A review of: D GEIER, J KERN, C GARVER, J ADAMS, T AUDHYA, R NATAF, M GEIER (2008). Biomarkers of environmental toxicity and susceptibility in autism☆ Journal of the Neurological Sciences DOI: 10.1016/j.jns.2008.08.021
One bio-social model of the etiology of autism suggests that a genetic predisposition, in the form of limited ability to remove toxins from the body (e.g., mercury), combined with exposure to such toxins, leads to an increased risk for developing autism. As I previously described in this study, researchers have examined urinary porphyrins as a measure of mercury exposure, and some studies have found increased levels of porphyrins in children with autism. In this study, the authors examined urinary porphyrin metabolites (a proposed measure of heavy metal toxicity) and plasma sulfates (a proposed measure of detoxification capacity) among children with autism.
The sample included 28 children between the ages of 2 and 16 recruited from the Dallas/Fort Worth community. These children had a diagnosis of autism (Childhood Autism Rating Scale scores above 30). This group was categorized into a mild (CARS
38.5) autism. Blood and urine samples were collected for analysis. A laboratory standard control sample of typically developing children was also included in the plasma analysis only.
The mild ASD group had significantly lower ratios of key porphyrin levels when compared with kids with severe ASD. The following group means are statistically significantly different from each other:
MILD ASD = 4.92±2.79 VS. SEVERE ASD = 6.0±1.58
MILD ASD = 17.3±8.9 VS. SEVERE ASD = 24.05±7.28
Pentacarboxyporphyrin/uroporphyrins I and III
MILD ASD = 0.19±0.06 VS. SEVERE ASD = 0.27±0.08
Precoprophyrin/uroporphyrins I and III
MILD ASD = 0.68±0.28 VS. SEVERE ASD = 1.09±0.36
Coproporphyrins I and III/ uroporphyrins I & and III
MILD ASD = 9.54±2.97 VS. SEVERE ASD = 12.64±3.47
(Precoproporphyrin+ pentacarboxyporphyrin) / (uroporphyrins I & and III+ heptacarboxyporphryin)
MILD ASD = 0.73±0.26 VS. SEVERE ASD = 1.1±0.29
The authors concluded that increased urinary porphyrin metabolites were associated with more severe autism based on CARS scores. Urinary porphyrin are believed to represent mercury toxicity.
Furthermore, the authors found significantly lower levels of plasma sulfates (Plasma cysteine, Plasma reduced glutathione, Plasma oxidized glutathione) among children with autism when compared to typically developing kids. Decreased sulfation (low plasma levels of sulfates) can indicate limited detoxification capacity, especially of heavy metals such as mercury.
In conclusion, the study presents some compelling evidence regarding differences in urinary porphyrin metabolites between kids with mild and severe autism symptoms, as well as differences in plasma sulfates between kids with autism when compared to neurotypical kids. This is consistent with the author’s theory that mercury exposure plays a role in autism. However, given the controversy regarding the mercury-autism association, I would like to clarify that these results do not indicate that mercury causes autism. Yes, it is possible that mercury toxicity and reduced detoxification capacity plays a role in autism, both, in the onset and severity. However, it is also possible that Autism itself results in reduced detoxification capacity and mercury toxicity via other mechanisms, but that such toxicity is not associated at all with the development of the disorder. For example, erythrocyte sedimentation rate and C-reactive protein are tests used in arthritis. Atypical results on these tests are found in people with arthritis. Yet, neither one is related to any of the proposed causes of arthritis, and instead reflect a consequence of the disorder itself (inflammation).
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