By way of definition, Autism is a neurodevelopmental disorder characterized by impairments in communication and social behavior, and by repetitive behaviors. Recent research has shone a light on the fact that while genetic factors are largely responsible for the occurrence of autism, specific environmental factors might act as risk factors triggering the development of autism in some instances. Thus, the confluence of environmental triggers and autism related genes is currently an area of keen research interest. As highlighted by Ashwood et. al. in a 2006 paper, for successful development of the central nervous system to occur, a functional or normal balance of the immune response is paramount. Ergo, the brains of Autistic patients are characterized by structural and signaling synaptic deficiencies as well as a dysregulation of neuronal survival and growth factors named neurotrophins, all of which seem to be tied to a common thread of Zn 2+ and Immune system abnormalities, among other pertinent but less significant environmental factors.
A few of the environmental factors that trigger the mutation or expression of mutant autism related genes, affect Zn 2+ homeostasis, and proper immune system function include maternal diabetes, heavy metal poisoning, prenatal stress, parental age, malnutrition, psychiatric drugs, toxins, and melatonin deficiency. Regarding immune system abnormalities, a cytokine imbalance is characteristic in the CSF of autistic individuals, and could be the starting point of the inflammatory state, leading to the disruption of trophic factors and increased apoptotic signaling in the cytoarchitecture in the CNS. Consequently, neurodevelopmental arrest or slowed down growth occurs. In the case of the cytokine IL-6, an associated increased expression of proteins called metallothioneins (MTs) that cause Zinc sequestration has been noted. Its worth noting that Zinc is a necessary co-factor for the proper activity of a vast amount of enzymes and proteins. Furthermore, both Zn 2+ deficiency and IL-6 have been shown to cause a reduction in the activity of Insulin-like Growth Factor 1 (IGF-1), a substrate for the IGF-1 receptor that is a component of the PI3K-Akt and Erk- pathways. The former modulates neuronal growth as well as dendritic and axonal maturation and the latter, the expression of neurotrophins imperative for proper neurodevelopment.
While deciphering all the interconnections involved in the physiological state of autism might seem like trying to pick needles out of a haystack, the best that you the reader can do is to avoid the environmental stressors that trigger the expression of autism related genes. For instance, plan on having your children at a younger age to avoid autoimmunity issues, ensure that you are not over or malnourished, ladies avoid taking psychotic medications when pregnant and manage your Zn 2+ and blood sugar levels when pregnant. Special mention to researches working to elucidate the pathophysiology of autism and highlight possible treatment targets, I implore you the reader to support research efforts in this regard.