Ricerca
che associa un legame patofisiologico plausibile tra esposizione a CEM ed
autismo ……………….
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AUTISM AND EMF? PLAUSIBILITY OF A
PATHOPHYSIOLOGICAL LINK - PART I.
1TRANSCEND
Research Program Neurology, Massachusetts General Hospital, Harvard Medical
School, Boston, MA 02129, USA. Electronic address: drmarthaherbert@gmail.com.
ABSTRACT
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.