Brain development, structure and function can suffer from a number of adverse environmental influences. A paper published in the journal Acta Pædiatrica review some of the environmental risk factors for ADHD.
“Converging evidence from epidemiologic, neuropsychology, neuroimaging, genetic and treatment studies shows that ADHD is a valid medical disorder…The majority of studies performed to assess genetic risk factors in ADHD have supported a strong familial nature of this disorder…However, several biological and environmental factors have also been proposed as risk factors for ADHD, including food additives/diet, lead contamination, cigarette and alcohol exposure, maternal smoking during pregnancy, and low birth weight.“
The authors review numerous studies that examine some these extraneous risk factors. They conclude by stating:
“Although a substantial fraction of the aetiology of ADHD is due to genes, the studies reviewed in this article show that many environmental risk factors and potential gene–environment interactions also increase the risk for the disorder.”
A study published in the journal Neuropediatrics investigates specifically the association between blood levels of mercury and ADHD in Hong Kong children:
“Fifty-two children with ADHD aged below 18 years diagnosed by DSM IV criteria without perinatal brain insults, mental retardation or neurological deficits were recruited from a developmental assessment center. Fifty-nine normal controls were recruited from a nearby hospital. Blood mercury levels were measured by cold vapor atomic absorption spectrophotometry.”
The authors uncovered a significant difference in blood mercury levels between the children with ADHD and the controls (‘normal’ children) which remained apparent after adjusting for age, gender and parents’ occupations:
“Children with blood mercury level above 29 nmol/L had 9.69 times higher risk of having ADHD after adjustment for confounding variables.”
The average blood mercury levels were higher for both the inattentive and combined subtypes of ADHD. Let’s bear in mind that this is one possible causal factor among many, not ‘THE’ cause. The authors conclude by stating:
“High blood mercury level was associated with ADHD. Whether the relationship is causal requires further studies.”
We can see a similar biological mechanism at play when we consider research recently published in Pediatric Allergy and Immunology that examines the association of heavy metals and Tourette syndrome. The authors state:
“Tourette syndrome (TS) is a childhood-onset and relapsing disorder characterized by involuntary simple or complex tics and high co-morbidity with behavioral anomalies…We investigated immunologic alternations and serum heavy metal levels in patients with TS to elucidate the unclarified mechanisms.”
Their findings illuminate a key point:
“In exacerbation, there were reverse CD4/CD8 (in two), higher percentages of natural killer cells (in five) and memory T cells (in eight), diminished lymphocyte activation CD69 marker (in three) and impaired NK cytotoxicity (in six) that showed a trend of lower inhibitory CD94 (NKG2A), activating NKp46, and perforin expression compared to those of patients with stable TS and healthy controls…Serum ASLO, mycoplasma antibody and the levels of heavy metals were not significantly different.”
In other words, the levels of heavy metals were pretty much the same but the immune system reaction to them was different. This is why it is impossible to make absolute statements about sub-acute levels of any heavy metal or toxin. Whether it elicits a dysregulated immune response leading to brain inflammation depends on the individual. The authors note this in their conclusion:
“Our study demonstrated that, in some patients with TS, consistently higher memory T cells and lower cytotoxicity in exacerbation status reflect immune alterations and underscore the potential for immunomodulation or immunosuppressive treatment.”
A paper published not long ago in Annals of Clinical Psychiatry carries the point further. The authors summarize the laboratory findings and other data in evidence for an autoimmune pathogenesis for autism:
“ Autoimmune markers were analyzed in the sera of autistic and normal children, but the cerebrospinal fluid (CSF) of some autistic children was also analyzed. Laboratory procedures included enzyme-linked immunosorbent assay and protein immunoblotting assay.”
Their findings certainly revealed the fire behind the smoke:
“Autoimmunity was demonstrated by the presence of brain autoantibodies, abnormal viral serology, brain and viral antibodies in CSF, a positive correlation between brain autoantibodies and viral serology, elevated levels of proinflammatory cytokines and acute-phase reactants, and a positive response to immunotherapy. Many autistic children harbored brain myelin basic protein autoantibodies and elevated levels of antibodies to measles virus and measles-mumps-rubella (MMR) vaccine. Measles might be etiologically linked to autism because measles and MMR antibodies (a viral marker) correlated positively to brain autoantibodies (an autoimmune marker)—salient features that characterize autoimmune pathology in autism. Autistic children also showed elevated levels of acute-phase reactants—a marker of systemic inflammation.”
Here again we see why it is impossible to argue for an environmental factor (heavy metal, virus, vaccine) as an absolute cause for autism or any other condition. Children at risk are those whose immune system is dysregulated and predisposed to an autoimmune triggering agent.
The authors state in their conclusion:
“The scientific evidence is quite credible for our autoimmune hypothesis, leading to the identification of autoimmune autistic disorder (AAD) as a major subset of autism. AAD can be identified by immune tests to determine immune problems before administering immunotherapy.”
We can also consider mild traumatic brain injury as a kind of ‘environmental risk factor’ for disorders neurodevelopment, learning and behavior. A study just published in the journal Pediatrics tests the link between postconcussion syndrome (PCS) and brain injury:
“Much disagreement exists as to whether postconcussion syndrome (PCS) is attributable to brain injury or to other factors such as trauma alone, preexisting psychosocial problems, or medicolegal issues. We investigated the epidemiology and natural history of PCS symptoms in a large cohort of children with a mild traumatic brain injury (mTBI) and compared them with children with an extracranial injury (ECI).”
The authors followed 670 children with mTBI and 197 children with ECI (non-cranial injury) and used the the Post Concussion Symptom Inventory, Rivermead Postconcussion Symptom Questionnaire, Brief Symptom Inventory, and Family Assessment Device to determine outcomes. Their data led to this conclusion:
“Among school-aged children with mTBI, 13.7% were symptomatic 3 months after injury. This finding could not be explained by trauma, family dysfunction, or maternal psychological adjustment. The results of this study provide clear support for the validity of the diagnosis of PCS in children.“
Environmental factors can be so severe that anyone would be affected. For most, however, the response depends on the individual. A skilled and experienced clinician knows when and where to focus suspicion. In the functional medicine model there are numerous resources available to test objectively when a question about environmental factors needs an answer, followed by the appropriate therapies when indicated.
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