Zinc in Gut-Brain Interaction in Autism and Neurological Disorders

Figure 3

A model for Zinc in gut-brain interaction in ASD and other neurological disorders. Zinc is taken up from our dietary sources and/or supplements in the proximal small intestine. However, absorption of zinc can be decreased in response to various agents such as iron and/or calcium supplements, high copper levels, folic acid, phytate, high fructose corn syrup (HFCS), and/or several drugs. Alternatively, zinc levels may be low due to genetic variants in zinc homeostasis genes or general low availability of zinc in the diet. As a result of this, zinc deficiency of the embryo may occur. Zinc deficiency might influence embryonic and fetal development affecting the GI system through impaired function of several key proteins contributing to many of the reported GI problems associated with ASD such as metallothionein dysfunction, plasma Cu/Zn inversion, heavy metal overload, Candida and Clostridium overgrowth, constipation and/or diarrhea, leaky gut, food sensitivities and allergies, inefficient processing of gluten and casein, enzyme deficiency, vitamin and mineral malabsorption, inefficient fat digestion and metabolism, and esophagitis and GI ulcers. These GI symptoms can give rise to behavioral difficulties.