Abstract
Numerous neurological disorders including fragile X syndrome, Down syndrome, autism, and Alzheimer’s disease are co-morbid with epilepsy. We have observed elevated seizure propensity in mouse models of these disorders dependent on diet. Specifically, soy-based diets exacerbate audiogenic-induced seizures in juvenile mice. We have also found potential associations between the consumption of soy-based infant formula and seizure incidence, epilepsy comorbidity, and autism diagnostic scores in autistic children by retrospective analyses of medical record data. In total, these data suggest that consumption of high levels of soy protein during postnatal development may affect neuronal excitability. Herein, we present our theory regarding the molecular mechanism underlying soy-induced effects on seizure propensity. We hypothesize that soy phytoestrogens interfere with metabotropic glutamate receptor signaling through an estrogen receptor-dependent mechanism, which results in elevated production of key synaptic proteins and decreased seizure threshold.
Highlights
Soy was first grown in the United States in the 1760s
In the SFARI autism population described in the previous section, we observe a statistically significant increase in attention deficit/hyperactivity disorder (ADHD) with the consumption of soy-based infant formula (6.7% soy, 3.9% non-soy, 1.7-fold increase, P = 0.04)
CONCLUDING REMARKS In summary, soy infant formula has been used in the United States since 1909 as an alternative for infants allergic to cow’s milk
Summary
Soy was first grown in the United States in the 1760s. This leguminous plant is native to East Asia and related to peas, alfalfa, and clover. We have found potential associations between the consumption of soy-based infant formula and seizure incidence, epilepsy comorbidity, and autism diagnostic scores in autistic children by retrospective analyses of medical record data. Our research, which is reviewed below, suggests that soy-based diets are associated with increased seizure susceptibility in both rodent and human models of neurological disease.
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