Journal of Child and Adolescent Behavior
Open Access

Research Article

Increased Autism Incidence: Is there a Single Cause?

Sarah Crawford^*

Department of Biology, Southern Connecticut State University, USA

*Corresponding Author:

Sarah Crawford
Department Biology, Southern Connecticut
State University, 501 Crescent Street, Room
311c Academic Science Laboratory
New Haven, Connecticut 06515, USA
Tel: +1-203-392-6215
E-mail: crawfords2@southernct.edu

Received Date: January 06, 2016; Accepted Date: February 09, 2016; Published Date: February 12, 2016

Citation: Crawford S (2016) Increased Autism Incidence: Is there a Single Cause?. J Child Adolesc Behav 4:273. doi:10.4172/2375-4494.1000273

Copyright: © 2016 Crawford S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

The Quantitative Threshold Exposure (QTE) hypothesis proposes that Autism Spectrum Disorder (ASD) is triggered by the cumulative effects of high-level exposure to endogenous and environmental factors that act as antigens to impair normal immune system (IS) and associated central nervous system (CNS) functions during critical prenatal and early childhood developmental stages. The hypothesis predicts that the greater the number of risk factors and the quantitative amounts of each to which a child is exposed prenatally and in early postnatal life, the greater the likelihood the child will develop some form of ASD as a result of their effects on critically integrated IS and CNS pathways active during prenatal, neo-natal and early childhood brain maturation. These risk factors have been identified in extensive epidemiological studies to include genetic predisposition, maternal fetal exposure to infectious disease, inflammatory and autoimmune phenomena, as well as exposure to antigenic and proinflammatory environmental factors. The incidence rates of several potential risk factors for ASD correlates with observed increases in ASD incidence over the past several decades, including increased incidence of pediatric infectious disease, increased obesity/ diabetes type-2 in parents of child-bearing age and Increased use of tetrahydrocannabinol (THC) during childbearing years. This model may be useful even when the individual contributions of specific risk factors cannot be quantified, as it proposes that the combined quantitative level of exposure to risk factors for ASD rather than exposure to any one risk factor per se defines threshold occurrence rates. The model has important predictive value, as it suggests that, rather than attempting to identify a specific causative agent linked to ASD, the combined risk factor profile should be evaluated in population studies in order to specify more accurately the limits of pre- threshold exposure.

Keywords