Is autism a developmental zinc deficiency?

Abstract

Autism spectrum disorder (ASD) is a complex condition influenced by genetic and environmental factors, particularly prenatal ones such as maternal infections, medications, toxins, and nutritional deficiencies. These factors interfere with brain development, leading to the core traits of ASD. Despite extensive research using animal and cell models, few fully replicate the complexity of ASD, highlighting the need to reassess our understanding of its biological processes. Prenatal zinc deficiency has emerged as a significant risk factor, inducing various ASD-related pathologies in studies and potentially uncovering fundamental disrupted biological processes. We propose that a core issue in ASD is metal homeostasis, especially abnormal zinc signaling. This review consolidates current evidence linking zinc to ASD and examines its critical roles in biological functions often affected in individuals with ASD. The findings suggest that prenatal zinc deficiency could reveal the fundamental biological processes disrupted in ASD, which other risk factors might mimic to a lesser extent. Consequently, this narrative review, based on a thorough synthesis of secondary data, provides a critical overview of the growing evidence connecting zinc to ASD while exploring its vital roles in biological functions frequently impaired in affected individuals.