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


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

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. 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 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 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). Carbamate (-)

One review found no association between carbamates and ADHD.49 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 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 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 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.)) 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. HIV

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

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

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