposition, which makes people more susceptible to COVID-19, showed no signs of an increased risk of ADHD. Conversely, ADHD and Tourette’s are associated with an increased risk of COVID-19 and a more severe course of COVID-19.130

  1. Ku, Tsai, Wang, Su, Sun, Wang, Wang (2019): Prenatal and childhood phthalate exposure and attention deficit hyperactivity disorder traits in child temperament: A 12-year follow-up birth cohort study. Sci Total Environ. 2019 Aug 29;699:134053. doi: 10.1016/j.scitotenv.2019.134053. ↥

  2. Riddell, Malin, Flora, McCague, Till (2019): Association of water fluoride and urinary fluoride concentrations with attention deficit hyperactivity disorder in Canadian youth. Environ Int. 2019 Oct 22;133(Pt B):105190. doi: 10.1016/j.envint.2019.105190. n = 980 ↥

  3. Bashash M, Marchand M, Hu H, Till C, Martinez-Mier EA, Sanchez BN, Basu N, Peterson KE, Green R, Schnaas L, Mercado-García A, Hernández-Avila M, Téllez-Rojo MM (2018): Prenatal fluoride exposure and attention deficit hyperactivity disorder (ADHD) symptoms in children at 6-12 years of age in Mexico City. Environ Int. 2018 Dec;121(Pt 1):658-666. doi: 10.1016/j.envint.2018.09.017. PMID: 30316181. ↥

  4. Bashash M, Thomas D, Hu H, Martinez-Mier EA, Sanchez BN, Basu N, Peterson KE, Ettinger AS, Wright R, Zhang Z, Liu Y, Schnaas L, Mercado-García A, Téllez-Rojo MM, Hernández-Avila M (2017): Prenatal Fluoride Exposure and Cognitive Outcomes in Children at 4 and 6-12 Years of Age in Mexico. Environ Health Perspect. 2017 Sep 19;125(9):097017. doi: 10.1289/EHP655. PMID: 28937959; PMCID: PMC5915186. ↥

  5. Wang A, Duan L, Huang H, Ma J, Zhang Y, Ma Q, Guo Y, Li Z, Cheng X, Zhu J, Zhou G, Ba Y (2022): Association between fluoride exposure and behavioural outcomes of school-age children: a pilot study in China. Int J Environ Health Res. 2022 Jan;32(1):232-241. doi: 10.1080/09603123.2020.1747601. PMID: 32281876. ↥

  6. Fiore G, Veneri F, Di Lorenzo R, Generali L, Vinceti M, Filippini T (2023): Fluoride Exposure and ADHD: A Systematic Review of Epidemiological Studies. Medicina (Kaunas). 2023 Apr 19;59(4):797. doi: 10.3390/medicina59040797. PMID: 37109754; PMCID: PMC10143272. REVIEW ↥

  7. Bundesinstitut für Risikobewertung: Information Nr. 037/2005 des BfR vom 12. Juli 2005: Durchschnittlicher Fluoridgehalt in Trinkwasser ist in Deutschland niedrig ↥

  8. Ibarluzea J, Subiza-Pérez M, Arregi A, Molinuevo A, Arranz-Freijo E, Sánchez-de Miguel M, Jiménez A, Andiarena A, Santa-Marina L, Lertxundi A. Association of maternal prenatal urinary fluoride levels with ADHD symptoms in childhood. Environ Res. 2023 Jul 19;235:116705. doi: 10.1016/j.envres.2023.116705. PMID: 37479215. ↥

  9. Reddy YP, Tiwari S, Tomar LK, Desai N, Sharma VK (2021): Fluoride-Induced Expression of Neuroinflammatory Markers and Neurophysiological Regulation in the Brain of Wistar Rat Model. Biol Trace Elem Res. 2021 Jul;199(7):2621-2626. doi: 10.1007/s12011-020-02362-x. PMID: 32865723. ↥

  10. Geier, Kern, Geier (2018): A cross-sectional study of the relationship between blood lead levels and reported attention deficit disorder: an assessment of the economic impact on the United States. Metab Brain Dis. 2018 Feb;33(1):201-208. doi: 10.1007/s11011-017-0146-6. n = 2109 ↥

  11. Khalid, Abdollahi (2019): Epigenetic modifications associated with pathophysiological effects of lead exposure. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2019 Aug 12:1-53. doi: 10.1080/10590501.2019.1640581. ↥

  12. van de Bor (2019): Fetal toxicology. Handb Clin Neurol. 2019;162:31-55. doi: 10.1016/B978-0-444-64029-1.00002-3. ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥

  13. Reuben A, Ward R, Rothbaum AO, Cornelison VL, Huffman S, McTeague LM, Schmidt MG, Specht AJ, Kilpatrick DG (2024): Who tests for lead and why? A 10-year analysis of blood lead screening, follow-up and CNS outcomes in a statewide US healthcare system. Occup Environ Med. 2024 Jan 25:oemed-2023-109210. doi: 10.1136/oemed-2023-109210. PMID: 38272665. ↥

  14. Muñoz, Rubilar, Valdés, Muñoz-Quezad, Gómez, Saavedra, Iglesias (2020): Attention deficit hyperactivity disorder and its association with heavy metals in children from northern Chile. Int J Hyg Environ Health. 2020 May;226:113483. doi: 10.1016/j.ijheh.2020.113483. PMID: 32106053. ↥ ↥

  15. Levin ED, Bowman RE, Wegert S, Vuchetich J (1987): Psychopharmacological investigations of a lead-induced long-term cognitive deficit in monkeys. Psychopharmacology (Berl). 1987;91(3):334-41. doi: 10.1007/BF00518187. PMID: 3104955. ↥

  16. Cory-Slechta DA (1997): Relationships between Pb-induced changes in neurotransmitter system function and behavioral toxicity. Neurotoxicology. 1997;18(3):673-88. PMID: 9339816. REVIEW ↥

  17. Zuch CL, O’Mara DJ, Cory-Slechta DA. Low-level lead exposure selectively enhances dopamine overflow in nucleus accumbens: an in vivo electrochemistry time course assessment. Toxicol Appl Pharmacol. 1998 May;150(1):174-85. doi: 10.1006/taap.1998.8396. PMID: 9630467. ↥

  18. Jones, Miller (2008): The effects of environmental neurotoxicants on the dopaminergic system: A possible role in drug addiction. Biochem Pharmacol. 2008 Sep 1;76(5):569-81. doi: 10.1016/j.bcp.2008.05.010. PMID: 18555207. REVIEW ↥

  19. Kim, Kim, Lee, Yun, Sohn, Shin, Kim, Chae, Roh, Kim (2018): Interaction between DRD2 and lead exposure on the cortical thickness of the frontal lobe in youth with attention-deficit/hyperactivity disorder. Prog Neuropsychopharmacol Biol Psychiatry. 2018 Mar 2;82:169-176. doi: 10.1016/j.pnpbp.2017.11.018. ↥

  20. Nilsen, Tulve (2019): A systematic review and meta-analysis examining the interrelationships between chemical and non-chemical stressors and inherent characteristics in children with ADHD. Environ Res. 2019 Nov 1:108884. doi: 10.1016/j.envres.2019.108884. REVIEW ↥ ↥ ↥

  21. Amos-Kroohs, Graham, Grace, Braun, Schaefer, Skelton, Vorhees, Williams (2016): Developmental stress and lead (Pb): Effects of maternal separation and/or Pb on corticosterone, monoamines, and blood Pb in rats. Neurotoxicology. 2016 May;54:22-33. doi: 10.1016/j.neuro.2016.02.011. PMID: 26943976; PMCID: PMC4875812. ↥

  22. Desrochers-Couture, Courtemanche, Forget-Dubois, Bélanger, Boucher, Ayotte, Cordier, Jacobson, Jacobson, Muckle (2019): Association between early lead exposure and externalizing behaviors in adolescence: A developmental cascade. Environ Res. 2019 Aug 19;178:108679. doi: 10.1016/j.envres.2019.108679. ↥

  23. Sprowles JLN, Amos-Kroohs RM, Braun AA, Sugimoto C, Vorhees CV, Williams MT (2018): Developmental manganese, lead, and barren cage exposure have adverse long-term neurocognitive, behavioral and monoamine effects in Sprague-Dawley rats. Neurotoxicol Teratol. 2018 May-Jun;67:50-64. doi: 10.1016/j.ntt.2018.04.001. PMID: 29631003; PMCID: PMC5970996. ↥

  24. http://www.adhs.org/genese/ mit weiteren Nachweisen ↥

  25. Smith DR, Strupp BJ. Animal Models of Childhood Exposure to Lead or Manganese: Evidence for Impaired Attention, Impulse Control, and Affect Regulation and Assessment of Potential Therapies. Neurotherapeutics. 2023 Feb 28. doi: 10.1007/s13311-023-01345-9. PMID: 36853434. ↥ ↥

  26. Dellefratte, Stingone, Claudio (2019): Combined association of BTEX and material hardship on ADHD-suggestive behaviours among a nationally representative sample of US children. Paediatr Perinat Epidemiol. 2019 Nov;33(6):482-489. doi: 10.1111/ppe.12594. n = 4.650 ↥

  27. http://www.adhs.org/genese/ ↥ ↥ ↥ ↥ ↥ ↥ ↥

  28. Müller, Candrian, Kropotov (2011): ADHS – Neurodiagnostik in der Praxis, Springer, Seite 88 ↥

  29. http://de.statista.com/statistik/daten/studie/261015/umfrage/praevalenz-des-rauchens-in-deutschland-nach-geschlecht/ ↥

  30. Mariussen E, Fonnum F (2006): Neurochemical targets and behavioral effects of organohalogen compounds: an update. Crit Rev Toxicol. 2006 Mar;36(3):253-89. doi: 10.1080/10408440500534164. PMID: 16686424. REVIEW ↥

  31. Regan SL, Williams MT, Vorhees CV (2022): Review of rodent models of attention deficit hyperactivity disorder. Neurosci Biobehav Rev. 2022 Jan;132:621-637. doi: 10.1016/j.neubiorev.2021.11.041. PMID: 34848247; PMCID: PMC8816876.) REVIEW ↥ ↥ ↥ ↥

  32. Sagiv SK, Thurston SW, Bellinger DC, Tolbert PE, Altshul LM, Korrick SA (2010): Prenatal organochlorine exposure and behaviors associated with attention deficit hyperactivity disorder in school-aged children. Am J Epidemiol. 2010 Mar 1;171(5):593-601. doi: 10.1093/aje/kwp427. PMID: 20106937; PMCID: PMC2842227. ↥

  33. Bushnell PJ, Moser VC, MacPhail RC, Oshiro WM, Derr-Yellin EC, Phillips PM, Kodavanti PR (2002): Neurobehavioral assessments of rats perinatally exposed to a commercial mixture of polychlorinated biphenyls. Toxicol Sci. 2002 Jul;68(1):109-20. doi: 10.1093/toxsci/68.1.109. PMID: 12075116. ↥ ↥

  34. Schantz SL (1996): Developmental neurotoxicity of PCBs in humans: what do we know and where do we go from here? Neurotoxicol Teratol. 1996 May-Jun;18(3):217-27; discussion 229-76. doi: 10.1016/s0892-0362(96)90001-x. PMID: 8725628. REVIEW ↥

  35. Pessah, Lein, Seegal, Sagiv (2019): Neurotoxicity of polychlorinated biphenyls and related organohalogens. Acta Neuropathol. 2019 Apr 11. doi: 10.1007/s00401-019-01978-1. ↥

  36. Sable HJ, Eubig PA, Powers BE, Wang VC, Schantz SL. Developmental exposure to PCBs and/or MeHg: effects on a differential reinforcement of low rates (DRL) operant task before and after amphetamine drug challenge. Neurotoxicol Teratol. 2009 May-Jun;31(3):149-58. doi: 10.1016/j.ntt.2008.12.006. Epub 2009 Jan 21. PMID: 19344642; PMCID: PMC2730353. ↥ ↥

  37. Chishti, Fisher, Seegal (1996): Aroclors 1254 and 1260 reduce dopamine concentrations in rat striatal slices. Neurotoxicology. 1996 Fall-Winter;17(3-4):653-60. ↥ ↥ ↥ ↥

  38. Faroon O, Jones D, de Rosa C (2000): Effects of polychlorinated biphenyls on the nervous system. Toxicol Ind Health. 2000 Sep;16(7-8):305-33. doi: 10.1177/074823370001600708. PMID: 11693948. REVIEW ↥

  39. Seegal RF, Brosch KO, Okoniewski RJ (1997): Effects of in utero and lactational exposure of the laboratory rat to 2,4,2’,4’- and 3,4,3’,4’-tetrachlorobiphenyl on dopamine function. Toxicol Appl Pharmacol. 1997 Sep;146(1):95-103. doi: 10.1006/taap.1997.8226. PMID: 9299601. ↥

  40. Seegal RF, Bush B, Brosch KO (1994): Decreases in dopamine concentrations in adult, non-human primate brain persist following removal from polychlorinated biphenyls. Toxicology. 1994 Jan 26;86(1-2):71-87. doi: 10.1016/0300-483x(94)90054-x. PMID: 8134924. ↥

  41. Seegal RF, Bush B, Brosch KO (1991): Comparison of effects of Aroclors 1016 and 1260 on non-human primate catecholamine function. Toxicology. 1991 Feb;66(2):145-63. doi: 10.1016/0300-483x(91)90215-m. PMID: 2014516. ↥

  42. Seegal RF, Bush B, Shain W (1990): Lightly chlorinated ortho-substituted PCB congeners decrease dopamine in nonhuman primate brain and in tissue culture. Toxicol Appl Pharmacol. 1990 Oct;106(1):136-44. doi: 10.1016/0041-008x(90)90113-9. PMID: 2123577. ↥

  43. Caudle WM, Richardson JR, Delea KC, Guillot TS, Wang M, Pennell KD, Miller GW (2006): Polychlorinated biphenyl-induced reduction of dopamine transporter expression as a precursor to Parkinson’s disease-associated dopamine toxicity. Toxicol Sci. 2006 Aug;92(2):490-9. doi: 10.1093/toxsci/kfl018. Erratum in: Toxicol Sci. 2022 Feb 28;186(1):175. PMID: 16702228. ↥

  44. Jacobson JL, Jacobson SW. Intellectual impairment in children exposed to polychlorinated biphenyls in utero. N Engl J Med. 1996 Sep 12;335(11):783-9. doi: 10.1056/NEJM199609123351104. PMID: 8703183. ↥

  45. Grandjean P, Weihe P, Burse VW, Needham LL, Storr-Hansen E, Heinzow B, Debes F, Murata K, Simonsen H, Ellefsen P, Budtz-Jørgensen E, Keiding N, White RF (2001): Neurobehavioral deficits associated with PCB in 7-year-old children prenatally exposed to seafood neurotoxicants. Neurotoxicol Teratol. 2001 Jul-Aug;23(4):305-17. doi: 10.1016/s0892-0362(01)00155-6. PMID: 11485834. ↥

  46. Stewart P, Fitzgerald S, Reihman J, Gump B, Lonky E, Darvill T, Pagano J, Hauser P (2003): Prenatal PCB exposure, the corpus callosum, and response inhibition. Environ Health Perspect. 2003 Oct;111(13):1670-7. doi: 10.1289/ehp.6173. PMID: 14527849; PMCID: PMC1241692. ↥

  47. Stewart P, Reihman J, Gump B, Lonky E, Darvill T, Pagano J (2005): Response inhibition at 8 and 9 1/2 years of age in children prenatally exposed to PCBs. Neurotoxicol Teratol. 2005 Nov-Dec;27(6):771-80. doi: 10.1016/j.ntt.2005.07.003. PMID: 16198536. ↥

  48. Xi, Wu (2021): A Review on the Mechanism Between Different Factors and the Occurrence of Autism and ADHD. Psychol Res Behav Manag. 2021 Apr 9;14:393-403. doi: 10.2147/PRBM.S304450. PMID: 33859505; PMCID: PMC8044340. REVIEW ↥

  49. Abreu-Villaça Y, Levin ED (2017): Developmental neurotoxicity of succeeding generations of insecticides. Environ Int. 2017 Feb;99:55-77. doi: 10.1016/j.envint.2016.11.019. Epub 2016 Nov 28. PMID: 27908457; PMCID: PMC5285268. REVIEW ↥ ↥ ↥ ↥ ↥

  50. Makris, Chrousos, Anesiadou, Sabico, Abd-Alrahman, Al-Daghri, Chouliaras, Pervanidou (2019): Serum concentrations and detection rates of selected organochlorine pesticides in a sample of Greek school-aged children with neurodevelopmental disorders. Environ Sci Pollut Res Int. 2019 Aug;26(23):23739-23753. doi: 10.1007/s11356-019-05666-1. ↥

  51. Sagiv SK, Kogut K, Harley K, Bradman A, Morga N, Eskenazi B (2021): Gestational Exposure to Organophosphate Pesticides and Longitudinally Assessed Behaviors Related to Attention-Deficit/Hyperactivity Disorder and Executive Function. Am J Epidemiol. 2021 Nov 2;190(11):2420-2431. doi: 10.1093/aje/kwab173. PMID: 34100072; PMCID: PMC8757311. ↥

  52. (Marks, Harley, Bradman, Kogut, Barr, Johnson, Calderon, Eskenazi (2010): Organophosphate pesticide exposure and attention in young Mexican-American children: the CHAMACOS study. Environ Health Perspect. 2010 Dec;118(12):1768-74. doi: 10.1289/ehp.1002056. PMID: 21126939; PMCID: PMC3002198. ↥

  53. Chang CH, Yu CJ, Du JC, Chiou HC, Chen HC, Yang W, Chung MY, Chen YS, Hwang B, Mao IF, Chen ML (2018): The interactions among organophosphate pesticide exposure, oxidative stress, and genetic polymorphisms of dopamine receptor D4 increase the risk of attention deficit/hyperactivity disorder in children. Environ Res. 2018 Jan;160:339-346. doi: 10.1016/j.envres.2017.10.011. PMID: 29054088. n = 207 ↥

  54. Zhou W, Deng Y, Zhang C, Dai H, Guan L, Luo X, He W, Tian J, Zhao L (2022): Chlorpyrifos residue level and ADHD among children aged 1-6 years in rural China: A cross-sectional study. Front Pediatr. 2022 Oct 14;10:952559. doi: 10.3389/fped.2022.952559. PMID: 36313880; PMCID: PMC9616114. ↥ ↥

  55. Mostafalou, Abdollahi (2018): The link of organophosphorus pesticides with neurodegenerative and neurodevelopmental diseases based on evidence and mechanisms. Toxicology. 2018 Nov 1;409:44-52. doi: 10.1016/j.tox.2018.07.014. ↥

  56. van den Dries, Guxens, Pronk, Spaan, El Marroun, Jusko, Longnecker, Ferguson, Tiemeier (2019): Organophosphate pesticide metabolite concentrations in urine during pregnancy and offspring attention-deficit hyperactivity disorder and autistic traits. Environ Int. 2019 Jul 29;131:105002. doi: 10.1016/j.envint.2019.105002. n = 784 ↥

  57. Quirós-Alcalá, Alkon, Boyce, Lippert, Davis, Bradman, Barr, Eskenazi (2011): Maternal prenatal and child organophosphate pesticide exposures and children’s autonomic function. Neurotoxicology. 2011 Oct;32(5):646-55. doi: 10.1016/j.neuro.2011.05.017. n > 500 ↥

  58. Banhela N, Naidoo P, Naidoo S (2020): Association between pesticide exposure and paraoxonase-1 (PON1) polymorphisms, and neurobehavioural outcomes in children: a systematic review. Syst Rev. 2020 May 9;9(1):109. doi: 10.1186/s13643-020-01330-9. PMID: 32386510; PMCID: PMC7211330. ↥

  59. Berg EL, Ching TM, Bruun DA, Rivera JK, Careaga M, Ellegood J, Lerch JP, Wöhr M, Lein PJ, Silverman JL (2020): Translational outcomes relevant to neurodevelopmental disorders following early life exposure of rats to chlorpyrifos. J Neurodev Disord. 2020 Dec 16;12(1):40. doi: 10.1186/s11689-020-09342-1. PMID: 33327943; PMCID: PMC7745485. ↥

  60. Gómez-Giménez B, Felipo V, Cabrera-Pastor A, Agustí A, Hernández-Rabaza V, Llansola M. Developmental Exposure to Pesticides Alters Motor Activity and Coordination in Rats: Sex Differences and Underlying Mechanisms. Neurotox Res. 2018 Feb;33(2):247-258. doi: 10.1007/s12640-017-9823-9. Epub 2017 Oct 3. PMID: 28975519. ↥

  61. Ito, Tomizawa, Suzuki, Shirakawa, Ono, Adachi, Suzuki, Shimomura, Nabeshima, Kamijima (2020): Organophosphate agent induces ADHD-like behaviors via inhibition of brain endocannabinoid-hydrolyzing enzyme(s) in adolescent male rats. J Agric Food Chem. 2020 Jan 30;10.1021/acs.jafc.9b08195. doi: 10.1021/acs.jafc.9b08195. PMID: 31995978. ↥

  62. Eadeh HM, Davis J, Ismail AA, Abdel Rasoul GM, Hendy OM, Olson JR, Bonner MR, Rohlman DS (2023): Evaluating how occupational exposure to organophosphates and pyrethroids impacts ADHD severity in Egyptian male adolescents. Neurotoxicology. 2023 Jan 5;95:75-82. doi: 10.1016/j.neuro.2023.01.001. PMID: 36621468. n = 226 ↥ ↥

  63. Wagner-Schuman M, Richardson JR, Auinger P, Braun JM, Lanphear BP, Epstein JN, Yolton K, Froehlich TE. Association of pyrethroid pesticide exposure with attention-deficit/hyperactivity disorder in a nationally representative sample of U.S. children. Environ Health. 2015 May 28;14:44. doi: 10.1186/s12940-015-0030-y. PMID: 26017680; PMCID: PMC4458051. ↥

  64. Richardson JR, Taylor MM, Shalat SL, Guillot TS 3rd, Caudle WM, Hossain MM, Mathews TA, Jones SR, Cory-Slechta DA, Miller GW (2015): Developmental pesticide exposure reproduces features of attention deficit hyperactivity disorder. FASEB J. 2015 May;29(5):1960-72. doi: 10.1096/fj.14-260901. PMID: 25630971; PMCID: PMC4415012. ↥

  65. Dreiem, Shan, Okoniewski, Sanchez-Morrissey, Seegal (2009): Methylmercury inhibits dopaminergic function in rat pup synaptosomes in an age-dependent manner. Neurotoxicol Teratol. 2009 Sep-Oct;31(5):312-7. doi: 10.1016/j.ntt.2009.05.001. PMID: 19464365. ↥

  66. Lin, Wang, Chiang, Lai, Chang, Chi (2017): Risk of subsequent attention-deficit/hyperactivity disorder among children and adolescents with amalgam restorations: A nationwide longitudinal study. .Community Dent Oral Epidemiol. 2017 Aug 7. doi: 10.1111/cdoe.12327 ↥

  67. Torrey EF, Simmons W (2023): Mercury and Parkinson’s Disease: Promising Leads, but Research Is Needed. Parkinsons Dis. 2023 Sep 16;2023:4709322. doi: 10.1155/2023/4709322. PMID: 37744289; PMCID: PMC10517869. REVIEW ↥

  68. Shih, Zeng, Lin, Chen, Chen, Wu, Tseng, Wu (2018): Association between peripheral manganese levels and attention-deficit/hyperactivity disorder: a preliminary meta-analysis. Neuropsychiatr Dis Treat. 2018 Jul 18;14:1831-1842. doi: 10.2147/NDT.S165378. eCollection 2018. ↥

  69. Howard SL, Beaudin SA, Strupp BJ, Smith DR (2023): Maternal choline supplementation: A potential therapy for developmental Manganese exposure? bioRxiv [Preprint]. 2023 Jun 26:2023.06.23.546356. doi: 10.1101/2023.06.23.546356. PMID: 37425833; PMCID: PMC10327095. ↥

  70. Salazar, Villaseca, Cisternas, Inestrosa (2021). Neurodevelopmental impact of the offspring by thyroid hormone system-disrupting environmental chemicals during pregnancy. Environ Res. 2021 Jun 1;200:111345. doi: 10.1016/j.envres.2021.111345. PMID: 34087190. ↥

  71. Liu H, Wang J (2022): The association between bisphenol a exposure and attention deficit hyperactivity disorder in children: a meta-analysis of observational studies. Rev Environ Health. 2022 Dec 8. doi: 10.1515/reveh-2022-0184. PMID: 36480489. n = 5.710 ↥

  72. Lee (2019): Potential health effects of emerging environmental contaminants perfluoroalkyl compounds. Yeungnam Univ J Med. 2018 Dec 31;35(2):156-164. doi: 10.12701/yujm.2018.35.2.156. ↥

  73. Dórea (2019): Environmental exposure to low-level lead (Pb) co-occurring with other neurotoxicants in early life and neurodevelopment of children. Environ Res. 2019 Oct;177:108641. doi: 10.1016/j.envres.2019.108641. ↥

  74. Smith, Gozal, Hunter, Kheirandish-Gozal (2017): Parent-Reported Behavioral and Psychiatric Problems Mediate the Relationship between Sleep-Disordered Breathing and Cognitive Deficits in School-Aged Children. Front Neurol. 2017 Aug 11;8:410. doi: 10.3389/fneur.2017.00410. eCollection 2017. ↥

  75. Niederhofer (2011): Association of Attention-Deficit/Hyperactivity Disorder and Celiac Disease: A Brief Report; Prim Care Companion CNS Disord. 2011; 13(3): PCC.10br01104; doi: 10.4088/PCC.10br01104; PMCID: PMC3184556, n = 67 ↥

  76. ähnlich: Okusaga, Yolken, Langenberg, Sleemi, Kelly, Vaswani, Giegling, Hartmann, Konte, Friedl, Mohyuddin, Groer, Rujescu, Postolache (2013): Elevated gliadin antibody levels in individuals with schizophrenia. World J Biol Psychiatry. 2013 Sep;14(7):509-15. doi: 10.3109/15622975.2012.747699. ↥

  77. Lachance, McKenzie (2013): Biomarkers of gluten sensitivity in patients with non-affective psychosis: a meta-analysis. Schizophr Res. 2014 Feb;152(2-3):521-7. doi: 10.1016/j.schres.2013.12.001. ↥

  78. Stevenson J, Sonuga-Barke E, McCann D, Grimshaw K, Parker KM, Rose-Zerilli MJ, Holloway JW, Warner JO (2010): The role of histamine degradation gene polymorphisms in moderating the effects of food additives on children’s ADHD symptoms. Am J Psychiatry. 2010 Sep;167(9):1108-15. doi: 10.1176/appi.ajp.2010.09101529. PMID: 20551163. RCT ↥

  79. Kwak MJ, Kim SH, Kim HH, Tanpure R, Kim JI, Jeon BH, Park HK (2023): Psychobiotics and fecal microbial transplantation for autism and attention-deficit/hyperactivity disorder: microbiome modulation and therapeutic mechanisms. Front Cell Infect Microbiol. 2023 Jul 24;13:1238005. doi: 10.3389/fcimb.2023.1238005. PMID: 37554355; PMCID: PMC10405178. REVIEW ↥ ↥ ↥

  80. Galland L. The gut microbiome and the brain (2014): J Med Food. 2014 Dec;17(12):1261-72. doi: 10.1089/jmf.2014.7000. PMID: 25402818; PMCID: PMC4259177. REVIEW ↥ ↥ ↥ ↥ ↥ ↥ ↥

  81. Lyte M (2011): Probiotics function mechanistically as delivery vehicles for neuroactive compounds: Microbial endocrinology in the design and use of probiotics. Bioessays. 2011 Aug;33(8):574-81. doi: 10.1002/bies.201100024. PMID: 21732396. ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥

  82. O’Mahony SM, Clarke G, Borre YE, Dinan TG, Cryan JF (2015): Serotonin, tryptophan metabolism and the brain-gut-microbiome axis. Behav Brain Res. 2015 Jan 15;277:32-48. doi: 10.1016/j.bbr.2014.07.027. Epub 2014 Jul 29. PMID: 25078296. REVIEW ↥

  83. O’Mahony SM, Clarke G, Borre YE, Dinan TG, Cryan JF (2015): Serotonin, tryptophan metabolism and the brain-gut-microbiome axis. Behav Brain Res. 2015 Jan 15;277:32-48. doi: 10.1016/j.bbr.2014.07.027. PMID: 25078296. REVIEW ↥ ↥ ↥ ↥ ↥ ↥ ↥

  84. Bravo JA, Forsythe P, Chew MV, Escaravage E, Savignac HM, Dinan TG, Bienenstock J, Cryan JF (2011): Ingestion of Lactobacillus strain regulates emotional behavior and central GABA receptor expression in a mouse via the vagus nerve. Proc Natl Acad Sci U S A. 2011 Sep 20;108(38):16050-5. doi: 10.1073/pnas.1102999108. PMID: 21876150; PMCID: PMC3179073. ↥ ↥ ↥

  85. Wang L, Xie Z, Li G, Li G, Liang J (2023): Two-sample Mendelian randomization analysis investigates causal associations between gut microbiota and attention deficit hyperactivity disorder. Front Microbiol. 2023 Apr 24;14:1144851. doi: 10.3389/fmicb.2023.1144851. PMID: 37168108; PMCID: PMC10166206. ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥

  86. Tengeler, Dam, Wiesmann, Naaijen, van Bodegom, Belzer, Dederen, Verweij, Franke, Kozicz, Arias Vasquez, Kiliaan (2020): Gut microbiota from persons with attention-deficit/hyperactivity disorder affects the brain in mice. Microbiome. 2020 Apr 1;8(1):44. doi: 10.1186/s40168-020-00816-x. PMID: 32238191; PMCID: PMC7114819. ↥

  87. Hooi, Dwiyanto, Rasiti, Toh, Wong RKM, Lee JWJ (2022): A case report of improvement on ADHD symptoms after fecal microbiota transplantation with gut microbiome profiling pre- and post-procedure. Curr Med Res Opin. 2022 Sep 26:1-13. doi: 10.1080/03007995.2022.2129232. PMID: 36164761. ↥

  88. Bull-Larsen, Mohajeri (2019): The Potential Influence of the Bacterial Microbiome on the Development and Progression of ADHD. Nutrients. 2019 Nov 17;11(11). pii: E2805. doi: 10.3390/nu11112805. REVIEW ↥ ↥

  89. Yang LL, Stiernborg M, Skott E, Gillberg T, Landberg R, Giacobini M, Lavebratt C (2022): Lower plasma concentrations of short-chain fatty acids (SCFAs) in patients with ADHD. J Psychiatr Res. 2022 Sep 28;156:36-43. doi: 10.1016/j.jpsychires.2022.09.042. PMID: 36228390. n = 269 ↥

  90. Eicher, Mohajeri (2022): Overlapping Mechanisms of Action of Brain-Active Bacteria and Bacterial Metabolites in the Pathogenesis of Common Brain Diseases. Nutrients. 2022 Jun 27;14(13):2661. doi: 10.3390/nu14132661. PMID: 35807841. ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥

  91. Borre, O’Keeffe, Clarke, Stanton, Dinan, Cryan (2020): Microbiota and neurodevelopmental windows: implications for brain disorders. Trends Mol Med. 2014 Sep;20(9):509-18. doi: 10.1016/j.molmed.2014.05.002. PMID: 24956966. REVIEW ↥

  92. Wang, Yang, Chou, Lee, Chou, Kuo, Yeh, Lee, Huang, Li (2019): Gut microbiota and dietary patterns in children with attention-deficit/hyperactivity disorder. Eur Child Adolesc Psychiatry. 2019 May 22. doi: 10.1007/s00787-019-01352-2. ↥ ↥ ↥ ↥ ↥

  93. Sukmajaya AC, Lusida MI, Soetjipto, Setiawati Y (2021): Systematic review of gut microbiota and attention-deficit hyperactivity disorder (ADHD). Ann Gen Psychiatry. 2021 Feb 16;20(1):12. doi: 10.1186/s12991-021-00330-w. PMID: 33593384; PMCID: PMC7888126. REVIEW ↥

  94. Wan, Ge, Zhang, Sun, Wang, Yang (2020): Case-Control Study of the Effects of Gut Microbiota Composition on Neurotransmitter Metabolic Pathways in Children With Attention Deficit Hyperactivity Disorder. Front Neurosci. 2020 Feb 18;14:127. doi: 10.3389/fnins.2020.00127. PMID: 32132899; PMCID: PMC7040164. ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥

  95. Jiang, Zhou, Zhou, Li, Yuan, Li, Ruan (2018): Gut microbiota profiles in treatment-naïve children with attention deficit hyperactivity disorder. Behav Brain Res. 2018 Jul 16;347:408-413. doi: 10.1016/j.bbr.2018.03.036. PMID: 29580894. n = 83 ↥ ↥

  96. Gkougka, Mitropoulos, Tzanakaki, Panagouli, Psaltopoulou, Thomaidis, Tsolia, Sergentanis, Tsitsika (2022): Gut microbiome and attention deficit/hyperactivity disorder: a systematic review. Pediatr Res. 2022 Mar 30. doi: 10.1038/s41390-022-02027-6. PMID: 35354932. METASTUDIE ↥ ↥ ↥

  97. Prehn-Kristensen A, Zimmermann A, Tittmann L, Lieb W, Schreiber S, Baving L, Fischer A (2018): Reduced microbiome alpha diversity in young patients with ADHD. PLoS One. 2018 Jul 12;13(7):e0200728. doi: 10.1371/journal.pone.0200728. PMID: 30001426; PMCID: PMC6042771. ↥

  98. Szopinska-Tokov J, Dam S, Naaijen J, Konstanti P, Rommelse N, Belzer C, Buitelaar J, Franke B, Bloemendaal M, Aarts E, Arias Vasquez A (2020): Correction: Szopinska-Tokov et al. Investigating the Gut Microbiota Composition of Individuals with Attention-Deficit/Hyperactivity Disorder and Association with Symptoms. Microorganisms 2020, 8, 406. Microorganisms. 2021 Jun 23;9(7):1358. doi: 10.3390/microorganisms9071358. Erratum for: Microorganisms. 2020 Mar 13;8(3): PMID: 34201905; PMCID: PMC8306196. ↥

  99. Lee MJ, Lai HC, Kuo YL, Chen VC (2022): Association between Gut Microbiota and Emotional-Behavioral Symptoms in Children with Attention-Deficit/Hyperactivity Disorder. J Pers Med. 2022 Oct 2;12(10):1634. doi: 10.3390/jpm12101634. PMID: 36294773; PMCID: PMC9605220. ↥ ↥ ↥ ↥ ↥ ↥ ↥

  100. Taş E, Ülgen KO (2023): Understanding the ADHD-Gut Axis by Metabolic Network Analysis. Metabolites. 2023 Apr 26;13(5):592. doi: 10.3390/metabo13050592. PMID: 37233633; PMCID: PMC10223614. ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥

  101. Xiao L, Liu S, Wu Y, Huang Y, Tao S, Liu Y, Tang Y, Xie M, Ma Q, Yin Y, Dai M, Zhang M, Llamocca E, Gui H, Wang Q (2023): The interactions between host genome and gut microbiome increase the risk of psychiatric disorders: Mendelian randomization and biological annotation. Brain Behav Immun. 2023 Aug 8;113:389-400. doi: 10.1016/j.bbi.2023.08.003. PMID: 37557965. ↥ ↥ ↥

  102. Aarts, Ederveen, Naaijen, Zwiers, Boekhorst, Timmerman, Smeekens, Netea, Buitelaar, Franke, van Hijum, Arias Vasquez (2017): Gut microbiome in ADHD and its relation to neural reward anticipation. PLoS One. 2017 Sep 1;12(9):e0183509. doi: 10.1371/journal.pone.0183509. PMID: 28863139; PMCID: PMC5581161. ↥

  103. Eicher TP, Mohajeri MH (2022): Overlapping Mechanisms of Action of Brain-Active Bacteria and Bacterial Metabolites in the Pathogenesis of Common Brain Diseases. Nutrients. 2022 Jun 27;14(13):2661. doi: 10.3390/nu14132661. PMID: 35807841; PMCID: PMC9267981. ↥

  104. Bergwerff CE, Luman M, Blom HJ, Oosterlaan J (2016): No Tryptophan, Tyrosine and Phenylalanine Abnormalities in Children with Attention-Deficit/Hyperactivity Disorder. PLoS One. 2016 Mar 3;11(3):e0151100. doi: 10.1371/journal.pone.0151100. PMID: 26938936; PMCID: PMC4777504. ↥

  105. Pärtty A, Kalliomäki M, Wacklin P, Salminen S, Isolauri E (2015): A possible link between early probiotic intervention and the risk of neuropsychiatric disorders later in childhood: a randomized trial. Pediatr Res. 2015 Jun;77(6):823-8. doi: 10.1038/pr.2015.51. PMID: 25760553. ↥

  106. Vasiliu O (2023) The current state of research for psychobiotics use in the management of psychiatric disorders-A systematic literature review. Front Psychiatry. 2023 Feb 23;14:1074736. doi: 10.3389/fpsyt.2023.1074736. PMID: 36911130; PMCID: PMC9996157. REVIEW ↥

  107. Swann JR, Diaz Heijtz R, Mayneris-Perxachs J, Arora A, Isaksson J, Bölte S, Tammimies K (2023): Characterizing the metabolomic signature of attention-deficit hyperactivity disorder in twins. Neuropharmacology. 2023 Apr 24:109562. doi: 10.1016/j.neuropharm.2023.109562. PMID: 37100381. ↥

  108. Bundgaard-Nielsen C, Lauritsen MB, Knudsen JK, Rold LS, Larsen MH, Hindersson P, Villadsen AB, Leutscher PDC, Hagstrøm S, Nyegaard M, Sørensen S (2023): Children and adolescents with attention deficit hyperactivity disorder and autism spectrum disorder share distinct microbiota compositions. Gut Microbes. 2023 Jan-Dec;15(1):2211923. doi: 10.1080/19490976.2023.2211923. PMID: 37199526; PMCID: PMC10197996. ↥

  109. Cho YJ, Shin B, Lee SH, Park S, Kim YK, Kim JJ, Kim E (2023): Altered Urine Microbiome in Male Children and Adolescents with Attention-Deficit Hyperactivity Disorder. Microorganisms. 2023 Aug 11;11(8):2063. doi: 10.3390/microorganisms11082063. PMID: 37630623; PMCID: PMC10458914. ↥

  110. Rodriguez-Paris, Remlinger-Molenda, Kurzawa, Głowińska, Spaczyński, Rybakowski, Pawełczyk, Banaszewska (2019): Psychiatric disorders in women with polycystic ovary syndrome. Psychiatr Pol. 2019 Aug 31;53(4):955-966. doi: 10.12740/PP/OnlineFirst/93105. ↥

  111. Merzon, Grossman, Vinker, Merhasin, Levit, Golan-Cohen (2020): Factors associated with withdrawal from insulin pump therapy: a large-population-based study. Diabetes Metab Res Rev. 2020 Jan 10. doi: 10.1002/dmrr.3288. n = 707 ↥

  112. Welsh (1996): A prefrontal dysfunction model of early-treated phenylketonuria. Eur J Pediatr. 1996 Jul;155 Suppl 1:S87-9. doi: 10.1007/pl00014259. PMID: 8828618. ↥

  113. Beckhauser, Beghini Mendes Vieira, Moehlecke Iser, Rozone, Luca, Rodrigues Masruha, Lin, Luiz Streck (2020): Attention Deficit Disorder with Hyperactivity Symptoms in Early-Treated Phenylketonuria Patients. Iran J Child Neurol. 2020 Winter;14(1):93-103. PMID: 32021633; PMCID: PMC6956970. n = 34 ↥

  114. Kildal, Hassel, Bjørnebekk (2022): ADHD symptoms and use of anabolic androgenic steroids among male weightlifters. Sci Rep. 2022 Jun 8;12(1):9479. doi: 10.1038/s41598-022-12977-w. PMID: 35676515; PMCID: PMC9178025. ↥

  115. Nudel R, Hougaard DM, Werge T, Benros ME (2023): Genetic and epidemiological analyses of infection load and its relationship with psychiatric disorders. Epidemiol Infect. 2023 May 18;151:e93. doi: 10.1017/S0950268823000687. PMID: 37197974; PMCID: PMC10311684. ↥

  116. Michos AG, Syriopoulou VP, Hadjichristodoulou C, Daikos GL, Lagona E, Douridas P, Mostrou G, Theodoridou M. (2007): Aseptic meningitis in children: analysis of 506 cases. PLoS One. 2007 Aug 1;2(7):e674. doi: 10.1371/journal.pone.0000674. PMID: 17668054; PMCID: PMC1933255. ↥

  117. Fowlkes AL, Honarmand S, Glaser C, Yagi S, Schnurr D, Oberste MS, Anderson L, Pallansch MA, Khetsuriani N. (2008): Enterovirus-associated encephalitis in the California encephalitis project, 1998-2005. J Infect Dis. 2008 Dec 1;198(11):1685-91. doi: 10.1086/592988. PMID: 18959496. ↥

  118. Lin HY, Chen YL, Chou PH, Gau SS, Chang LY (2022): Long-term psychiatric outcomes in youth with enterovirus A71 central nervous system involvement. Brain Behav Immun Health. 2022 Jun 1;23:100479. doi: 10.1016/j.bbih.2022.100479. PMID: 35694176; PMCID: PMC9184869. ↥

  119. Goh M, Joy C, Gillespie AN, Soh QR, He F, Sung V (2023): Asymptomatic viruses detectable in saliva in the first year of life: a narrative review. Pediatr Res. 2023 Dec 22. doi: 10.1038/s41390-023-02952-0. PMID: 38135726. REVIEW ↥

  120. Chang LY, Huang LM, Gau SS, Wu YY, Hsia SH, Fan TY, Lin KL, Huang YC, Lu CY, Lin TY (2007): Neurodevelopment and cognition in children after enterovirus 71 infection. N Engl J Med. 2007 Mar 22;356(12):1226-34. doi: 10.1056/NEJMoa065954. PMID: 17377160. ↥

  121. Nozyce, Lee SS, Wiznia, Nachman, Mofenson, Smith, Yogev, McIntosh, Stanley, Pelton (2006): A behavioral and cognitive profile of clinically stable HIV-infected children. Pediatrics. 2006 Mar;117(3):763-70. doi: 10.1542/peds.2005-0451. PMID: 16510656. n = 274 ↥

  122. Dale, Church, Heyman (2003): Striatal encephalitis after varicella zoster infection complicated by Tourettism. Mov Disord. 2003 Dec;18(12):1554-6. doi: 10.1002/mds.10610. PMID: 14673900. ↥

  123. Wilson, Thomas (2022): Peridontitis as a Risk Factor for Attention Deficit Hyperactivity Disorder: Possible Neuro-inflammatory Mechanisms. Neurochem Res. 2022 Jun 28. doi: 10.1007/s11064-022-03650-9. PMID: 35764847. ↥

  124. Elmehy DA, Elmansory BM, Gamea GA, Abdelhai DI, Abd-Elsalam SM, Salamah AM, Ata DS, Mahmoud EF, Ibrahim HA, Salama AM (2023): Parasitic infections as potential risk factors for attention deficit hyperactivity disorder (ADHD) in children. J Parasit Dis. 2023 Mar;47(1):82-92. doi: 10.1007/s12639-022-01542-x. PMID: 36910322; PMCID: PMC9998788. ↥

  125. Merzon E, Magen E, Ashkenazi S, Weizman A, Manor I, Krone B, Green I, Golan-Cohen A, Vinker S, Faraone SV, Israel A (2023): The Association between Glucose 6-Phosphate Dehydrogenase Deficiency and Attention Deficit/Hyperactivity Disorder. Nutrients. 2023 Nov 29;15(23):4948. doi: 10.3390/nu15234948. PMID: 38068806; PMCID: PMC10708268. ↥

  126. Daniels LB, Roberts S, Moreno E, Tremoulet AH, Gordon JB, Burns JC (2022): Long-term health outcomes in young adults after Kawasaki disease. Int J Cardiol Heart Vasc. 2022 May 4;40:101039. doi: 10.1016/j.ijcha.2022.101039. PMID: 35573651; PMCID: PMC9096130. n = 406 ↥

  127. Kuo HC, Chang WC, Wang LJ, Li SC, Chang WP (2016): Association of Attention deficit hyperactivity disorder and Kawasaki disease: a nationwide population-based cohort study. Epidemiol Psychiatr Sci. 2016 Dec;25(6):573-580. doi: 10.1017/S2045796015000840. PMID: 26392050; PMCID: PMC7137668. n = 651 ↥

  128. Lin CH, Lin WD, Chou IC, Lee IC, Hong SY (2019): Heterogeneous neurodevelopmental disorders in children with Kawasaki disease: what is new today? BMC Pediatr. 2019 Nov 4;19(1):406. doi: 10.1186/s12887-019-1786-y. PMID: 31684911; PMCID: PMC6827201. n = 612 ↥

  129. Huangfu N, Lu Y, Ma H, Hu Z, Cui H, Yang F (2023): Genetic liability to mental disorders in relation to the risk of hypertension. Front Cardiovasc Med. 2023 Feb 27;10:1087251. doi: 10.3389/fcvm.2023.1087251. PMID: 36923957; PMCID: PMC10008891. ↥

  130. Chen F, Cao H, Baranova A, Zhao Q, Zhang F (2023): Causal associations between COVID-19 and childhood mental disorders. BMC Psychiatry. 2023 Dec 8;23(1):922. doi: 10.1186/s12888-023-05433-0. PMID: 38066446; PMCID: PMC10704772. ↥

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