Central Causation of Autism/ASDs via Excessive [Ca2+]i Impacting Six Mechanisms Controlling Synaptogenesis during the Perinatal Period: The Role of Electromagnetic Fields and Chemicals and the NO/ONOO(-) Cycle, as Well as Specific Mutations

Abstract

Overview

The study discusses novel viewpoints on the causation of autism and ASDs, focusing particularly on synaptic development during the perinatal period. The disruption in synaptogenesis emerges through an intricate interplay of intracellular calcium levels and genetic and environmental factors.

Findings

• Impact of EMFs and Chemicals: Autism causation is significantly associated with electromagnetic fields and various chemical exposures. EMFs trigger autism via activation of voltage-gated calcium channels leading to elevated [Ca2+]i levels, while chemicals also induce [Ca2+]i elevation, primarily through NMDA receptor activation.
• Genetic and Epigenetic Contributions: In many cases, genetic factors concerning calcium levels influence synaptogenesis, complemented by MeCP2 epigenetic dysfunctions driving the chronic nature of ASDs.
• Systematic Review Consistency: A thorough examination of relevant literature confirms the predictive model's consistency, suggesting a multifaceted approach could benefit ASD prevention and treatment.

Conclusion

The integration of avoidance strategies for EMFs and certain chemicals along with dietary and environmental enhancements like high levels of Nrf2, vitamin D, and omega-3 fatty acids could potentially mitigate ASD risks. These findings underscore the complexity of autism causation and highlight potential pathways for prevention and therapeutic interventions.