The Environment and Autism

While attending IMFAR 2016 I had the opportunity to listen to the plenary lecture on environment and autism by Irva Hertz Picciotto. In the opinion of many Irva is the top environmental epidemiologist in our nation. She presently works at UC Davis within the Department of Public Health, where she joined the MIND institute in 2000, and is the Director of an NIH-funded study called CHARGE. The latter is the first large-scale comprehensive study of environmental risk factors in autism.

Irva’s lecture started by mentioning historical antecedents of environmental pollutants, primarily metals, causing neuropsychiatric disorders. These chemical agents are poisonous to animals and humans and are presently considered neurotoxins that accumulate in, among other tissues, the brain causing damage to the same. Among the most prominent offenders was the chemical element lead, which causes seizures and abdominal symptoms. Levels of lead in the teeth of children are associated with diminished intellectual abilities, impaired auditory processing and an increase in behavioral problems. Lead was considered the culprit of a “silent epidemic” that affected thousands of children until laws were enacted restricting its use in paints. (Note: lead was an additive in paints used to speed up drying and increase durability, that is, a fresh appearance). In a similar way another chemical element, mercury, causes physical and mental disabilities. Curiously both high and low levels of mercury are considered harmful and play a role in congenital defects. What we learned about this early history of environmental epidemiology is that there is a particular vulnerability for children to the effects of these toxins, especially when exposed during pregnancy when the brain is still developing.

In terms of autism, Irva went on to dispel many myths regarding the etiology of autism. These myths included: 1) There is a single cause responsible for all cases of autism, 2) It is all genetic, 3) It is all environmental (e.g., nutritional, neighborhood location), and 4) It is the parent’s fault. Indeed, Irva argued that recent evidence supports a multifactorial genesis for autism.

A major part of Irva’s lecture went to discuss whether there has been a real increase in the prevalence rates of autism. Her own studies showed a 600% increase in prevalence over the past couple of decades. The painstaking research showed that changes in DSM criteria accounted for 120% of the increase, the trend towards a younger diagnosis accounted for 44%, broadening of criteria to include milder cases accounted for 56%, and older age of mothers accounted for 4%. Overall, even when accounting for diagnostic substitution (e.g., cases of intellectual disability now being diagnosed as autistics), the reasons for explaining the increased prevalence accounted for only a portion of the increase, a far cry from the reported 600%. The available results leave a lot to explain.

Regarding the increased prevalence rates Irva explained the misconception that because the rates were increasing the cause(s) should also be increasing. In effect if we considered the possibility of multiple causation some risk factors could be increasing while others could be decreasing. In order to answer some of these questions, Irva started the CHARGE study at the MIND Institute. This study has 3 arms: children with autism, children with environmental delays, and a control group. They have detailed physical, laboratory and history examination. The study focuses on environmental exposures: 1) pesticides, 2) metals, 3) organic pollutants, 4) viruses and bacterias, 5) medical procedures, and 6) nutritional factors. Results from the CHARGE study and a revision of the literature has made Irva suggest a number of risk factors for autism. These risk factors include (note: the strength of the association is marked by the number of +) : both maternal and paternal age ++++, diabetes in mother +++, short interpregnancy interval ++, pesticides ++, and season of conception at birth ++. Other risk factors discussed in the literature, like smoking, have offered contradictory findings and are in need of further study.

Note: The lecture did not touch upon the recent report by the CCD claiming a stabilization of the prevalence rates. Also, Irva’s subject population has come from California. It would be interesting to see whether the results can be generalized to other states and countries.




3 responses to “The Environment and Autism

  1. I agree with Irva’s statement that “autism” cause is multifactorial like many other psychiatric anomalies. “Autism” is an uncertain diagnosis in the absence of established biomarkers. The suggested astronomical number of epistatic combinations of SNPs, (Koefoed and Mellerup Genet Epidemiol. 2011 Jul;35(5):318-32.) like other psychiatric anomalies, are also reported as the major influence. In addition, far more parents than ever take their children to a physician for a diagnosis of sometimes minor behavioral responses. This last I suggest as the major increase.
    I also agee with “the increased prevalence rates Irva explained the misconception that because the rates were increasing the cause(s) should also be increasing.”

    Liked by 1 person

  2. Interesting research. For our son, the issue was lead. However, we switched pediatricians four times before someone thought to check this. Because the issue was lead, chelation was miraculous for him.

    His zinc levels were also very low due to the lead poisoning. While we were going through chelation and for quite some time after, we supplemented with zinc. His bruxism also went away.

    Wonderful research by UC Davis. Hope this makes it mainstream!


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