Author: Herbert MR, Sage C.
Affiliation:
TRANSCEND Research Program Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02129, USA. Electronic address: drmarthaherbert@gmail.com.
Conference/Journal: Pathophysiology.
Date published: 2013 Oct 3
Other:
Pages: S0928-4680(13)00037-0 , Special Notes: doi: 10.1016/j.pathophys.2013.08.001 , Word Count: 380
Although autism spectrum conditions (ASCs) are defined behaviorally, they also involve multileveled disturbances of underlying biology that find striking parallels in the physiological impacts of electromagnetic frequency and radiofrequency exposures (EMF/RFR). Part I of this paper will review the critical contributions pathophysiology may make to the etiology, pathogenesis and ongoing generation of core features of ASCs. We will review pathophysiological damage to core cellular processes that are associated both with ASCs and with biological effects of EMF/RFR exposures that contribute to chronically disrupted homeostasis. Many studies of people with ASCs have identified oxidative stress and evidence of free radical damage, cellular stress proteins, and deficiencies of antioxidants such as glutathione. Elevated intracellular calcium in ASCs may be due to genetics or may be downstream of inflammation or environmental exposures. Cell membrane lipids may be peroxidized, mitochondria may be dysfunctional, and various kinds of immune system disturbances are common. Brain oxidative stress and inflammation as well as measures consistent with blood-brain barrier and brain perfusion compromise have been documented. Part II of this paper will review how behaviors in ASCs may emerge from alterations of electrophysiological oscillatory synchronization, how EMF/RFR could contribute to these by de-tuning the organism, and policy implications of these vulnerabilities. Changes in brain and autonomic nervous system electrophysiological function and sensory processing predominate, seizures are common, and sleep disruption is close to universal. All of these phenomena also occur with EMF/RFR exposure that can add to system overload ('allostatic load') in ASCs by increasing risk, and worsening challenging biological problems and symptoms; conversely, reducing exposure might ameliorate symptoms of ASCs by reducing obstruction of physiological repair. Various vital but vulnerable mechanisms such as calcium channels may be disrupted by environmental agents, various genes associated with autism or the interaction of both. With dramatic increases in reported ASCs that are coincident in time with the deployment of wireless technologies, we need aggressive investigation of potential ASC - EMF/RFR links. The evidence is sufficient to warrant new public exposure standards benchmarked to low-intensity (non-thermal) exposure levels now known to be biologically disruptive, and strong, interim precautionary practices are advocated.
Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.
KEYWORDS:
Autism, Cellular stress, Children, EMF/RFR, Environment, Fetus, Mitochondrial dysfunction, Oscillatory synchronization, Oxidative stress, Radiofrequency, Wireless
PMID: 24095003