4. Age-independent physical stress as 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
- 4.2.1. Parents smoking
- 4.2.2. Polychlorinated biphenyls (PCBs) / Polychlorinated biphenyl ethers
- 4.2.3. Polyvenyl chloride (PVC)
- 4.2.4. Pesticides
- 4.2.5. Mercury / Amalgam (Mercury)
- 4.2.6. Manganese or formaldehyde
- 4.2.7. Lead (Lead)
- 4.2.8. Bisphenol A
- 4.2.9. Perfluoroalkyl compounds
- 4.2.10. Fluoridated drinking water
- 4.2.11. Benzene, toluene, ethylbenzene, xylene/xylene (BTEX)
- 4.2.12. Phthalates
- 4.2.13. Inorganic arsenic
- 4.2.14. Synergistic effects of neurotoxins
- 4.3. Food intolerances, allergies
- 4.4. Gut bacteria, Gut-brain-axis (gut-brain-axis)
- 4.5. Polycystic ovary syndrome (PCOS)
- 4.6. (Untreated) type 1 diabetes
- 4.7. Phenlylketonuria (PKU)
- 4.8. Anabolic androgenic steroids (AAS)
- 4.9. Viral infections
- 4.10. Bacterial infections
4.1. Breathing pauses during sleep
Breathing pauses in children’s sleep can trigger cognitive distress, causing symptoms that resemble ADHD.1
It is an open question whether breathing cessations during sleep may represent such a stress load that they may contribute to ADHD through epigenetic changes, or whether they merely cause symptoms resembling those of ADHD. In the latter case, people who did not previously have ADHD and who developed ADHD (like) symptoms due to breathing cessations during sleep would have to have these symptoms completely disappear again after elimination of the breathing cessations during sleep. We are not aware of any studies on this to date.
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, about 25% less of the total population smoke, 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
On pesticides in pregnancy and ADHD, see above.
22.214.171.124. Organochlorine compounds
A study of Greek schoolchildren with ADHD found no elevated blood serum levels of9
- Dichlorodiphenyltrichloroethane (DDT) Metabolites
- Hexachlorocyclohexane (HCH) isomers
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 specific 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
4.2.5. Mercury / Amalgam (Mercury)
4.2.6. Manganese or formaldehyde
4.2.7. Lead (Lead)
A connection between ADHD and lead is said to exist in particular if affected individuals have the DRD2 gene variant rs1800497r.21 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.22
A long-term study found no immediate increased ADHD risk in people with previous lead exposure, but increased externalizing behaviors and increased addiction risks.23
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.24
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.25
4.2.8. Bisphenol A
Bisphenol A is suspected of increasing the risk of ADHD.6 A connection with certain MAO-A gene variants that cause lower serotonin degradation is mentioned13 and an influence on thyroid balance is discussed.26
4.2.9. Perfluoroalkyl compounds
Elevated levels of perfluoroalkyl compounds have been observed in ADHD.27
4.2.10. 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-fold in 6- to 17-year-olds. 14-year-olds living in areas where fluoride was added to drinking water were found to have a 2.8-fold risk of an ADHD diagnosis compared with 14-year-olds in areas without fluoridated drinking water. Older children responded with a higher risk.28 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.29
4.2.11. 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.30
Higher phthalate metabolites in children’s urine correlated with increased likelihood of ADHD by 3 to 9-fold.31
4.2.13. 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).20
4.2.14. Synergistic effects of neurotoxins
- 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 assured 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.3334 The same was found in patients with non-affective psychosis.35
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.
For more details, see ⇒ Nutrition and diet in ADHD.
4.4. Gut bacteria, Gut-brain-axis (gut-brain-axis)
The primary functions of the microbiota include:36
- 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
Studies found abnormalities in gut flora in children with ADHD.36
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.37
Early disruption of the developing gut microbiota can affect neurological development and potentially lead to adverse mental health outcomes later in life.38
- Bacteroides coprocola (B. coprocola)39
- Faecalibacterium prausnitzii40
- Lachnospiraceae bacterium40
- Ruminococcus gnavus 40
- Eubacterium rectale
- Bacteroides uniformis (B. uniformis)39
- Bacteroides ovatus (B. ovatus)
- Increase correlated with ADHD symptoms39
- Sutterella stercoricanis (S. stercoricanis)
- Bacteroides caccae40
- Odoribacter splanchnicus40
- Paraprevotella xylaniphila40
- Veillonella parvula40
- 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.
- Differently a study according to which Odoribacter were reduced40
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.44
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.45
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.46
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.47 PKU has a prevalence of 1 in 8000 people.
One study found an ADHD rate of 38% in phenlylketonuria despite adequate treatment.48
ADHD is also related to 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.49
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.50 In addition to encephaltitis51, (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 increased ADHD risk 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 ADHD risk. In addition, increased autistic symptoms were found. Other psychiatric diagnoses were not elevated.52 Another study found ADHD particularly prevalent when A71 infection was associated with cardiopulmonary failure.53
EV-A71 often shows weakness, limb atrophy, seizures, hand-foot-mouth disease, encephalitis, and decreased intelligence.
A study of children and adolescents with HIV in stable health found ADHD symptoms in 20%.54
4.9.4. Zoster encephalitis
In an isolated case, ADHD was mentioned in association with zoster encephalitis.55
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.56
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