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Research on The Dangers of EMF’s and Autism


When I begin researching the dangers of EMF’s in relationship to our autistic son, I found this amazing, fully-referenced 100-page PDF article to show to my husband.

If you are not clear on how EMF’s can have a potentially hazardous impact on your autistic child, I encourage you to read this article in its entirety… or the parts you are most interested in.  There is a great table of contents.

Below I have excerpted and highlighted in bold some areas that I thought would be important to help show my husband that electromagnetic radiation was a serious potential threat to our son’s recovery, and certainly something we should work to address in our home.

By the way, you can cheaply and effectively mitigate the effects of harmful EMF’s from electricity, cell-phone towers, and Wi-Fi in your home, office, and car with a BioElectric Shield. 


Click here to learn more from the bioelectric shield developers’ own website, including several research studies showing its effectiveness.



The premise of this review is that although scant attention has been paid to possible links between electromagnetic fields and radiofrequency exposures (EMF/RFR) and Autism Spectrum Disorders (ASDs), such links probably exist. The rationale for this premise is that the physiological impacts of EMF/RFR and a host of increasingly well-documented pathophysiological phenomena in ASDs have remarkable similarities. Additional support may be found in the parallels between the rise in reported cases of ASDs and the remarkable increases in EMF/RFR exposures over the past few decades. Reviewing these similarities does not prove that these parallels imply causality – that kind of research has not been done. Moreover, the physiological processes affected by EMF/RFR are also impacted by other environmental factors. Yet EMF/RFR does not need to be a unique contributor to ASDs to add significantly to system overload (‘allostatic load’) and dysfunction. Even so these pathophysiological overlaps do suggest that the potential for an EMF/RFR-ASD connection should be taken seriously, and that their vulnerable biological features may make many with ASDs more likely to experience adverse EMF/RFR impacts. This is a sufficient basis to recommend that precautionary measures should be implemented and respected, that further research should be prioritized, and that policy level interventions based on existing and emerging data should be designed and pursued. Moreover, pursuing this link could help us understand ASDs better and find more ways to improve the lives of people with ASDs and of so many others.

A. How are Biology and Behavior Related?

Considering a potential link between ASDs and EMF/RFR (or indeed of any potential contributor to incidence or pathogenesis) requires taking account of the evolution that has been occurring in our understanding of the relationship between ASD’s behavioral and biological features. ASDs were first labeled as ‘autism’ in 1943 by Leo Kanner, a child psychiatrist who extracted several key behavioral features, related to communication and social interaction challenges and a tendency toward restricted interests and repetitive behaviors, characteristic of all 11 of the children in his first case series (Kanner 1943). Although in the seven decades since this condition was first constructed as a category there has been some modification of the way these behavioral features have been characterized, ASDs are still defined behaviorally, although sensory issues such as hypo- or hyper-reactivity have recently been included in the diagnostic criteria (Diagnostic and Statistical Manual of Mental Disorders or DSM-V) (American Psychiatric Association 2000, 2013, May).

1. Transduction is fundamental but poorly understood

Yet in considering how an environmental factor such as EMF/RFR could lead to autism and/or influence its severity or incidence, we need to think about how underlying biology is transduced into changes in nervous system electrical activity, and how these in turn generate the set of behaviors we have categorized as ‘autism.’ (Herbert 2005) This means not taking behaviors as given, or as purely determined by genetics, but exploring the full range of biology that generates these features and challenges.

2. More than brain

Although ‘autism’ has long been considered to be a psychiatric or neurological brain- based disorder (Rapin and Katzman 1998; Polleux and Lauder 2004), it has become undeniable that people diagnosed with ASDs often also have a multitude of biological features – including systemic pathophysiological disturbances (such as oxidative stress, mitochondrial dysfunction and metabolic and immune abnormalities) (Ming et al. 2012; Tsaluchidu et al. 2008; Pieczenik and Neustadt 2007; Gonzalez et al. 2011) as well as symptomatic medical comorbidities (such as gastrointestinal distress, recurrent infections, epilepsy, autonomic dysregulation and sleep disruption) (Nikolov et al. 2009; Kotagal and Broomall 2012; Kaartinen et al. 2012; Daluwatte et al. 2012; Tuchman and Cuccaro 2011; Canitano 2007; Malow 2004; Kang and Barnes 2013; Jyonouchi et al. 2011) – in addition to the core defining behaviors – and many of these occur commonly (Kohane et al. 2012). The problem has been that no one such biological feature has turned out to be present in every single person carrying an ASD diagnosis – and they are not specific to ASDs, either. Moreover there has been much variability in many of the features of autism – not only between individuals but in many cases within individuals at different points in time or under different circumstances. Because of this variability, the relevance of many of these biological features has been dismissed as secondary and not intrinsically related to the ‘autism.’ Instead, many have considered the behavioral features as fundamental not only to how autism manifests and is definedbut also to the core intrinsic nature of ASDs, even though the biological basis of these behaviors has by no means been established.

3. Heterogeneity: More genetic and environmental than physiological

It is not as if this variability is unique to the ‘environmental side.’ At the present time over 800 genes have been associated with ASDs, and over 100 different rare genetic syndromes are frequently accompanied by ASD, with no clear specific unifying mechanism uniting this remarkable heterogeneity (Trikalinos et al. 2006; Ring et al. 2008; Pelphrey et al. 2011; Mandell 2011; Hall et al. 2012; Bill and Geschwind 2009). Similarly a large number of potential environmental contributors are under investigation ranging from toxicants and Vitamin D deficiency or failure to take prenatal vitamins to air pollution and stress or infection in pregnancy (Whitehouse et al. 2012; Kocovska et al. 2012; Schmidt et al. 2011; Landrigan 2010; Roberts et al. 2007; Shelton, Hertz-Picciotto, and Pessah 2012; Becerra et al. 2012; Volk et al. 2011). Yet at the physiological level a smaller set of disturbances are showing up as common across substantial numbers of people with ASDs – and in fact not uniquely to ASDs but also in myriad other chronic conditions whose prevalence also appears to be increasing (Bilbo Jones, and Parker 2012; Knox 2010). Prominent among these are immune disturbances including inflammation, mitochondrial dysfunction, and oxidative stress, as well as toxic body burden. Vulnerability to all of these can be increased mildly or substantially by a variety of often common genetic mutations, but may remain latent without the overlay of environmental triggers. Conversely, with substantial enough environmental input, genetic vulnerability may not be necessary.

4. Mechanism is more than correlation

Just HOW biological features might be related to the behavioral features that have up until now defined ASDs has not been clarified; until recently the main research effort regarding pathophysiology in ASDs has been to establish the presence of these phenomena in the first place. Even so, some correlations between biological and behavioral features have been identified – e.g. a higher level of immune abnormalities correlates with more aberrant behaviors (Wei et al. 2012; Careaga and Ashwood 2012; Jyonouchi et al. 2011; Ashwood et al. 2011; Heuer et al. 2008; Zerrate et al. 2007; Curran et al. 2007). Still, such correlations in themselves do not explain the mechanisms by which the transduction of pathophysiology into behavior might actually occur. In order to do that, an important component would be to study the relationship between systemic pathophysiology and nervous system electrophysiology.

5. EMF/RFR research may help us understand how ASDs ‘work’

Assessing the potential contribution of EMF/RFR to ASDs puts this question of the nature of the pathophysiology-behavior transduction into an interesting and provocative light since the brain is simultaneously a tissue-based physical organ that can be compromised by cellular pathophysiology as well as altered developmental processes, and an information processing system that operates through networks of synchronized electrical oscillations (brain waves) – and EMF/RFR impacts may occur directly at both of these levels. To date the emphasis in ASD research has largely been on ‘structure- function’ relationships that have been anatomy-centered. This research has generated correlations between brain structures and behaviors, and has found some genetic correlates as well, but it has made assumptions that these phenomena are rooted in genetics and genetically perturbed molecular structures and substances. This leads to targeting the molecular level with pharmaceuticals, but not to the broader agenda of understanding environmental or physiological contributions or dynamic features of brain and behavior. Thus, exploring how EMF/RFR impacts ASDs may help to force the question of how these pathophysiological and electrophysiological/information processing levels actually interact, and how anatomy may in many ways be a product rather than a cause of physiology.

B. Time Courses of Mechanisms

For the most part, researchers have looked for causes of autism in mechanisms that occur early and create permanent change or damage. This approach is logical if one assumes that genetic influences are overwhelmingly predominant, and ‘autism’ is a fixed lifelong trait. However evidence is emerging that ASDs may in many respects be more state-like and variable than trait-like and fixed.

1. Plasticity

One of the remarkable shifts in conceptual thinking about ASDs is an appreciation of its brain plasticity (Helt et al. 2008). Growing numbers of reports of improvement and loss of diagnosis, reversal of neurological symptoms in a growing number of mouse models of genetic syndromes that in humans prominently feature autism (Cobb, Guy and Bird 2010; Ehninger et al. 2008; Goebel-Goody et al. 2012; Henderson et al. 2012; Kaphzan et al. 2012; Liu, huang, and Smith 2012; Mehta, Gandal, and Siegel 2011; Paylor et al. 2008; Rotschafer et al. 2012; Sato et al. 2012; Suvrathan et al. 2010), short-term pharmaceutically induced improvement in brain connectivity (Narayanan et al. 2010), and transient reversal or abeyance of symptomatology under various circumstances (including fever, fluid-only diet, and certain antibiotic treatments (Sandler et al. 2000; Curran et al. 2007)) – all of these throw into question the long-standing assumption that we are simply dealing with a ‘broken brain.’ Indeed, how could a ‘broken brain’ produce markedly improved function with such a short turnaround time? (Herbert 2009) Such a time frame cannot possibly be accounted for by remodeling of the brain’s anatomical substrate. ‘Brain waves’ and their synchronization, on the other hand, could easily vary over short time periods. Looking into physiological and environmental modulators not only of brain development but also of everyday brain function becomes increasingly imperative.

In addition, documentation of average to superior intelligence in most people with autism (Edelson 2006; Dawson et al. 2007), as well as of domains of perceptual superiority (Soulieres, Zeffiro, et al. 2011; Soulieres, Dawson et al. 2011; Samson et al. 2011; Soulieres et al. 2010; Soulieres et al. 2009; Mottron et al. 2006; Mottron 2004; Bertone et al. 2005; Perreault et al. 2011), call into question the long-standing assumption that ASDs are intrinsically or for the most part associated with cognitive deficits – another strike against the outdated ‘deficit’ or ‘broken brain’ model.

2. Mechanisms that operate actively throughout the lifecourse

One particularly valuable lesson about ASDs that can be learned from looking at how EMF/RFR affects underlying biology is that these impacts are by no means confined to early development. We already have clinical reports of ‘intermittent autism’ – for example, some children with mitochondrial disease who have ups and downs of their bioenergetics status ‘have autism’ on their bad days but don’t display autistic features on their good days (Korson 2007). These children with their vulnerable, barely compensated mitochondria seem to be teetering right at the brink of the interface of metabolic and electrophysiological dysfunction, tipping back and forth on this knife edge. It makes one wonder what everyday exposures – allergens, infection, pesticide on the school playground, even perchance EMF/RFR – might contribute to the bad days (with their loss of electrophysiological optimization, probably on account of insufficient energy to drive fully integrated brain function), and conversely how many choices exist in everyday life that could tilt things in the direction of more good days (by helping to stabilize more optimal nervous system performance) (Herbert and Weintraub 2012).

The short time course needed for biologically effective EMF/RFR ‘doses’ to lead to observable impacts reflects that these exposures can affect cells without obstruction (unlike many chemical agents), and create impacts within minutes. This type of mechanism may also give us fresh and important ways of understanding the short-term variability – the good days and the bad days – that are so common in ASD even in those who do not have a formal diagnosis of mitochondrial disease.

3. Pathophysiology and allostatic load

Based on these considerations, the strategy to be pursued in this examination of a potential EMF/RFR – ASD link is to review the many parallels between underlying biology, or pathophysiology, in ASDs and the impacts of EMF/RFR on living organisms. EMF/RFR exposures have demonstrated impacts at just about every level at which biology and physiology have been shown to be disrupted in ASDs. EMF/RFR has been shown to potentiate the impact of various toxicants when both exposures occur together (Juutilainen, Kumlin, and Naarala 2006); this may be additive or more than additive. This suggests that EMF/RFR may synergize with other contributors and make things worse. With many different environmental factors piling on to a much smaller number of environmentally vulnerable physiological mechanisms (Herbert 2010), one must consider that the model of ‘allostatic load’ – the sum total of stressors and burdens – may be central to understanding how the many risk factors interact to create autism – and to create a spectrum of levels of severity across so many of ASD’s associated features. A cascade of exposures interacting with vulnerabilities can potentially lead to a tipping point for an individual, such as the phenomenon of autistic regression experienced by a substantial subset of people with ASDs. When exposures increase at the population level, we are likely to see trends of increase in the number of people passing that tipping point and getting diagnosed. EMF/RFR exposures have increased several thousand-fold or more in the past two decades from wireless technology innovations that have unplanned side effects from pulsed RFR, a newly classified human carcinogen (Baan et al, 2011). Nearly six billion people globally own wireless phones, for example. Many hundreds of thousands more are exposed to wireless whole-body transmissions from wireless antenna facilities (Sage and Carpenter, BioInitiative 2012 Report, Section 24). For this as well as for physiological reasons allostatic loading as a viable concept for the study of ASDs should reasonably address EMF/RFR as one of the collection of exposures of relevance to the overall stress load, since it is now a chronic and unremitting exposure in daily life at environmentally relevant levels shown to cause bioeffects from preconception and pregnancy through infancy, childhood and the whole lifecourse.

In an article entitled “Unrelenting Stress is Toxic,: The New Scientist (28 July 2012) describes stress in an eloquent way:

“Unrelenting stress is toxic because it can turn the body’s defense system against itself. Neuroendocrinologist Bruce McEwen at Rockefeller University in New York says the stress response that evolved to protect us from harm can be hijacked and actually cause harm when the stress level never abates. In a normal situation, the introduction of stress causes the body to deliver a boost of energy – by sending a surge of glucose to the muscles – and to increase heart rate, blood pressure and breathing to get oxygen to the muscles in hurry. At the same time, blood vessels constrict and clotting factors increase – ready to slow bleeding in case you are wounded. These responses are a part of a fight-or-flight survival kit, and once the stress has passed, these should subside. But for people under unrelenting stress, this response never quite switches off – leaving sugar levels unregulated, high blood pressure, increate risk of blood clots, depressed sex drive and an immune system buckling under the strain. Prolonged exposure to stress hormones can have other effects as well, including affecting the brain by altering the structure of the neurons and their connections, which in turn can influence behaviour and hormonal processes.”

This passage refers to effects on the hypothalamo-pituitary-adrenal axis (Aldad, 2012), but as will be discussed in the Part II, equally important is cellular stress from stress proteins (heat shock protein HSP) and from oxidative stress generated at very low- intensity EMF and RFR levels as detailed in the BioInitiative 2012 Update, Section 7 by Martin Blank, PhD; Blank, 2012). Both are significant kinds of stress that can add body- burdens via allostatic loading.


This is just a taste of some of this very well-researched article which makes a compelling case for caution when it comes to EMF’s and Autism.

I highly recommend you bookmark this article to send to your skeptical friends and read the rest of it as you have time.

Serious Research On The Dangers Of EMFs and Autism

If you’re convinced that caution in the face of EMF radiation is a good idea for your family, click here to find out what I recommend as an affordable and effective EMF shielding solution.

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