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

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

Certain physical illnesses, toxins, or food intolerances appear to be able to increase the risk of ADHD (or other mental disorders) throughout life.

4.1. Breathing pauses during sleep

Breathing pauses in children’s sleep can trigger cognitive distress, causing symptoms that resemble ADHD.1

It is open whether sleep breathing cessations can be such a stressor that they can contribute to ADHD through epigenetic changes, or whether they merely cause symptoms similar to those of ADHD. In the latter case, in people who did not have ADHD before, and who developed ADHD (similar) symptoms due to breathing pauses during sleep, these would have to disappear completely after elimination of the breathing pauses during sleep. So far, we are not aware of any studies on this.

4.2. Toxins

4.2.1. Parents smoking

Postnatal parental smoking correlates with a 1.3-fold risk (increased by 30%)2 for ADHD in the offspring.
This could be related to genetic factors, as ADHD sufferers smoke significantly more often. The comorbidity of smoking to ADHD is 40%.3 In contrast, of the total population, about 25% smoke less, namely 26.9% of women and 32.6% of men.4

4.2.2. Polychlorinated biphenyls (PCBs) / Polychlorinated biphenyl ethers

Polychlorinated biphenyls and polychlorinated biphenyl ethers are suspected of causing ADHD.

Polychlorinated biphenyls inhibit dopamine synthesis as well as the storage of dopamine in the vesicles and its release, thus causing a too low dopamine level. PBCs also cause hyperactivity and impulsivity (in rats already at subtoxic doses).56
There is weak evidence (= not proven) of relevance in ADHD.27
PCBs have been banned in Germany since 1989.

4.2.3. Polyvenyl chloride (PVC)

One review describes a suspected correlation of PVC exposure and ADHD.8

4.2.4. Pesticides

With regard to pesticides (especially organochlorine compounds, pyrethroids, organophosphates), there are indications (= not proven with certainty) of relevance in ADHD.26

On pesticides in pregnancy and ADHD, see above.

4.2.4.1. Organochlorine compounds

A study of Greek school children with ADHD found no elevated blood serum levels of9

  • Dichlorodiphenyltrichloroethane (DDT) Metabolites
  • Hexachlorocyclohexane (HCH) isomers
  • Cyclodienes
  • Methoxychlor
4.2.4.2. Organophosphates

Organophosphate pesticides have no effect according to two major studies,1011 while other studies found a correlation of prenatal and postnatal exposure and ADHD((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.)) or discussed a theoretically possible increase in ADHD risk.12 One source suggests an increased ADHD risk from organophosphates particularly when coinciding with a particular MAO-A gene variant that causes lower serotonin depletion.13

A study in rats was able to induce ADHD-like behaviors in Wystar and SHR rats by organosphates and shows strong circumstantial evidence that these are mediated by decreases in fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) via the cannabinoid receptor.14

Blood levels were measured in Egyptian adolescents, some of whom used pesticides, and parents were asked about ADHD symptoms in the adolescents:15
No correlation to ADHD was found with respect to chlorpyrifos.
Measured were:

  • Organophosphate
    • Urinary trichloro-2-pyridinol (TCPy) as a specific metabolite biomarker for exposure to chlorpyrifos

4.2.5. Pyrethroids

Blood levels were measured in Egyptian adolescents, some of whom used pesticides, and parents were asked about ADHD symptoms in the adolescents:15
A correlation to ADHD was found with respect to pyrethroid λCH by the Cis-DCCA reading (all subjects reported clinical ADHD symptoms).
Measured was:

  • Pyrethroids
    • urinary cis-3-(2,2-dichlorovinyl)-2,2-dimethylcyclopropanecarboxylic acid (cis-DCCA) as a specific biomarker of exposure to αCM
    • Lambda-cyhalothric acid (λCH-acid) as a specific biomarker for exposure to λCH
    • urinary 3-phenoxybenzoic acid (3-PBA) as a general metabolite biomarker for exposure to pyrethroids

4.2.6. Mercury / Amalgam (Mercury)

There is weak evidence (= not proven) of relevance in ADHD.2616
A large study with n = 2073 participants could not find any association between amalgam and ADHD.17

4.2.7. Manganese or formaldehyde

There is weak evidence of relevance in ADHD, with elevated levels of manganese found only in hair but not in blood levels in ADHD sufferers.218

4.2.8. Lead (Lead)

Elevated blood lead levels lead to an increased risk of ADHD.19206 A blood lead level of ≥ 5 μg/dl was found to increase the risk of ADHD by 1.33 (OR 2.33).21

A connection between ADHD and lead is said to exist in particular if affected individuals possess the DRD2 gene variant rs1800497r.22 A connection to certain MAO-A gene variants is also mentioned, which causes a lower serotonin degradation.13 A study in rats suggests interactions of lead exposure and early stress on the dopaminergic system.23
One long-term study found no immediate increased ADHD risk in people with past lead exposure, but increased externalizing behaviors and increased addiction risks.24
Lead disposition during pregnancy may increase ADHD risk. See above.
Even a lead content in drinking water below the limit values is said to be problematic.25
Increased lead absorption can occur from old water pipes. In principle, lead water pipes pose little risk in areas with calcareous water, since lime forms a reliably 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.

Lead increases dopaminergic activity and has been linked to attention deficits, Alzheimer’s disease, and increased drug sensitivity.26

4.2.9. Bisphenol A

Bisphenol A is suspected of increasing the risk of ADHD.6 A connection with certain MAO-A gene variants, which cause lower serotonin degradation13 and an influence on thyroid balance is discussed.27
A meta-study found a clear link between bisphenol exposure and ADS(H)S.28

4.2.10. Perfluoroalkyl compounds

Elevated levels of perfluoroalkyl compounds have been observed in ADHD.29

4.2.11. Fluoridated drinking water

In Canada, a study found that a 1 mg/liter increase in fluoride in drinking water increased the risk of ADHD by 6.1 times in 6- to 17-year-olds. Among 14-year-olds living in areas where fluoride was added to drinking water, a 2.8-fold risk of an ADHD diagnosis was found compared with 14-year-olds in areas without fluoridated drinking water. Older children responded with a higher risk.30 In contrast, fluorine urine levels did not correlate with ADHD (1,877 subjects).

In Germany, 90% of drinking water has a fluoride content of 0.3 mg/liter. Drinking water is not fluoridated in Germany.31

4.2.12. Benzene, toluene, ethylbenzene, xylene/xylene (BTEX)

Higher exposure to these airborne substances correlated with a 1.54-fold increased risk of ADHD in kindergarten-age children.32

4.2.13. Phthalates

Higher phthalate metabolites in children’s urine correlated with increased likelihood of ADHD by 3 to 9-fold.33

4.2.14. Inorganic arsenic

Those children in the 20% with the highest urinary arsenic levels were found to have a doubled risk of ADHD (OR 2.02).21

4.2.15. Synergistic effects of neurotoxins

The synergistic effects of neurotoxins should be noted:234

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

4.3. Food intolerances, allergies

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

However, individual food intolerances or allergies are just as much stressors as diseases, toxins or psychological stress and can therefore worsen the stress situation of affected individuals to such an extent that symptoms develop. This is not an ADHD-specific finding. For example, in a group of children with schizophrenia problems, dietary treatment of an existing gluten intolerance eliminated the schizophrenia symptoms in the children affected.3536 The same was found in patients with non-affective psychosis.37

To detect rarely occurring food intolerances (which, unlike allergies, cannot be detected by blood tests), an elimination diet may be helpful. However, such a diet is very difficult to implement and maintain, and is unlikely to be adhered to, especially in younger children. In particular, any advantages must be weighed against the sometimes serious social consequences.

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

When assessing the effectiveness of diets (and other “desirable” therapeutic avenues), parents often come up with assessments that far exceed what tests or teacher evaluations can confirm.

See ⇒ for more details Nutrition and diet in ADHD.

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

The primary functions of the microbiota include:38

  • Protection against pathogens by increasing mucus production and thus stabilizing the intestinal-blood barrier
  • Immune system support
  • Vitamins production
  • 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 Acetates Ethanoates 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 blood serum in ADHD compared to healthy family members found:39

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

Research found abnormalities in gut flora in children with ADHD38
ADHD correlated with leaky gut, neuroinflammation, and overactivated microglial cells. The colon microbiota exhibit a pro-inflammatory shift and harbor more gram-negative bacteria that contain immune-triggering lipopolysaccharides in their cell walls.40

Adults with ADHD had lower plasma concentrations of formic, acetic, propionic, and succinic acids than their healthy family members. Adjusting ADHD patients for SCFA-affecting factors, children had lower concentrations of formic, propionic, and isovaleric acid than adults, and those who had taken more antibiotic medications in the past two years had lower concentrations of formic, propionic, and succinic acid. 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 disruption of the developing gut microbiota can affect neurological development and potentially lead to adverse mental health outcomes later in life.41

Decreased were:

  • Bacteroides coprocola (B. coprocola)42
  • Enterococcus43
  • Faecalibacterium prausnitzii43
    • anti-inflammatory40
  • Faecalibacterium444543
    • Anti-inflammatory40
  • Lachnospiraceae bacterium43
  • Ruminococcus gnavus 43
  • Bifidobacterium
    • Anti-inflammatory40
  • Coprococcus
    • Anti-inflammatory40
  • Eucbacterium
    • anti-inflammatory40
  • Eubacterium rectale
    • anti-inflammatory40
  • Lactobacillus
    • anti-inflammatory40
  • Prevotella
    • anti-inflammatory40
  • Roseburia
    • anti-inflammatory40

Increased were

  • Bacteroides uniformis (B. uniformis)42
  • Bacteroides ovatus (B. ovatus)
    • Increase correlated with ADHD symptoms42
  • Sutterella stercoricanis (S. stercoricanis)
    • Increase correlated with intake of dairy products, nuts, seeds, legumes, iron, magnesium42
    • Increase correlated with ADHD symptoms42
  • Veillonellaceae43
  • Bacteroides caccae43
  • Odoribacter splanchnicus43
  • Paraprevotella xylaniphila43
  • Veillonella parvula43
  • Bifidobacterium46
    • 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 decreased reward anticipation, which is likely to suggest decreased levels of dopamine in the striatum. How these two seemingly contradictory pathways fit together is not explained to us at this time.
  • Eggerthella45
    • Pro-inflammatory40
  • Odoribacter45
    • Differently a study according to which Odoribacter were reduced43
  • Alistipes
    • Pro-inflammatory40
  • Flavonifractor
    • Pro-inflammatory40

No significant difference was found in the alpha diversity of the intestinal bacteria.4344

One study found that mice whose guts were contaminated with gut bacteria from people with ADHD had structural changes in the brain (white matter, gray matter, hippocampus, internal capsule), decreased connectivity between motor and visual cortices right in the resting state, and and higher anxiety than mice in which gut bacteria from people without ADHD were used.47

A single-case study reported improvement in ADHD symptoms in a young woman with intestinal bacterial exchange that occurred in relation to a recurrent Clostridioides difficile infection.48

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.49

4.6. (Untreated) type 1 diabetes

A study among diabetes sufferers with and without treatment using an insulin pump found a 2.45-fold increased risk of ADHD in those with type 1 diabetes who were not treated, with ADHD considered a risk factor for inconsistent diabetes treatment.50

4.7. Phenlylketonuria (PKU)

Phenylketonuria (Følling disease, phenylpyruvic acid oligophrenia) is a genetically caused metabolic disorder by which the amino acid phenylalanine cannot be broken down to tyrosine due to the lack of the enzyme phenylalanine hydroxylase (PAH). Tyrosine, in turn, is required for the synthesis of dopamine, so dopamine deficiency is a consequence of PKU.51 PKU has a prevalence of 1 in 8000 people.

One study found an ADHD rate of 38% in phenlylketonuria despite adequate treatment.52
ADHD is also associated with dopamine deficiency.

4.8. Anabolic androgenic steroids (AAS)

Power athletes who take anabolic androgenic steroids are significantly more likely to have ADHD than power athletes who do not.53

4.9. Viral infections

4.9.1. Enteroviruses in general

(Non-polio) enteroviruses cause a good half of all cases of aseptic meningitis, making them among the most important known causes.54 In addition to encephaltitis55, (non-polio) enteroviruses also frequently cause febrile illness, hand-foot-and-mouth disease, herpangina, aseptic meningitis, and encephalitis, as well as sometimes severe 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.00000000000707. PMID: 25906098; PMCID: PMC4602682.))

4.9.2. Enterovirus A71 (EV-A71)

A longitudinal study of 43 adolescents who had a central nervous system infection with enterovirus A71 (EV-A71) between the ages of 6 and 18 years found ADHD in 34.9%. This more than triples the risk of ADHD. In addition, increased autistic symptoms were found. Other psychiatric diagnoses were not elevated.56 Another study found ADHD particularly prevalent when A71 infection was associated with cardiopulmonary failure.57
EV-A71 often shows weakness, limb atrophy, seizures, hand-foot-mouth disease, encephalitis, and decreased intelligence.

4.9.3. HIV

A study of children and adolescents with HIV in stable health found ADHD symptoms in 20%.58

4.9.4. Zoster encephalitis

In an isolated case, ADHD was mentioned in association with zoster encephalitis.59

4.10. Bacterial infections

Periodontal disease is a bacterial inflammation of the gums caused by the bacterium P. gingivalis, which secretes toxins. Periodontal disease and is described as a risk factor for ADHD.60


  1. 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.

  2. http://www.adhs.org/genese/

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

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

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

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

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

  8. 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

  9. 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.

  10. 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

  11. 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

  12. 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.

  13. 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

  14. 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.

  15. 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

  16. 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.

  17. 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

  18. 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.

  19. 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

  20. 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.

  21. 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.

  22. 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.

  23. 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.

  24. 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.

  25. http://www.adhs.org/genese/ mit weiteren Nachweisen

  26. 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

  27. 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.

  28. 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

  29. 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.

  30. 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

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

  32. 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

  33. 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.

  34. 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.

  35. 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

  36. 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.

  37. 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.

  38. 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

  39. 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

  40. 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.

  41. 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

  42. 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.

  43. 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.

  44. 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

  45. 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. METASTUDY

  46. 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.

  47. 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.

  48. 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.

  49. 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.

  50. 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

  51. 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.

  52. 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

  53. 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.

  54. 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.

  55. 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.

  56. 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.

  57. 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.

  58. 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

  59. 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.

  60. 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.

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