Maternal antibodies to gliadin and autism spectrum disorders in offspring-A population-based case-control study in Sweden.
Mom's gluten antibodies do not cause autism and may even protect kids who have both autism and intellectual disability.
01Research in Context
What this study did
Swedish doctors tested blood from 1,000 moms. Half had kids later diagnosed with autism. Half did not.
They looked for anti-gliadin antibodies. These proteins show if mom ate gluten and her body reacted to it.
What they found
High antibody levels did NOT raise autism risk overall. The odds stayed flat at 1.0.
A surprise popped up in the subgroup with both autism and intellectual disability. High antibodies cut their odds in half (0.51). More gluten reaction, fewer cases.
How this fits with other research
Nicholson et al. (2017) also used Swedish baby blood spots. They found no link between neonatal thyroid levels and autism. Both studies show single biomarkers from early life fail to predict autism.
Nygren et al. (2012) ran an earlier Swedish screen. They proved systematic testing finds more autism cases. Higgins et al. (2021) used the same registry tricks but asked why autism starts instead of how many kids have it.
Moorthy et al. (2022) looked at sugar and cavities in kids with autism. They also found diet factors do not explain autism. Together these papers cool off simple food-blame stories.
Why it matters
You can stop telling moms that eating gluten during pregnancy causes autism. The data show zero overall risk. If you assess a child who has both autism and intellectual disability, remember the odd antibody finding, but do not over-read it. Focus your energy on evidence-based teaching tools, not gluten-free diets, when you write behavior plans.
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02At a glance
03Original abstract
While individuals diagnosed with autism spectrum disorders (ASD) have higher levels of antibodies directed towards gliadin, a component of wheat gluten, no study has examined anti-gliadin antibodies (AGA) in etiologically relevant periods before diagnosis. The objective of this study was to investigate if maternal levels of AGA, during pregnancy and at the time of birth, are associated with ASD in offspring. We analyzed AGA in archived neonatal dried blood spots (NDBS) for 921 ASD cases and 1090 controls, and in paired maternal sera collected earlier in pregnancy for a subset of 547 cases and 428 controls. We examined associations with ASD diagnoses as a group and considering common comorbidities (intellectual disability [ID] and attention-deficit/hyperactivity disorder). We compared 206 cases to their unaffected siblings to examine the potential for confounding by shared familial factors. Odds of ASD tended to be lower among those with the highest levels (≥90th percentile) of AGA compared to those with low levels (<80th percentile; OR 0.78, 95% CI 0.56-1.09, measured in NDBS). This pattern was more apparent for ASD with comorbid ID when measured in NDBS (0.51, 0.30-0.87), with a similar trend in maternal sera (0.55, 0.24-1.29). High levels of AGA were similarly associated with lower odds of ASD in the sibling comparison. In summary, we found little association between maternal antibodies raised against components of gluten and risk of ASD in general. Exposure to high levels of AGA in the pre- and perinatal periods may be protective in terms of risk for ASD with ID. LAY SUMMARY: There is a debate among both scientists and community members as to whether an immune reaction to gluten exposure could be considered a cause of autism. We examined antibodies that are directed against gliadin, a part of gluten, in samples collected from pregnant mothers and their newborn babies. We did not see any major differences in the antibody level among those children diagnosed with ASD or their mothers compared to children who were not diagnosed with ASD. High levels of the antibodies were in fact associated with a somewhat lower risk of ASD with co-occurring intellectual disabilities, though we cannot tell from this study why that might be the case.
Autism research : official journal of the International Society for Autism Research, 2021 · doi:10.1002/aur.2567