Interactive associations of eczema with glutathione S-transferase genes in relation to autism spectrum disorder and its severity in Jamaican children.
In Jamaican kids, eczema plus the GSTP1 Val/Val gene type doubles ASD risk, though eczema alone does nothing.
01Research in Context
What this study did
Saroukhani et al. (2023) asked whether eczema plus certain gene types raise autism risk in Jamaican kids. They compared children with ASD to typically developing peers. Each child was checked for eczema and for three GST gene variants that handle body toxins.
What they found
Eczema alone did not boost ASD odds. Yet kids who had both eczema and the GSTP1 Val/Val genotype showed double the chance of ASD. A second gene, GSTM1, gave a smaller, non-significant bump.
How this fits with other research
Giesbers et al. (2020) used the same Jamaican cohort and same GST genes. They saw heavy-metal exposure slightly more often in typical kids, but the link vanished after diet was counted. The pattern shows GST genes matter, yet the trigger changes.
Nijs et al. (2016) found normal brain glutathione in adults with ASD. That seems to clash, but their sample was older and looked inside the brain, while Sepideh studied kids and gene risk, not brain levels. Age and tissue explain the gap.
Song et al. (2024) also saw no brain GSH difference in autistic children aged 8–12. Again, direct brain chemistry looks normal, while peripheral gene–environment links still show up.
Why it matters
If a child has eczema and the Val/Val GSTP1 type, you now know ASD risk is higher. You can flag this combo to parents and push for early screening. No new intervention yet, but the info sharpens your developmental watch list.
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02At a glance
03Original abstract
BACKGROUND: Comorbidity of eczema with autism spectrum disorder (ASD) is increasing. We investigated the associations of eczema and its possible interaction with polymorphisms in glutathione S-transferase (GST) genes in relation to ASD and ASD severity. METHOD: Using data from 344 1:1 age- and sex-matched ASD cases and typically developing controls, we assessed additive and interactive associations of eczema with GST genes in relation to ASD by applying conditional logistic regression models, and in relation to ASD severity in ASD cases as measured by the Autism Diagnostic Observation Schedule-2nd Edition (ADOS-2) total and domain-specific comparison scores (CSs) by fitting general linear models. RESULTS: After adjusting for child's age and history of breastfeeding, eczema had no additive association with ASD [Matched Odds ratio (MOR) and 95% Confidence Intervals (CI): 1.04 (0.76, 1.41), P = 0.82] or ASD severity (all P > 0.20). Using a recessive genetic model, eczema was significantly associated with ASD only among children with the Val/Val genotype for the GSTP1 Ile105Val polymorphism [MOR (95% CI) = 2.04 (1.02, 4.08), P = 0.04, P for interaction = 0.03]. In addition, among ASD cases with the GSTM1 DD genotype, those with eczema had a marginally significant higher mean ADOS-2 Social Affect CS than those without eczema (7.3 vs. 6.8, P = 0.08, P for interaction = 0.09). CONCLUSION: Our findings suggest children with certain genotypes for GST genes may be more susceptible for comorbidity of eczema and ASD, which is consistent with the role of GST genes in both conditions.
Research in autism spectrum disorders, 2023 · doi:10.1016/j.bbi.2019.10.008