Although gastrointestinal (GI) disorders are not among the diagnostic criteria for autism, as many as
84% of children with autism present with GI issues. It's been long suggested that there is a correlation between the two:
1961: Asperger himself suggested a link between autism and celiac disease (an autoimmune digestive response to gluten intake).
1971: Goodwin noted malabsorption in autistic children.
1979: Panksepp described the neurochemistry of autism, suggesting that an incomplete breakdown and excessive absorption of dietary food peptides (gluten containing foods such as barley, rye, oats, etc) may exert central opioid-like effects.
1993: Murch suggested that a deficient in the phenol-sulfur-transferase systems in the GI wall may lead to increased GI permeability to food peptides leading to both intestinal inflammation and neuropsychiatric dysfunction.
In a 2009 journal article in Pediatrics (124;796-798) Ibrahim details a 18+ year study on the GI system and autism. In this study, participants from age 0-18 were followed and put into five different categories according to their GI symptoms: 1) Constipation 2) diarrhea 3) abdominal bloating, discomfort or irritability 4) gastroesophageal reflux or vomiting 5) feeding issues or food selectivity. The majority of the medical care throughout this study was conducted via the Mayo Clinic.
The study found that there were significant differences between cases with autism and controls in cumulative incidence of constipation and feeding issues/food selectivity. Relative risk ratios, however, determined no significant associations between cases with autism and controls in the overall incidence of diarrhea, reflux/vomiting, and bloating/irritability/discomfort.
The goal of this study was to compare the incidence of GI symptoms of autistic children to age and gender-matched controls. The studied concluded that the overall incidence of gastrointestinal symptoms "
did not differ between cases of autism and controls. The areas of difference, such as constipation and food issues/food selectivity, they attribute to neurobehavioral characteristics in children with autism rather than being indicative of primary gastrointestinal pathology. Of importance, they do suggest that subgroups of children may have gastrointestinal disorders that contribute to their autistic behaviors." However, Ibrahim did note that there are sub-categories that need to be investigated further, in order to lay the gastrointestinal prevalence in autistic children to rest.
It is important to note that this study's participants came from the same county within Wisconsin, and were made up of 98% caucasian ethnicity and that a generalized statement cannot be made from this one study.
Multiple theories currently exist over the possible enviromental triggers for autism including childhood vaccinations, mercury exposure and viral infections (all of these will eventually be discussed in this forum). Some more researched theories include the idea that the use of acetaminophen within the early years of childhood causes autism, hence the title and topic for this blog post.
Acetaminophen is metabolized via three pathways: glucuronidation (a process that makes any non-energy providing source available for excretion), sulfation (a process that decreases the toxological effects of the drug) and via the cytochrome P-450 system (a process that bioactivates the drug via a catalyzation of the oxidizing agents within the drug itself).
