The role of oxidative stress, inflammation and acetaminophen exposure from birth to early childhood in the induction of autism

Abstract

The wide range of factors associated with the induction of autism is invariably linked with either inflammation or oxidative stress, and sometimes both. The use of acetaminophen in babies and young children may be much more strongly associated with autism than its use during pregnancy, perhaps because of well-known deficiencies in the metabolic breakdown of pharmaceuticals during early development. Thus, one explanation for the increased prevalence of autism is that increased exposure to acetaminophen, exacerbated by inflammation and oxidative stress, is neurotoxic in babies and small children. This view mandates extreme urgency in probing the long-term effects of acetaminophen use in babies and the possibility that many cases of infantile autism may actually be induced by acetaminophen exposure shortly after birth.

Keywords: Autism; acetaminophen; inflammation; oxidative stress; paracetamol; paracetamolo.

Figure 1.

The role of oxidative stress (red), inflammation (blue), and possibly acetaminophen exposure after birth in the induction of autism.

Figure 2.

Apparent changes in the quality and quantity of autism extending over a decade, starting in the early 1980s. In the top diagram, data are from Rimland’s summary of the number of surveys (the “E-1 Diagnostic Checklist” and the “E-2 Diagnostic Checklist”) that were collected in a given time period through grass-roots efforts of the Autism Research Institute and the Autism Society of America, the only two national autism organizations in the United States at the time of the data collection. The Y-axis describes the actual number of surveys received, and changes in the number of reports received were attributed by Rimland to increases in the number of children with autism. “Shortly after birth” in this case refers to parents’ reports that symptoms of autism were evident within weeks of birth. In the lower diagram, the prevalence of autism in California as compiled by Nevison is shown. Data are a composite of “snapshot” data (information collected at one point in time) from the California Department of Developmental Services (collected in 2002 and covering birth years 1970–1997) and tracking data evaluating 5-year-olds collected under the US Individuals with Disabilities Education Act (covering birth years 1995–2005).

Figure 3.

Action and metabolism of acetaminophen in babies and children. Phase II metabolism involving glucorinadation, like sulfation, leads to detoxification of acetaminophen, but sulfation is the primary mechanism active in infants and children.