A Review of “Evidence of toxicity, oxidative stress, and neuronal insult in autism”
Kern & Jones (2006) is the propounding of a theory of the etiology of autism, via neuronal cell death and is deeply connected to the descriptive autism epidemiology. It is marred by the severe problems in the epidemiology referenced.
Kern & Jones (2006) have written a theory based on a review of literature advocating that some individuals’ autism could be caused by neuronal cell death or damage, shortly after birth, via environmental factors. They further propose that these persons were selectively susceptible to the environmental factors. They propose the view that some autistic children may “be like the canary in the coal mine, exposing policy and/or environmental issues that need to be addressed” (Kern & Jones, 2006).
In this review I will advocate the view that Kern & Jones theory is deeply tied to the descriptive epidemiology. I will also point out the problems with the epidemiology referenced therein.
Criticism of Epidemiology Referenced
Criticism of USDE Data
Kern & Jones cite the Autism Society of America's (ASA) claim that there is an autism epidemic. This is factual in that the ASA has indeed loudly and clearly claimed that the US is undergoing an autism epidemic. At one point, the Autism Society of America was alarmed enough to send out an email to their list subscribers (Gernsbacher, Dawson, Goldsmith, 2005).
The ASA bases this conclusion on a review of the United States Department of Education (USDE) yearly reports to the US Congress on the implemenetation of the Individuals with Disabilities Education Act (IDEA), which includes various data on child counts from every State.
The problem is that these data in no way constitute reliable/valid descriptive epidemiology. Laidler (2005) points out that an assignment to the autism category is not the same a diagnosis of Autistic Disorder or any of the PDD’s via the DSM-IV. These crtiteria vary State to State. Since this is merely a service category, children who are actually autistic may be missed or not assigned to this category at all if their IEP team decides that autism is not their primary disability. Given the potential for errors in the USDE data, accurate decision making based on autism data changes may be flawed (Sahttuck, 2006).
It is also true that the USDE autism data and descriptive epidemiology, do not match in terms of increase or in terms of prevalence rate. The USDE data lag significantly behind the epidemiology and the epidemiology implies that the birth cohorts starting in mid 1990s have had a stable prevalence rate (Chakrabarti & Fombonne, 2005). This is not necessarily surprising since the special education autism service category and therefore the USDE autism counts, only came into existance following IDEA revision of 1990. It ahs been proposed that as with any new system, it has taken time for the data to catch up to the epidemiology (Gernsbacher et al., 2005) and I note, that it still has a lot of catching up left to do.
Criticism of the ASA
I would propose that the logic of the ASA’s decision to declare an autism epidemic can be aptly summerized by the comments of its board members last winter who denounded a study by the researcher Paul Shattuck, who called into question the appropriatness of using the USDE data. This what some ASA board members said:
“We need to move away from a dialogue about prevalence”
“The fact remains that the numbers of those with autism have reached epidemic proportions, and we need to address this now,"
“Any study that diverts our focus or that diminishes the perception of this need hurts us all.”
-Cathy Pratt, Ph.D
“significant number of individuals with autism and their families who aren't mere statistics in a study, but rather, real people with real needs”
-Diane Twachtman-Cullen, Ph.D
“regardless of Shattuck's study findings, more and more people are being diagnosed with autism and the focus must be on the services agenda.”
-Jim Ball, Ed.D
These brings bring to light the focus of the ASA on providing assistance and treatment to autistic persons. The ASA would like the only discussion to be on "how to help persons with autism". This may have a noble intent, but is deeply misguided, as applied science is informed and directed by basic and descriptive research.
However, more needs to be said here. The ASA has repeatedly violated their own recommendations about what topics of autism are permitted. This failure to be consistent in their standards is well presented in the above comments when Lee Grossman states that, there is, for sure, an autism epidemic.
The ASA has no problem with research which increases the view of “need”, but evidently opposes that which calls such into question even when such seems to be the more accurate position. I propose that an organization where dissenting science is not permitted, has left the path of science, and should never be referenced when making attempting to make a scientific statement.
Review of Bryson and Sugiyama & Abe
Kern and Jones invoke the standard wisdom that the base rate of autism was 1 per 1,000 children or 10 per 10,000 in the 1980s. To this end they cite Bryson et al. (1988) at 10.01 per 10,000 and Sugiyama & Abe (1989) at 13.0 per 10,000. Unfortunately, they are comparing the single categories of Autism from the New RDC and Infantile Autism from the DSM-III (respectively) to whole spectrum analyses based on the DSM-IV and ICD-10. In other words they are comparing one category to 4. This is unfortunate as one of these new categories the older studies failed to account for is PDD-NOS, in which ¾ of the current autism total resides (Chakrabarti & Fombonne, 2005). Also, Wing et al. (1976) give a rate of autism plus some PDDs as twice what is seen here at 21.2 per 10,000.The authors are effectively comparing an apple, to a mango, lemon, grape, and coconut.
Review of the Reference of Palmer et al.
The authors reference Palmer et al. (2006). This study showed used USDE data to correlate nearness to power plants (which emit mercury in the air via burning coal). The authors note an increased risk of those living near power plants to having autism. This has been taken by some to be a proof of a mercury etiology of autism. But this is the fallacy of non causa, pro causa; correlation is not causation. This finding also does not explain why a spike did not occur in CDDS data in cohorts who were very young pre-schoolers following the 1987 eruption of Mt. St. Helens which caused a significant spike in atmospheric mercury levels. And again, we have the problem of using the unreliable USDE data in the place.
Review of the Environmental triggers
To establish the validity of environmental triggers in the etiology of autism. The authors cite 3 sources. The 2003 UDES report to Congress. Which I do not have and can not comment on. The 2001 Chakrabarti & Fombonne article. And Palmer et al. (2006) which I already addressed.
I find it strange the authors would cite Chakrabarti & Fombonne who have been decidedly critical of environmental trigger based theories of autism (Fombonne, 2003; Chakrabarti & Fombonne, 2005; Fombonne et al. 2006).
Kern & Jones (2006) view some autistic children as the evidence that certain political and environmental issues have led to harm. Unfortunately they do this by invoking a epidemiology that is quite poorly established. I am again reminded of Gernsbacher, Dawson, & Goldmsith, 2005) who wrote “Epidemics, invoke causes, false epidemic invoke false causes.”
American Psychiatric Association. (1980). Diagnostic and Statistical Manual of Mental Disorders, Third Edition. Washington, DC: American Psychiatric Association; 1980.
American Psychiatric Association. (1987). Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised. Washington, DC:
American Psychiatric Association; 1980.American Psychiatric Association. (1994). Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Washington, DC:
American Psychiatric Association; 1994.American Psychiatric Association. (2000). Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. Washington, DC: American Psychiatric Association; 1994.
Bryson, S. E., Clark, B. S., & Smith, I. M. (1988). First report of a Canadian epidemiological study of autistic syndromes. Journal of Child Psychology and Psychiatry, 4, 433-445.
Chakrabarti, S., & Fombonne, E. (2001). Pervasive developmental disorders in preschool children. Journal of the American Medical Association, 285, 3093-3099.
Chakrabarti, S., Fombonne, E., (2005). Pervasive developmental disorders in preschool children: confirmation of high prevalence. American Journal of Psychiatry, 162(6), 1133-41
Fombonne, E. (2003). Epidemiological surveys of autism and other pervasive developmental disorders: an update. Journal of Autism and Developmental Disorders. 33, 365-382.
Fombonne, E., Zakarian, R., Bennett, A., Meng, L., McLean-Heywood, D. (2006). Pervasive developmental disorders in Montreal, Quebec, Canada: Prevalence and links with immunizations. Pediatrics. 118(1) 139-150.
Gernsbacher MA, Dawson M, & Goldsmith HH. (2005). Three reasons not to believe in an autism epidemic. Current directions in psychological science. In press.
Kern, J, K., Jones, A, M. (2006). Evidence of toxicity, oxidative stress, and neuronal insult in autism. Journal of Toxicology and Environmental Health, 9, 485-499.
Sugiyama, T., & Abe, T. (1989). The prevalence of autism in Nagoya, Japan: a total population study. Journal of Autism & Developmental Disorders, 19, 1, 87-96.
Wing, L., Yeates, S. R., Brierly, L. M., & Gould, J. (1976). The prevalence of early childhood autism: comparison of administrative and epidemiological studies. Psychological Medicine, 6, 89-100.
World Health Organization. (1992). International Classification of Diseases, 10th Revision (ICD-10). Geneva, Switzerland: World Health Organization; 1992.