Dear reader of ADxS.org, please excuse the disruption.

ADxS.org needs around €58,500 in 2024. Unfortunately 99,8 % of our readers do not donate. If everyone reading this appeal made a small contribution, our fundraising campaign for 2024 would be over after a few days. This appeal is displayed 23,000 times a week, but only 75 people donate. If you find ADxS.org useful, please take a minute to support ADxS.org with your donation. Thank you very much!

Since 01.06.2021 ADxS.org is supported by the non-profit ADxS e.V. Donations to ADxS e.V. are tax-deductible in Germany (up to €300, the remittance slip is sufficient as a donation receipt).

If you would prefer to make an active contribution, you can find ideas for Participation or active support here.

$45213 of $63500 - as of 2024-10-31
71%
ADxS.org Logo
ADxS.org Logo
Search Donations Addresses Recent changes ADHS-Forum Deutsche Version
Register

Already have an account? Login

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

Sitemap

The ADxS.org project
Abstract from ADxS.org
Symptoms
Consequences of ADHD
Origin
Stress
Neurological aspects
Diagnostics
Prevention
Treatment: Guide and Effect size
Treatment: Medication for ADHD
Non-drug treatment
Addresses
This and that about ADHD
Tests and surveys
Forum

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

Previous page Next page

Author: Ulrich Brennecke
Review: Dipl.-Psych. Waldemar Zdero

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 children’s urine correlated with increased likelihood of ADHD by 3 to 9 times.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 by 6.1 times in 6- to 17-year-olds. 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 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.1011121314 A blood lead level of ≥ 5 μg/dl was found to increase the risk of ADHD by 1.33 (OR 2.33).15

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 exposure16
    • in the nucleus accumbens17
  • Increased dopamine signaling
    • in mesolimbic pathways (nucleus accumbens)18
    • Lead increases dopaminergic activity and has been linked to attention deficits, Alzheimer’s disease and increased drug sensitivity.19

The DRD2 gene variant rs1800497r is said to promote a link between ADHD and lead.20 A connection to certain MAO-A gene variants is also mentioned, which causes lower serotonin degradation.21 A study in rats suggests interactions between lead exposure and early stress on the dopaminergic system.22 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 addiction23

In one study, lead altered neostriatal serotonin and norepinephrine levels, increased anxiety and decreased open-field activity.24

Lead exposure during pregnancy may increase the risk of ADHD. See there.
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 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 barely 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.26

4.1.4. Inorganic arsenic (+ 102 %)

Those children who were among the 20% with the highest urinary arsenic levels were found to have double the risk of ADHD (OR 2.02).15

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.27

4.1.6. Smoking by parents (+ 30 %)

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

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.3132

Even low levels of PCB exposure during development impair neurobiological, cognitive and behavioral functions.32
One study found a 26% to 92% increased risk of ADHD.33 Individual studies found contradictory or weak impairments,3435 however, the vast majority show evidence of relevance in ADHD.2836

Polychlorinated biphenyls affect the dopamine system.37 PCBs inhibit dopamine synthesis as well as the storage of dopamine in the vesicles and its release, thereby causing low dopamine levels3813 in the basal ganglia and PFC3940 38 41 42 43 , as well as reduced DAT in the striatum44, 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)3813
  • IQ, memory, attention 45
  • Memory, attention46
  • Impulsivity (via corpus callosum)4748 in rats even at subtoxic doses3813
  • 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.37
  • no effect on sustained attention34

4.1.8. Polyvinyl chloride (PVC)

One review describes a suspected correlation between PVC exposure and ADHD.49

4.1.9. Pesticides

With regard to pesticides (especially organochlorine compounds, pyrethroids, organophosphates), there are indications of relevance in ADHD.2813

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.281350

A study of Greek schoolchildren with ADHD found no elevated blood serum levels of51

  • 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 3252 53 54 50 55 or a theoretically possible increase in ADHD risk.56 One source suggests an increased risk of ADHD from organophosphates, particularly when coinciding with a particular MAO-A gene variant that causes lower serotonin degradation.21
In contrast, two larger studies found no influence 5758
With regard to hyperactivity, 2 studies found an association between organophosphates and hyperactivity, 4 studies found no association.59
One study found no correlation of chlorpyrifos with hyperactivity in rats60 while another found it in females.61
A study in rats was able to induce ADHD-like behaviors in Wystar and SHR rats by organophosphates and found strong circumstantial evidence that these are mediated by reductions in fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) via the cannabinoid receptor.62
Blood values were measured in Egyptian adolescents, some of whom used pesticides, and the parents were asked about ADHD symptoms in the adolescents:63 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.55

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 64 Other studies also found an association with ADHD6550 , ASD or developmental delay.32
Blood levels were measured in Egyptian adolescents, some of whom used pesticides, and the parents were asked about ADHD symptoms in the adolescents:63 A correlation to ADHD was found in relation to the pyrethroid λCH through the measured value Cis-DCCA (all persons with ADHD reported clinical ADHD symptoms).

4.1.9.4. Carbamate (-)

One review found no associations between carbamates and ADHD.50

4.1.9.5. Neonicotinoids (- ?)

One review found no links between neonicotinoids and ADHD, although there were few studies on this topic.50

4.1.10. Mercury / Amalgam (Mercury)

There is weak evidence (= not proven) of relevance in ADHD.281366
A large study with n = 2073 participants was unable to establish a connection between amalgam and ADHD.67
Mercury is also suspected of being a possible contributory cause of Parkinson’s disease.68 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, but not in blood levels, of people with ADHD.2869
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.26
A doubling of the manganese content in teeth from the prenatal and postnatal period increased the risk of attention problems and ADHD symptoms in the school years by 5%. Manganese from the childhood period showed no influence70
A study reports benefits of choline supplementation during pregnancy in rats to prevent manganese-induced developmental disorders in the offspring71

4.1.12. Bisphenol A

Bisphenol A is suspected of increasing the risk of ADHD.13 A connection with certain MAO-A gene variants that cause lower serotonin degradation21 and an influence on the thyroid balance is being discussed.72
A meta-analysis found a clear link between bisphenol exposure and ADD(H)S.73

4.1.13. Perfluoroalkyl compounds

Elevated levels of perfluoroalkyl compounds have been observed in ADHD.74

4.1.14. Triclosan

Prolonged exposure to the environmental pollutant triclosan induced ADHD symptoms in rats. Triclosan appears to cause a reduction in dopamine levels in the PFC.75

A 60-day continuous exposure of rats to triclosan caused ADHD-like behavior in the offspring. It activated microglia in the PFC, which led to the release of inflammatory factors. In vitro, triclosan increased the levels of inflammatory cytokines, including IL-1β, IL-6 and TNF-α, in HMC3 cells. In addition, triclosan upregulated PKM2 via hnRNPA1, which affects the STAT3 signaling pathway and thus continuously activates microglia, promoting the release of inflammatory cytokines.76

4.1.15. Synergy effects of neurotoxins

The synergistic effects of neurotoxins must be taken into account:2877

  • 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.78

It remains to be seen whether breathing interruptions during sleep can cause such stress 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 have 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 people with ADHD 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 was able to eliminate the schizophrenia symptoms in the children affected by this.7980 The same was found in people with ADHD and non-affective psychosis.81

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 - in carriers of certain gene variants of the genes that encode histamine-degrading enzymes - increase ADHD symptoms82

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 maintain and is barely adhered to, especially 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-brain axis, gut bacteria, gut flora

See under Gut-brain axis

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.83

4.6. (Untreated) type 1 diabetes

A study of persons with ADHD with and without insulin pump treatment found a 2.45-fold increased risk of ADHD in untreated people with type 1 diabetes, with ADHD considered a risk factor for inconsistent diabetes treatment.84

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, so dopamine deficiency is a consequence of PKU.85 PKU has a prevalence of 1 in 8000 people.

One study found an ADHD rate of 38% in phenylketonuria despite adequate treatment.86
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.87

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 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 of88

  • 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.89 In addition to encephaltitis90, (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 who had a central nervous system infection with enterovirus A71 (EV-A71) between the ages of 6 and 18 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.9192 Another study found ADHD to be particularly common when the A71 infection was accompanied by cardiopulmonary failure.93
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 stable health found ADHD symptoms in 20%.94

4.9.2.4. Zoster encephalitis

In one isolated case, ADHD was mentioned in association with zoster encephalitis.95

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 and is described as a risk factor for ADHD.96

4.9.4. Parasitic infections

A study of 100 children with ADHD and 100 healthy children found a correlation of ADHD with:97

  • 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%98

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 people with ADHD99, other studies found only a tendency100 or no association.101

4.12. Lipodystrophy (lack of fatty tissue)

One study found evidence of a greatly increased prevalence of ADHD in lipodystrophy.102

4.13. Dystrophinopathy (muscular dystrophy, muscle weakness)

One study found evidence of a greatly increased ADHD prevalence of 18.4% for dystrophinopathy and 12.73% for ASD.103
There are also links between ADHD gene candidates and genes associated with dystrophies. See there.

4.14. Hyperthyroidism / hypothyroidism

In addition to other cognitive deficits, hyperthyroidism can also cause inattention and hyperarousal. Depending on the degree of hypothyroidism, the cognitive effects can range from mild impairment of memory and attention to complete dementia.104105

The THRA gene encodes the thyroid receptor alpha, TRα1, TRHB the thyroid receptor isoforms TRβ1 and TRβ2.
The pituitary hormone TSH (thyroid-stimulating hormone) stimulates the thyroid gland to produce thyroxine (T4; prohormone) and then triiodothyronine (T3). The thyroid hormones (T3 and T4) in the blood in turn regulate the pituitary release of TSH within the hypothalamic-pituitary-thyroid axis, which is mediated by the receptor isoform TRβ2.

In the case of a (rarely occurring genetic) resistance to thyroid hormone β, this negative feedback loop, which stabilizes the TH level in the blood, is disrupted. This leads to increased TH and unsuppressed, i.e. normal TSH levels106

4.15. Gender diversity

A multinational study found evidence that the frequency and severity of ADHD symptoms was particularly high in gender-diverse individuals.107

4.16. Factors without relevant contribution

4.16.1. High blood pressure

One study found no statistical significance for a genetic link between high blood pressure and ADHD.108

4.16.2. COVID-19 gene therapy

Gene predisposition, which makes people more susceptible to COVID-19, showed no signs of an increased risk of ADHD. Conversely, however, ADHD and Tourette’s are associated with an increased risk of COVID-19 and a more severe course of COVID-19.109

  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. Rosenauer V, Schwarz MI, Vlasak T, Barth A (2024): Childhood lead exposure increases the risk of attention-deficit-hyperactivity disorder: A meta-analysis. Sci Total Environ. 2024 Nov 15;951:175574. doi: 10.1016/j.scitotenv.2024.175574. PMID: 39153625. REVIEW ↥

  11. 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 ↥

  12. 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. ↥

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

  14. 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. ↥

  15. 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. ↥ ↥

  16. 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. ↥

  17. 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 ↥

  18. 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. ↥

  19. 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 ↥

  20. 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. ↥

  21. 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 ↥ ↥ ↥

  22. 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. ↥

  23. 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. ↥

  24. 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. ↥

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

  26. 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. ↥ ↥

  27. 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 ↥

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

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

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

  31. 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 ↥

  32. 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 ↥ ↥ ↥ ↥

  33. 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. ↥

  34. 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. ↥ ↥

  35. 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 ↥

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

  37. 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. ↥ ↥

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

  39. 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 ↥

  40. 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. ↥

  41. 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. ↥

  42. 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. ↥

  43. 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. ↥

  44. 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. ↥

  45. 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. ↥

  46. 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. ↥

  47. 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. ↥

  48. 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. ↥

  49. 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 ↥

  50. 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 ↥ ↥ ↥ ↥ ↥

  51. 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. ↥

  52. 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. ↥

  53. (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. ↥

  54. 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 ↥

  55. 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. ↥ ↥

  56. 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. ↥

  57. 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 ↥

  58. 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 ↥

  59. 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. ↥

  60. 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. ↥

  61. 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. ↥

  62. 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. ↥

  63. 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 ↥ ↥

  64. 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. ↥

  65. 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. ↥

  66. 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. ↥

  67. 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 ↥

  68. 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 ↥

  69. 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. ↥

  70. Schildroth S, Bauer JA, Friedman A, Austin C, Coull BA, Placidi D, White RF, Smith D, Wright RO, Lucchini RG, Arora M, Horton M, Claus Henn B (2023): Early life manganese exposure and reported attention-related behaviors in Italian adolescents. Environ Epidemiol. 2023 Oct 19;7(6):e274. doi: 10.1097/EE9.0000000000000274. PMID: 38912396; PMCID: PMC11189689. ↥

  71. 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. ↥

  72. 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. ↥

  73. 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 ↥

  74. 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. ↥

  75. Cui H, Shu C, Peng Y, Wei Z, Ni X, Zheng L, Shang J, Liu F, Liu J (2024): Long-life triclosan exposure induces ADHD-like behavior in rats via prefrontal cortex dopaminergic deficiency. Ecotoxicol Environ Saf. 2024 Jul 23;282:116766. doi: 10.1016/j.ecoenv.2024.116766. PMID: 39047361. ↥

  76. Shu C, Cui H, Peng Y, Wei Z, Ni X, Zheng L, Shang J, Liu F, Liu J (2024): Understanding the molecular pathway of triclosan-induced ADHD-like behaviour: Involvement of the hnRNPA1-PKM2-STAT3 feedback loop. Environ Int. 2024 Sep;191:108966. doi: 10.1016/j.envint.2024.108966. PMID: 39167854. ↥

  77. 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. ↥

  78. 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. ↥

  79. 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 ↥

  80. 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. ↥

  81. 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. ↥

  82. 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 ↥

  83. 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. ↥

  84. 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 ↥

  85. 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. ↥

  86. 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 ↥

  87. 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. ↥

  88. 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. ↥

  89. 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. ↥

  90. 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. ↥

  91. 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. ↥

  92. 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 ↥

  93. 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. ↥

  94. 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 ↥

  95. 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. ↥

  96. 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. ↥

  97. 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. ↥

  98. 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. ↥

  99. 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 ↥

  100. 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 ↥

  101. 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 ↥

  102. Demir T, Simsir IY, Tuncel OK, Ozbaran B, Yildirim I, Pirildar S, Ozen S, Akinci B (2024): Impact of lipodystrophy on health-related quality of life: the QuaLip study. Orphanet J Rare Dis. 2024 Jan 5;19(1):10. doi: 10.1186/s13023-023-03004-w. PMID: 38183080; PMCID: PMC10768358. ↥

  103. Diehl E, O’Neill M, Gray L, Schwaede A, Kuntz N, Rao VK (2024): Prevalence of Attention-Deficit/Hyperactivity Disorder and Autism Spectrum Disorder in Individuals With Dystrophinopathy at a Tertiary Care Center in Chicago. Pediatr Neurol. 2024 May 19;158:94-99. doi: 10.1016/j.pediatrneurol.2024.05.011. PMID: 39024712. ↥

  104. Göbel A, Heldmann M, Göttlich M, Dirk AL, Brabant G, Münte TF (2016): Effect of Mild Thyrotoxicosis on Performance and Brain Activations in a Working Memory Task. PLoS One. 2016 Aug 18;11(8):e0161552. doi: 10.1371/journal.pone.0161552. PMID: 27536945; PMCID: PMC4990413. ↥

  105. Bauer M, Goetz T, Glenn T, Whybrow PC (2008): The thyroid-brain interaction in thyroid disorders and mood disorders. J Neuroendocrinol. 2008 Oct;20(10):1101-14. doi: 10.1111/j.1365-2826.2008.01774.x. PMID: 18673409. REVIEW ↥

  106. Göttlich M, Chatterjee K, Moran C, Heldmann M, Rogge B, Cirkel A, Brabant G, Münte TF (2024): Altered brain functional connectivity in patients with resistance to thyroid hormone ß. PLoS One. 2024 Aug 22;19(8):e0306538. doi: 10.1371/journal.pone.0306538. PMID: 39172991; PMCID: PMC11341041. ↥

  107. Lewczuk K, Marcowski P, Wizła M, Gola M, Nagy L, Koós M, Kraus SW, Demetrovics Z, Potenza MN, Ballester-Arnal R, Batthyány D, Bergeron S, Billieux J, Briken P, Burkauskas J, Cárdenas-López G, Carvalho J, Castro-Calvo J, Chen L, Ciocca G, Corazza O, Csako RI, Fernandez DP, Fujiwara H, Fernandez EF, Fuss J, Gabrhelík R, Gewirtz-Meydan A, Gjoneska B, Grubbs JB, Hashim HT, Islam MS, Ismail M, Jiménez-Martínez MC, Jurin T, Kalina O, Klein V, Költő A, Lee SK, Lin CY, Lin YC, Lochner C, López-Alvarado S, Lukavská K, Mayta-Tristán P, Miller DJ, Orosová O, Orosz G; Sungkyunkwan University’s research team; Ponce FP, Quintana GR, Quintero Garzola GC, Ramos-Diaz J, Rigaud K, Rousseau A, Tubino Scanavino M, Schulmeyer MK, Sharan P, Shibata M, Shoib S, Sigre-Leirós V, Sniewski L, Spasovski O, Steibliene V, Stein DJ, Ünsal BC, Vaillancourt-Morel MP, Claire Van Hout M, Bőthe B (2024): Cross-Cultural Adult ADHD Assessment in 42 Countries Using the Adult ADHD Self-Report Scale Screener. J Atten Disord. 2024 Feb;28(4):512-530. doi: 10.1177/10870547231215518. PMID: 38180045. ↥

  108. 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. ↥

  109. 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. ↥

Diese Seite wurde am 27.10.2024 zuletzt aktualisiert.
Previous page Next page