Mechanisms of Disease Causation in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis

Will the real ringmaster please stand up?

By Arthur Brawer, MD, PA

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The unequivocal demonstration that patients suffering from chronic fatigue syndrome (CFS)/myalgic encephalomyelitis have pervasive metabolic abnormalities has led to a dramatic shift in efforts to identify mechanisms of disease causation.1,2 The complexity of the metabolic abnormalities is daunting, as they involve mitochondrial dysfunction, epigenetic factors, microbiota, cell membrane permeability, leukocyte respiration, enzymatic reactions, substrate availability, the central nervous system, the autonomic nervous system, adenosine triphosphate (ATP) production in muscle, oxidative phosphorylation, central sensitization, matrix macromolecules, endocrine receptor activity, and routine levels of metabolites.1-7 Compounding all of this are reports of endogenous viral reactivation and immune dysregulation in CFS.1,2,7 The latter includes cytokine elevations, reduced natural killer cell function, alterations of B-cell subunits and T-cell numbers, and changes in activation markers on T-cell surfaces.

What could possibly be causing such diverse pathophysiological disruptions? The answer may lie in studies of similar biochemical disturbances in women suffering from the recently identified (and decidedly real) recurrent public health debacle known as silicone breast implant toxicity (SBIT).5,6,8,9

Of the 2 million women in the United States who have had silicone implants over the past 11 years, 100,000 have had them permanently removed in the past 4 years, to alleviate a multitude of grievous ailments.9 Silicone gel–filled breast implants are just 1 of 60,000 man-made organosiloxane (organosilicon) compounds (OSCs) that contain artificial silicon-carbon bonds (bonds that never occur in nature).5,6,10,11 These 60,000 molecules, synthesized over the past 80 years, now contaminate every worldwide environmental compartment and are a “mission impossible” for any living organism to contend with.5,6,10-12 They are pervasive, and they routinely enter the body via inhalation, dermal absorption, and ingestion.5,10-12

Recent studies found elevated levels of OSCs and/or their degradation products (eg, silanols) in random household inhabitants, frogs, seals, and honeybees.5,13,14 These molecules can biointegrate into matrix macromolecules, disrupting an endless number of overlapping functions.6,8 They are harmful to bacteria, and they can disrupt enzyme functions, cross the blood-brain barrier and chelate neurotransmitters such as dopamine, block the parasympathetic activity of acetylcholine, stunt the demand for augmented energy production during exercise, perturb mitochondrial-induced immune activation, enhance nociception, suppress leukocyte respiration, enhance mast cell degranulation, alter cell membrane permeability (especially in muscle), donate methyl groups to mercury already accumulated in the body (producing the more powerful toxin, methyl mercury), and donate methyl groups to DNA.5,6,8,11,15,16

Enhanced DNA methylation proceeds simultaneously with biointegration changes in other epigenetic determinants (eg, histones and micro RNAs), in large part because silicon behaves like a metal at times, altering electromagnetic fields.5,16-18 The resulting disruption of communication networking may skew human DNA expression to trigger immune dysregulation and reactivate Epstein-Barr virus and other latent viral genomic materials acquired during a lifetime.16 These changes can create the illusion that CFS is triggered by an acute viral infection when, in fact, lymphadenopathy, fever, and sore throats may be manifestations of a disease process already well underway.

Silicone gel–filled breast implant toxicity provides a model that can inform CFS research; SBIT is mediated by multiple disruptions of the body’s biochemistry that are virtually identical to observations in CFS.

The biointegration and altered communication phenomena can be extrapolated to other life-sustaining molecules, such as the electron transfer system of mitochondria.5,16,19 This creates a double-edged sword, since mitochondria typically orchestrate cell danger–responses to metabolic disruptions caused by environmental toxicity.7 Thus, OSCs are more harmful to life on earth than pesticides, phthalates, polyhalogenated compounds, and endocrine receptor disruptors.5,7,20

Decades of assertions by physical chemists that OSCs are chemically and biologically inert are now untenable. National Aeronautics and Space Administration (NASA) scientists routinely restrict astronauts’ exposure to OSCs to minimize illness during space exploration. We now know that the decimation of honeybees, previously thought to be related to pesticide-induced immune suppression, is caused by OSC surfactants added to enhance insecticide stickiness.18 The resulting distortion of electromagnetic fields in honeybee brains prevents them from honing back to the hive; instead, they fly around in disarray before succumbing to exhaustion.16

Do you know any patients with CFS who drive into the wrong neighborhood on their way home?

Many, if not all, of the above physiologic and metabolic malfunctions are transmissible when cell division occurs, explaining the term “chronic” in CFS.20 Silicone gel–filled breast implant toxicity provides a model that can inform CFS research; SBIT is mediated by multiple disruptions of the body’s biochemistry that are virtually identical to observations in CFS.5,6,8,9 However, CFS itself is a gross oversimplification of SBIT, which manifests as a vast array of clinical phenomena that are often life-threatening. Manifestations of SBIT are particularly harmful due to biochemical chaos caused by in vivo exposure to an exceedingly excessive polymer presence. Therefore, SBIT may be an extreme form of a more subtle metabolic toxicity that manifests as CFS in the general population.5,6

Should we discard all perspectives on the cause of CFS from narrowly focused specialists, such as endocrinologists, immunologists, neurologists, psychiatrists, muscle physiologists, cardiologists, and infectious disease specialists?

Not really, because their unicompartmental observations can provide clarification in the aggregate.

However, cytokine elevations, immune dysregulations, and endogenous viral reactivations observed in patients with CFS are likely to be epiphenomena and not primary events, arising as amplification loops in symptomatic individuals after OSCs initiate pervasive biochemical and metabolic dysfunctions.

It has taken decades to determine that the controversial and vague illness known as CFS is a medical reality. Now it is time for all researchers to get on the same page.

Errata: In the original publication of this article, some of the references were attributed incorrectly due to an error on the part of the editorial team. The author's submission correctly attributed the references. The citations were corrected on December 7, 2018.

About the Author

Arthur Brawer, MD, PA is an arthritis specialist whose educational career developed at Brandeis University, Boston University School of Medicine and Boston University Medical Center. For the past thirty-eight years he has maintained a private practice in Long Branch, New Jersey, and has been the Director of Rheumatology at Monmouth Medical Center. He has held the position of Associate Clinical Professor of Medicine at both Robert Wood Johnson Medical School and Hahnemann/Drexel College of Medicine. His research topics include arthritis, alternative medicine, environmentally-related ailments and others, which have been published in multiple peer-reviewed medical journals.

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