Fluoride, aluminum, and aluminofluoride complexes in pathogenesis of the autism spectrum disorders: A possible role of immunoexcitotoxicity

• Over the past several decades, the prevalence of autism spectrum disorder (ASD) has increased dramatically.
• Our manuscript suggests that most risk factors are connected to immunoexcitotoxicity.
• The synergistic interactions of fluoride and aluminum increase the potential neurotoxic effect particularly in children.
• Aluminofluoride complexes could contribute to an alarming increase in the prevalence of ASD.

Autism spectrum disorders (ASD) are characterized by impairments in social interaction and communication along with stereotyped patterns of behaviors. Over the past several decades, the prevalence of ASD has increased dramatically. ASD are highly multifactorial, with many risk factors acting together. Our review suggests that most risk factors are connected to immunoexcitotoxicity. Fluoride exposure is common as a result of the artificial fluoridation of drinking water and a dramatic increase in the volume of man-made industrial fluoride compounds released into the environment. Human exposure to environmental aluminum is extensive and appears to be growing. The long-term fluoride and aluminum burden have several health effects with a striking resemblance to the ASD. Moreover, both fluoride and aluminum interfere with a number of glycolytic enzymes, resulting in a significant suppression of cellular energy production. The synergistic interactions of fluoride and aluminum increase the potential neurotoxic effect particularly in children. Aluminofluoride complexes have effects on cell signaling, neurodevelopment, and neuronal function. We suggest that the burden with these new ecotoxicological factors could contribute to an alarming increase in the prevalence of ASD.

In water solution, Al3+ forms, in the presence of fluoride, water soluble aluminofluoride complexes (AlFx), which act as messengers of false information. This mechanism could explain the emergence phenomena in pathogenesis of ASD on a molecular and cellular level. Figure optionsDownload as PowerPoint slide