Interaction between GSTT1 and GSTP1 allele variants as a risk modulating-factor for autism spectrum disorders.
In Jamaican toddlers, carrying two specific gene types nearly triples autism odds, yet the finding needs repeat studies before clinical use.
01Research in Context
What this study did
Scientists looked at two genes in Jamaican children. One gene helps the body clean toxins. The other helps too.
Kids were two to eight years old. Some had autism. Some did not. The team checked who carried both gene types.
What they found
Children with both gene versions had almost three times the chance of autism. Each gene alone showed no extra risk. Only the pair mattered.
How this fits with other research
Zhao et al. (2024) also found a near-triple autism risk in Chinese toddlers. Their trigger was an unplanned pregnancy without folic acid. Different cause, same size effect.
Talmi et al. (2020) saw a smaller risk from low birth weight. That result lines up here: both show only slight odds jumps.
Hollowood et al. (2018) used mom’s blood to sort pregnancies into high- or low-risk groups. Their test could not tell if this baby would get autism. The gene pair in Doughty et al. (2015) is more specific, but it still needs repeat studies before use.
Why it matters
You can’t change genes, but you can explain risk to families. If Jamaican parents ask about autism odds, tell them this gene pair is a clue, not a verdict. Watch for replication work before adding gene tests to your practice.
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02At a glance
03Original abstract
We investigated the role of glutathione S-transferase (GST) genes in Autism Spectrum Disorder (ASD). We used data from 111 pairs of age- and sex-matched ASD cases and typically developing (TD) controls between 2-8 years of age from Jamaica to investigate the role of GST pi 1 (GSTP1), GST theta 1 (GSTT1), and GST mu 1 (GSTM1) polymorphisms in susceptibility to ASD. In univariable conditional logistic regression models we did not observe significant associations between ASD status and GSTT1, GSTM1, or GSTP1 genotype (all P > 0.15). However, in multivariable conditional logistic regression models, we identified a significant interaction between GSTP1 and GSTT1 in relation to ASD. Specifically, in children heterozygous for the GSTP1 Ile105Val polymorphism, the odds of ASD was significantly higher in those with the null GSTT1 genotype than those with the other genotypes [Matched Odds Ratio (MOR) = 2.97, 95% CI (1.09, 8.01), P = 0.03]. Replication in other populations is warranted.
Research in autism spectrum disorders, 2015 · doi:10.1016/j.rasd.2014.12.008