One of the mysteries of immunology: the function of B cells (green) in the thymus gland was previously unknown. Researchers have now been able to show that the immune cells help to prevent T cells from attacking the body. [Jan Böttcher, Thomas Korn / TUM]
Researchers from the Technical University of Munich (TUM) and the Ludwig Maximilian University of Munich (LMU) have discovered that the immune cells known as B cells contribute to the “training” of the T cells in the thymus gland. If this process fails, autoimmune diseases can develop.
“Neuromyelitis optica is a paradigmatic autoimmune disease of the central nervous system, in which the water-channel protein AQP4 is the target antigen,” the researchers wrote. “The immunopathology in neuromyelitis optica is largely driven by autoantibodies to AQP42. However, the T cell response that is required for the generation of these anti-AQP4 antibodies is not well understood. Here we show that B cells endogenously express AQP4 in response to activation with anti-CD40 and IL-21 and are able to present their endogenous AQP4 to T cells with an AQP4-specific T cell receptor (TCR).”
The team was led by Thomas Korn, PhD, professor of experimental neuroimmunology at TUM and a principal investigator in the SyNergy Cluster of Excellence, and Ludger Klein, PhD, professor of immunology at LMU’s Biomedical Center (BMC).
Neuromyelitis optica is an autoimmune disease similar to multiple sclerosis (MS). While it is not yet known which molecules are attacked in MS, it is well-established that T cells respond to the protein AQP4 in neuromyelitis optica. AQP4 is most prominently expressed in cells of the nervous tissue, which then becomes the target of the autoimmune reaction. Frequently, the optic nerve is affected.
The researchers were able to show that in the thymus gland of humans and mice not only the epithelial cells but also B cells express and present AQP4 to the T cell precursors. If the B cells were prevented from doing so in animal experiments, AQP4-reactive T cell precursors were not eliminated and the autoimmune disease developed. This was also the case when the epithelial cells still presented the molecule. The team concludes from this that B cells in the thymus are a necessary condition for immune tolerance regarding AQP4.
“We suspect that this previously unknown process has evolved particularly to prevent dangerous interactions between autoreactive T and B cells in the lymph nodes and spleen, the so-called peripheral immune compartment,” explained Klein. Once the immune system is developed, B and T cells can communicate and thus trigger highly effective immune reactions. This is useful when it comes to fighting pathogens quickly. On occasion, however, B cells may accidentally present the body’s own proteins, such as AQP4. If the T cells that react to AQP4 had not been sorted out in the thymus, this could lead to a sudden and violent large-scale attack on the body.
“We assume that problems with the training of T cells by the B cells in the thymus can cause other autoimmune diseases as well,” said Korn. “After all, the B cells in the thymus present a whole range of the body’s own proteins. The corresponding interactions must be investigated in further studies.”
According to the researchers, likely suspects include antiphospholipid syndrome (APS) and certain forms of cerebral amyloid angiopathy. “Looking further into the future, this interaction in the thymus might be exploited to treat existing autoimmune diseases in a very targeted manner,” said Korn.
Two years after the end of a randomized trial that showed a benefit of daily vitamin D and omega-3 fatty acid (n-3 FA) supplementation for reducing risk for autoimmune diseases, the salubrious effects of daily vitamin D appear to have waned after the supplement was discontinued, while the protection from n-3 lived on for at least 2 additional years.
As previously reported, the randomized VITAL, which was designed primarily to study the effects of vitamin D and n-3 supplementation on incident cancer and cardiovascular disease, also showed that 5 years of vitamin D supplementation was associated with a 22% reduction in risk for confirmed autoimmune diseases, and 5 years of n-3 FA supplementation was associated with an 18% reduction in confirmed and probable incident autoimmune diseases.
Now, investigators Karen H. Costenbader, MD, MPH, of Brigham & Women’s Hospital in Boston, Massachusetts, and colleagues reported that among 21,592 participants in VITAL who agreed to be followed for an additional 2 years after discontinuation, the protection against autoimmune diseases from daily vitamin D (cholecalciferol; 2000 IU/d) was no longer statistically significant, but the benefits of daily marine n-3 FAs (1 g/d as a fish-oil capsule containing 460 mg of eicosapentaenoic acid and 380 mg of docosahexaenoic acid) remained significant.
“VITAL observational extension results suggest that vitamin D supplementation should be given on a continuous basis for long-term prevention of [autoimmune diseases]. The beneficial effects of n-3 fatty acids, however, may be prolonged for at least 2 years after discontinuation,” they wrote in an article published on January 25 in Arthritis & Rheumatology.
Costenbader told Medscape Medical News that the results of the observational extension study suggest that the benefits of vitamin D “wear off more quickly, and it should be continued for a longer period of time or indefinitely, rather than only for 5 years.”
In addition to the disparity in the duration of the protective effect, the investigators also saw differences in the effects across different autoimmune diseases.
In an interview with Medscape Medical News, Janet Funk, MD, MS, vice chair of research in the Department of Medicine and professor in the School of Nutritional Science and Wellness at the University of Arizona, Tucson, Arizona, who was not involved in the study, saidthat the results suggest that while each supplement may offer protection against autoimmune diseases, the effects are inconsistent and may not apply to all patients.
“I think the VITAL extension results suggest that either supplement (or both together) may have benefits in reducing risk of autoimmune diseases, including possible persistent effects posttreatment, but that these effects are nuanced (ie, only in normal weight post-vitamin D treatment) and possibly not uniform across all autoimmune diseases (including possible adverse effects for some — eg, inverse association between prior omega-3 and psoriasis and tendency for increased autoimmune thyroid disease for vitamin D), although the study was not powered sufficiently to draw disease-specific conclusions,” she said.
In an editorial accompanying the study, rheumatologist Joel M. Kremer, MD, of Albany Medical College and the Corrona Research Foundation in Delray Beach, Florida, wrote that “[T]he studies by Costenbader, et al. have shed new light on the possibility that dietary supplements of n-3 FA [fatty acid] may prevent the onset of [autoimmune disease]. The sustained benefits they describe for as long as 2 years after the supplements are discontinued are consistent with the chronicity of FA species in cellular plasma membranes where they serve as substrates for a diverse array of salient metabolic and inflammatory pathways.”
VITAL Then
To test whether vitamin D or marine-derived long-chain n-3 FA supplementation could protect against autoimmune disease over time, Costenbader and colleagues piggybacked an ancillary study onto the VITAL trial, which had primary outcomes of cancer and cardiovascular disease incidence.
A total of 25,871 participants were enrolled, including 12,786 men aged 50 and older and 13,085 women aged 55 and older. The study had a 2 × 2 factorial design, with patients randomly assigned to vitamin D 2000 IU/d or placebo and then further randomized to either 1 g/d n-3 FAs or placebo in both the vitamin D and placebo primary randomization arms.
In multivariate analysis adjusted for age, sex, race, and other supplement arm, vitamin D alone was associated with a hazard ratio (HR) of 0.68 (P = .02) for incident autoimmune disease, n-3 alone was associated with a nonsignificant HR of 0.74, and the combination was associated with an HR of 0.69 (P = .03). However, when probable incident autoimmune disease cases were included, the effect of n-3 became significant, with an HR of 0.82.
VITAL Now
In the current analysis, Costenbader and colleagues reported observational data on 21,592 VITAL participants, a sample representing 83.5% of those who were initially randomized, and 87.9% of those who were alive and could be contacted at the end of the study.
As in the initial trial, the investigators used annual questionnaires to assess incident autoimmune diseases during the randomized follow-up. Participants were asked about new-onset, doctor-diagnosed rheumatoid arthritis, polymyalgia rheumatica, psoriasis, autoimmune thyroid disease, and inflammatory bowel disease. Participants could also write in any other new autoimmune disease diagnoses.
There were 236 new cases of confirmed autoimmune disease that occurred since the initial publication of the trial results, as well as 65 probable cases identified during the median 5.3 years of the randomized portion, and 42 probable cases diagnosed during the 2-year observational phase.
The investigators found that after the 2-year observation period, 255 participants initially randomized to receive vitamin D had a newly developed confirmed autoimmune disease, compared with 259 of those initially randomized to a vitamin D placebo. This translated into a nonsignificant HR of 0.98.
Adding probable autoimmune cases to the confirmed cases made little difference, resulting in a nonsignificant adjusted HR of 0.95.
In contrast, there were 234 confirmed autoimmune disease cases among patients initially assigned to n-3, compared with 280 among patients randomized to the n-3 placebo, translating into a statistically significant HR of 0.83 for new-onset autoimmune disease with n-3.
Costenbader and colleagues acknowledged that the study was limited by the use of doses intended to prevent cancer or cardiovascular disease and that higher doses intended for high-risk or nutritionally deficient populations might reveal larger effects of supplementation. In addition, they noted the difficulty of identifying the timing and onset of incident disease, and that the small number of cases that occurred during the 2-year observational period precluded detailed analyses of individual autoimmune diseases.
X chromosome inactivation is a crucial biological process with some inadvertent autoimmune consequences.
Shaped by thousands of years of evolution, the body’s immune system is a vigilant guardian primed against external infectious threats. Too much vigilance, however, and this guardian of potent cells and chemicals instead becomes our own adversary. The result is a myriad of autoimmune diseases affecting around one in five Americans and around four percent worldwide.
While one’s risk for autoimmune disease is partly genetic, individuals who are disproportionately affected tend to be those assigned female at birth — a shocking 78 percent. Why there’s such a staggering difference has been a mystery, but scientists have been narrowing down suspects to risk factors like hormones, the gut microbiome, and now, the X chromosome itself.
Researchers led by Stanford University found that a routine biological process that silences one X chromosome in females (called X chromosome inactivation) may be a risk factor for autoimmune diseases. In particular, proteins that help with the silencing process might seem foreign to our bodies, and the body might create antibodies against them, setting the stage for autoimmune diseases.
When male mice prone to autoimmune disease were genetically engineered with the Xist gene, they also showed signs of autoimmunity similar to what’s seen in their female counterparts. In blood samples collected from human participants with autoimmune diseases, the researchers also found antibodies against the proteins involved in X chromosome inactivation.
“Scientists have a better idea now of pinpointing the autoimmune risk associated in different sexes, and this comes from the chromosomal basis, individual molecules we can now perhaps pin this [to],” Howard Chang, professor of cancer research and genetics at Stanford University of Medicine, who led the study, tells Inverse.
THE MASTER SILENCER
All humans and many other mammals have a pair of sex chromosomes: two Xs for biological females and one X and one Y for biological males. Because chromosomes are basically individual recipe books that a cell uses whenever it needs to make something, having duplicates of the same book means the cell would end up making more than it needs, like making twice as many cakes. Twice as many cakes may sound benign, but for a cell, having that many genes turned on and baking all their proteins and other molecules they code for would be lethal.
To balance out the books, each cell randomly chooses an X chromosome to muffle during early embryonic development. As you might guess, this doesn’t happen in biological males, as they only have one X chromosome.
This biological silencing is handled by a gene found on the X chromosome called Xist, which was first discovered in the early 1990s. Xist doesn’t code for any protein — almost 99 percent of DNA doesn’t; instead, this gene manufactures something called long noncoding RNA, RNA being a Xerox copy of DNA that’s free to float around in the cell, unlike DNA packed away in chromosomes and confined to the nucleus.
Paradoxically, Xist is turned on in whichever X chromosome gets the short stick, says Chang. Its long noncoding RNA recruits other proteins to join in on the silencing, the whole mass of RNA and proteins sticking together to form what scientists call a ribonucleoprotein complex. This complex then coats the X chromosome like some sort of form-fitting molecular bodysuit.
In 2015, Chang and a group of other researchers published a paper cataloging the proteins forming the ribonucleoprotein complex. They didn’t have autoimmune disease on their minds, per se, when conducting their study but discovered many of the proteins associated with the complex could become parts of autoantibodies, aka antibodies that respond to and attack your own cells and tissues.
This discovery had the researchers wondering: Is Xist, the master silencer, somehow nefariously involved in autoimmune disease?
GENETICS + ENVIRONMENT
To answer that question, Chang and his colleagues inserted the Xist gene into the genome of male mice, some of whom were susceptible to autoimmune disease and others resistant. The Xist gene was tweaked so it could be turned on and off at will by chemical means, and the portion of the gene that instructs its RNA to silence the X chromosome was deleted. However, the long noncoding RNA could still mingle with other proteins to make its ribonucleoprotein complex. The experiment also included male mice where Xist wasn’t turned on, female mice, and healthy, otherwise normal mice.
Turning on Xist itself didn’t trigger autoimmunity, but when the mice were injected with pristane, a compound known to cause a lupus-like disease in the animals, that’s where Chang and his colleagues noticed signs of autoimmune disease in the genetically vulnerable mice on par with some of the female mice injected with pristane.
“Because we made a male mouse get [autoimmune] disease just with this RNA, that really shows that you don’t need female hormones,” says Chang. “You don’t even need a second X chromosome, just this RNA can confer a lot of the risk.”
In mice with Xist who weren’t susceptible to autoimmune disease, nothing really happened to them, which Chang says highlights how not just Xist alone but one’s genetic susceptibility for conditions like lupus, inflammatory bowel disease, or multiple sclerosis (and exposures to potential environmental triggers) needs to be present to explain one’s risk for autoimmune disease.
These findings are just the first step in unraveling the complexity of autoimmune disease and identifying more precise diagnostics and treatments to better help patients, says Chang. However, there are some limitations, namely the fact this study was in mice using an engineered form of Xist, not the one normally found in the X chromosome.
“If you use a version [of Xist] that’s slightly different, that could lead to slightly different results,” he says.
In a separate but parallel study, the researcher analyzed blood samples obtained from anonymous donations to the Stanford Blood Center. In those whose blood demonstrated signs of autoimmunity with autoantibodies, those antibodies were reactive to 79 out of the 81 proteins part of Xist’s ribonucleoprotein complex. So there is a basis for Xist potentially mediating autoimmune disease in humans, although Chang says he would love to see these results replicated in a larger population.
For upcoming studies, the researchers would also like to suss out how exactly the immune system chances upon this ribonucleoprotein complex since it’s otherwise sequestered inside the cell’s nucleus, out of sight by immune cells.
“Understanding what different triggers do, whether they cause cell death in a way that leaks out small or large amounts of Xist, that would be a useful thing to think about in the future,” says Chang.
Low-dose rituximab may be effective for patients with newly diagnosed generalized myasthenia gravis and may reduce the need for rescue therapies.
Little randomized trial evidence exists to support use of rituximab for myasthenia gravis (MG). In this trial, adults with non-thymomatous generalized MG, symptoms for <12 months, and a Quantitative Myasthenia Gravis (QMG) score of 6 or more (out of 39 points, with higher scores representing more-severe disease) were randomized without stratification to a single infusion of rituximab 500 mg (n=25) or placebo (n=22). Patients taking prednisolone >40 mg daily or other steroid-sparing immunosuppressants were excluded. Only two participants did not have acetylcholine receptor (AChR) antibodies. There were baseline differences between the groups: Rituximab recipients were older than placebo recipients (mean, 67 years vs. 58 years), had lower AChR antibody titers (25.1 nmol/L vs. 70.7 nmol/L), and were less severely affected according to Myasthenia Gravis Foundation of America classification (MGFA), but were more likely to be on prednisolone (64% vs. 55%).
The primary endpoint, reaching minimal manifestation status (QMG score ≤4) and prednisolone dose ≤10 mg daily at 16 weeks, differed significantly between the rituximab and placebo groups (71% vs. 29%). A treatment benefit was also observed at 24, 36, and 48 weeks. Secondary endpoints did not differ, including AChR antibody titers at 24 weeks, although they trended toward favoring rituximab use. Fewer rituximab than placebo recipients required rescue treatments (4% vs. 36%) or were hospitalized (0 vs. 3 patients). A fatal cardiac event in a patient with preexisting heart disease occurred in the rituximab group.
Comment
The authors postulate that the benefit of rituximab treatment in early myasthenia gravis may be related to the reduction of long-lived plasma cells responsible for antibody secretion, although they considered other mechanisms given the lack of difference in acetylcholine receptor antibody titers after treatment. The role for rituximab among newer treatments and the ideal long-term dosing schedule remain uncertain, but this trial supports its use as an option for some newly diagnosed patients.
Increased awareness of autoimmune encephalitis has led to two unintended consequences: a high frequency of misdiagnoses and the inappropriate use of diagnostic criteria for antibody-negative disease. Misdiagnoses typically occur for three reasons: first, non-adherence to reported clinical requirements for considering a disorder as possible autoimmune encephalitis; second, inadequate assessment of inflammatory changes in brain MRI and CSF; and third, absent or limited use of brain tissue assays along with use of cell-based assays that include only a narrow range of antigens. For diagnosis of possible autoimmune encephalitis and probable antibody-negative autoimmune encephalitis, clinicians should adhere to published criteria for adults and children, focusing particularly on exclusion of alternative disorders. Moreover, for diagnosis of probable antibody-negative autoimmune encephalitis, the absence of neural antibodies in CSF and serum should be well substantiated. Neural antibody testing should use tissue assays along with cell-based assays that include a broad range of antigens. Live neuronal studies in specialised centres can assist in resolving inconsistencies with respect to syndrome-antibody associations. Accurate diagnosis of probable antibody-negative autoimmune encephalitis will identify patients with similar syndromes and biomarkers, which will provide homogeneous populations for future assessments of treatment response and outcome.
Our disconnection from the virtually infinite and accessible storehouse of electrons at the earth’s surface is an overlooked cause of autoimmune disease. Revolutionary research is uncovering that physical contact with the ground provisions free radical-neutralizing electrons that circulate through the living matrix of our body and act as our primary antioxidant defense system
One characteristic intrinsic to the human experience is connection with the earth, that indelible interdependence with a foundational and primordial element, representing the antecedents from which we came and the soil to which we will return. Grounding to the earth galvanizes our senses and reawakens our ancient connection with the limitless free electron source residing in our planet.
Free Radical Excess is a Harbinger of Disease
In essence, the ground represents a reservoir of free and mobile electrons, or negative charges that have the potential to neutralize the positively charged free radicals, or reactive oxygen species (ROS), that can damage cell constituents and lead to disease and degeneration. Free radicals, such as hydrogen peroxide, hydroxyl radical, and superoxide anion radical are inherently unstable compounds that are both byproducts of aerobic metabolism and synthesized through different physiochemical and pathological states (1).
Admittedly, free radicals play hormetic or adaptive roles as signaling molecules in redox biology for maintenance of cellular homeodynamics (2), and may have in fact evolved as an essential signal transduction mechanism to enable changes in response to accessibility of environmental nutrients (3, 4). However, free radicals present in excess lead to a condition known as oxidative stress, which is the breeding ground for autoimmune disease and other chronic conditions including diabetes mellitus, cancer, ischemic diseases such as coronary artery disease, stroke, hypertension and preeclampsia, and neurodegenerative diseases including Parkinson’s and Alzheimer’s (1).
With respect to autoimmune disorders such as rheumatoid arthritis, systemic lupus erythematosus, and Sjögren’s syndrome, studies have shown that most patients have excessive burdens of oxidative stress or inadequate antioxidant defense systems compared to healthy controls (5). Oxidative stress is implicated in the pathophysiology of autoimmune disorders because an imbalance between free radicals and antioxidants up-regulates inflammation, stimulates apoptosis or cell suicide, and also induces loss of immunological tolerance, or the ability to distinguish self from non-self (5).
Grounding Counterbalances Free Radicals
Defined as “molecular species capable of independent existence that contain an unpaired electron in an atomic orbital,” free radicals tend to donate or accept electrons from other molecules, causing damage to nucleic acids, which contain the genetic material, as well as carbohydrates, lipids, and proteins (6). In effect, putting your bare feet on the ground may elicit an antioxidant effect, scavenging these free radicals and mitigating their harm. According to scientists,
The surface of the planet is electrically conductive…and its negative potential is maintained (i.e. its electron supply replenished) by the global atmospheric electrical circuit. Mounting evidence suggests that the Earth’s negative potential can create a stable internal bioelectrical environment for the normal functioning of all body systems (Chevalier et al. 2011).
The living matrix of the human, comprised of a “continuous molecular fabric of the organism, consisting of fascia, the other connective tissues, extracellular matrices, integrins, cytoskeletons, nuclear matrices and DNA,” participates in the exchange of electrical charges in order to maintain a state of equilibrium or homeostasis, allowing the transfer of charges as a preemptive strategy to mount an inflammatory response should infection or injury occur (7). To illustrate the magnitude of exchange of electrons in health, researchers discuss that patients with inflammatory disorders may actually deplete therapists during body work, massage, or hands-on energy medicine sessions (7). Thus, the influx of free electrons through barefoot contact with the earth, which are disseminated through intracellular biopolymers and the amorphous gelatinous material known as the ground substance of the extracellular tissue, has the potential to reduce acute and chronic inflammation through this mechanism (7).
The Lost Art of Grounding
In modern industrial societies, we have forsaken our quintessential link to nature, no longer oscillating with the natural cycles and exhibiting sacred reverence for the day-night, cosmic, seasonal, and interstellar forces, but rather adopting attitudes of superiority over nature and perceiving nature as an entity to be exploited and conquered. This loss of harmony with the natural rhythms is not only detrimental to our human psyche, which evolved to be fundamentally attuned to nature, but it also negatively impacts our health which is so inextricably linked with exposure to sunlight, the sounds of the natural world, and grounding with the earth.
Throughout the majority of evolutionary history, human beings slept on the group, went shoeless, or wore footwear fashioned from animal hides that allowed equilibration with the electrical potential of the earth, practices which have been discarded with what is perceived as the linear trajectory of human kind towards a pinnacle of advancement. However, our divorce from the earth is in some ways a regression, since we lost that pivotal energetic transfer from the ground to the body. By deviating from these primordial practices, alongside inundation with toxicants, electromagnetic radiation, genetically engineered, irradiated, and nutrient-poor food, the modern lifestyle has bred a climate ripe for disease.
The advent of plastic or rubber soled shoes, elevated beds, and high-rise buildings, which insulate the body from the electrical field of the earth, has coincided with unparalleled increases in the epidemic of chronic illness, including autoimmune disease (8). Not only that, but it decimates our defenses against electromagnetic pollution, as studies have demonstrated that grounding reduces the voltage induced on the body by a factor of seventy upon exposure to alternating current (AC) electric potential (8). In other words, the transfer of electrons from the earth to the body prevents the ubiquitous electromagnetic frequencies from interfering with the electric charges and activities of molecules inside our bodies, which is not insignificant given that “there is no question that the body reacts to the presence of environmental electric fields” (8).
Although direct contact with the earth is optimal, there are various conductive grounding systems commercially available that come as sheets, mats, adhesive patches, footwear inserts, or bands which can be worn or used inside the home for those who live with inclement weather conditions or who want to use grounding in clinical scenarios (9).
Innumerable Benefits of Grounding for Autoimmune Disease
1. Enhanced Sleep and Pain Relief
When subjects are grounded during sleep using a conductive mattress pad, significant improvements in diurnal cortisol rhythm were observed, trending towards normalization (10). In other words, cortisol, the stress and awakening hormone, reverted to the normal pattern of being high in the morning and low at night. This normalizing effect on the circadian rhythm is important since prolonged stress, often a triggering factor in autoimmune disease, can cause glucocorticoid receptor resistance which culminates in an ongoing inflammatory responses (11).
In the experiment, grounding led to better sleep onset latency, or the time it takes to fall asleep at night, as well as less sleep disruption and reduced night-time pain (10). Other studies have shown that grounded subjects exhibit less sleep dysfunction and significant relief from chronic joint and muscle pain compared to those in sham grounding conditions (12). Not only are individuals with sleep disturbances at increased risk for developing autoimmune disease (13, but impaired sleep perpetuates a cycle of pain (14), so a trial of a benign intervention such as grounding, which can truncate the vicious cycle, is of merit.
In regards to chronic pain, a common affliction in autoimmune populations, grounding unequivocally altered biomarkers of pain and immune system activity in one study of delayed-onset muscle soreness (DOMS) in men following eccentric exercise. In the experiment, healthy men performed calf raises while carrying one-third of their body weight on their shoulders. Researchers witnessed that those in the sham group had a sharp spike in white blood cells and greater pain perception, indicative of an inflammatory reaction, whereas those who were grounded had a slight decrease in white blood cells, significantly less pain, and shorter recovery time (8).
2. Blood Sugar Regulation
Patients with autoimmune diseases, including conditions such as ulcerative colitis, psoriasis, rheumatoid arthritis, Graves disease, and Hashimoto’s thyroiditis, are at increased risk of type 2, non-insulin dependent diabetes due to common mechanistic pathways (15). Blood sugar dysregulation, as well as insulin resistance, are also common antecedents or predisposing factors in the onset of autoimmune disease. Thus, it is promising that earthing has been shown to decrease fasting glucose among diabetics with poor glycemic control when implemented over a three-day period (8).
3. Decreased Immune Reactivity
Grounding has been proven to produce measurable changes in immune hyper-responsiveness, including changes in white blood cell counts, concentrations of inflammation-mediating cytokines, and other molecules that are involved in mounting inflammatory responses (9). Not only does grounding mitigate the cardinal signs of inflammation, including dolor (pain), calor (heat), tumor (swelling), rubor (redness), and function laesa (loss of function), but medical infrared imaging studies have shown that grounding precipitates rapid resolution of inflammation (9).
Researchers Oschman and colleagues (2015) theorize that earth-derived electrons can contribute to resolution of smoldering or silent inflammation and also, “suggest that mobile electrons create an antioxidant microenvironment around the injury repair field, slowing or preventing reactive oxygen species (ROS) delivered by the oxidative burst from causing ‘collateral damage’ to healthy tissue, and preventing or reducing the formation of the so-called ‘inflammatory barricade’” (9).The oxidative burst is the rapid production of free radicals by neutrophils, a subset of immune cells that invade injured sites and generate signals to induce repair, clear cellular debris, and eradicate pathogens (16). However, ROS are also capable of inducing damage to healthy cells, and their detrimental effects can be alleviated by earthing.
On the other hand, the inflammatory barricade that is erected with insult or injury walls off damaged tissue or infection to effectively prohibit migration of pathogens or debris into healthy tissue. However, the inflammatory barricade can lead to chronic inflammation because it impedes the navigation of regeneration-promoting cells and antioxidants into the sequestered area. Researchers hypothesize that this cycle of persistent inflammation secondary to the inflammatory barricade can be arrested via grounding, which saturates the body with electrons, reverses the ‘electron deficiency’ that engenders the barricade in the first place, and enables wound healing (9).
4. Endocrine Balance
One hallmark of autoimmune rheumatic diseases is over-production of inflammation-inciting cellular messengers known as pro-inflammatory cytokines, which potently activate the hypothalamic-pituitary-adrenal (HPA) axis which oversees our stress response (17). This leads to a cellular milieu where pro-inflammatory autoimmune-exacerbating hormones predominate over anti-inflammatory hormones such as glucocorticoids, which sets up an inflammatory cascade favoring tissue destruction (17).
However, earthing has been observed to influence this often dysregulated hypothalamic-pituitary-adrenal-thyroid axis (8). In fact, some individuals need to taper down their dose of thyroid medication after beginning grounding in order to circumvent hyperthyroid symptoms, presumably because their thyroid glands begin to work more efficiently (8).
5. Blood Viscosity
Research has elucidated that the majority of autoimmune disorders, including as systemic lupus erythematosus (SLE), inflammatory bowel disease (IBD), and Behçet’s syndrome are all accompanied by increased propensity for venous thromboembolism (VTE), or blood clots that form in deep veins (18). This is likely because of perturbations in the innate immune system and the fact that “Systemic inflammation modulates thrombotic responses by suppressing fibrinolysis, upregulating procoagulant, and downregulating anticoagulant” (18). These processes favor clot formation and prevent the degradation of blood clots.
Luckily, experimenters found that healthy subjects grounded for two hours demonstrated significantly less aggregation of red blood cells, indicating a substantial reduction in blood clotting potential (19). In addition, the grounded participants possessed greater zeta potential, which is a marker for the ability of red blood cells to repel each other (19). In fact, the anticoagulant effect of earthing is so potent that international normalized ratios (INRs) must be supervised by physicians when an earthing regimen is undertaken by an individual on a blood-thinning medication like coumadin (8).
6. Autonomic Balance
Grounding has been shown to shift the autonomic nervous system from sympathetic fight-or-flight to parasympathetic rest-and-digest, also known as breed-and-feed. In fact, participants in an earthing condition exhibited immediate deactivation of the former and concomitant activation of the latter (20). Experimenters observed that subjects who were grounded exhibited various parameters, such as increased respiratory rate and stabilization of blood oxygenation, both indicative of a metabolic healing response that requires enhanced oxygen supply (20).
In addition, grounding improves heart rate variability (HRV), a measure of regulation of the autonomic nervous system and a surrogate marker for cardiovascular risk when low (21). Preliminary studies have revealed that between twenty-four and one hundred percent of patients with autoimmune disease experience autonomic dysfunction, also known as dysautonomia, meaning that they have impaired regulation of bodily functions governed by this all-encompassing system (22). The autonomic nervous system is responsible for diverse functions such as urination, defecation, digestion, heart rate, blood pressure, pupillary response, and sexual arousal, so dysautonomia can disrupt all of these largely unconscious physiological activities. Thus, grounding is suggested to be a viable complementary therapy for autoimmune disease, especially in cases where sympathetic tone predominates over parasympathetic.
Enhanced activity through the parasympathetic branch also improves the bidirectional communication network between the central nervous system (brain and spinal cord) and gut-associated lymphoid system (GALT) known as the gut-brain axis, leading to better intestinal blood flow, motility, and gastric secretions, all of which optimize digestion and discourage bacterial overgrowth, gastrointestinal infections, and intestinal permeability (23), which represent root causes of autoimmune disease.
Moreover, improved parasympathetic tone activates efferent or outward-conducting fibers of the longest cranial nerve in the body, known as the vagal nerve, which extends from the brainstem to the abdomen and interfaces with most internal organs including the heart, lungs, and digestive tract. Studies have revealed that electrical grounding improves vagal tone in both adults and preterm infants, possibly reducing neonatal morbidity, improving stress resilience, and engendering autonomic balance (24).
The vagal nerve also innervates or supplies receptors on immune cells, which have the effect of influencing the peripheral immune system in an anti-inflammatory direction when activated (25, 26, 27). In addition, stimulating anti-inflammatory neurotransmission through the vagal nerve dampens down the activity of glial cells, leukocytes, and macrophages, parts of the immune system which produce pro-inflammatory signaling molecules which can exacerbate autoimmune disease (28).
Changes in Electron Content Influence Cellular Function
In the absence of contact with the earth, distorted electrical gradients can amass due to heterogenous charge distribution. This uneven distribution of charges can in turn affect the functioning of enzymes, essential proteinaceous elements which catalyze the reactions that drive life itself. This occurs because the pH of biological fluids and even the three-dimensional conformation of molecules, upon which their proper activity is contingent, can be influenced by charge perturbations in the environment.
Binding of substrates, or the precursor molecules for chemical reactions, to active sites on enzymes, is influenced by the electrical microenvironment. Similarly, the ability to donate or accept hydrogen atoms, and the activity of voltage-gated ion channels which transport substances into or out of the cell, is all dictated by electrical charges. Correct timing of electrochemical impulses is vital to the functioning of the nervous system, so much so that variations in local electrical profiles can lead to aberrant firing and ensuing pathology (29).
Photo by Kelly Sikkema on Unsplash
The Evidence Supports Earthing
Rather than a woo-woo concept, flow of electrons, gravitating from the earth to the body, has been scientifically documented (30). Earthing has been transplanted from the realm of alternative medicine folklore to the domain of a scientifically substantiated therapy for ailments of many kinds, including aging, since aging is inextricably linked to inflammatory burden (31). In their review paper, Chevalier and colleagues (2012) discuss that undergoing an earthing practice has preliminary evidence of improving autoimmune conditions such as rheumatoid arthritis, multiple sclerosis, and lupus, presumably by the aforementioned biochemical mechanisms. Regular earthing may also elicit improvements in cardiovascular arrhythmias, hypertension, osteoporosis, asthma and other respiratory conditions, sleep apnea, and premenstrual syndrome (PMS) (8).
Moreover, electrons supercharge the electron transport chain of the mitochondria, our energy-producing organelles, preventing onset of chronic fatigue syndrome (CFS) symptomatology (9). By being semi-conducted and dispersed through our connective tissue matrixes made of ground substance, cytoskeleton, collagen corridors, and body fluids, the electrons from the earth are able to quickly offset oxidative damage and protect healthy tissue (9).
Throughout history, traditional cultures have referred to the biofields that surround our bodies as prana, cosmic ether, qi, the four humours, and the odic force, among multiple other names. The wisdom in these ancient concepts, which transcends cultural demarcations and spiritual designations, is being validated by the discovery that we reside within bioelectromagnetic bodies. Not only can we be conceptualized as beings of light, since we liberate quantum particles known as biophotons or ultra-weak photonic emissions, but we also emit electromagnetic fields, which are produced with the movement of electrical charges.
In addition, innovations in biophysics and cellular biology are illuminating that, “the human body is equipped with a system-wide collagenous, liquid-crystalline semiconductor network known as the living matrix” (9) which is capable of directing electrons to any bodily location in the event of injury or disease in order to confer protection at the cellular, tissue, and organ level (21). In fact, this vast whole-body redox network which includes cell membrane proteins called integrins, pores across the nuclear envelop, nucleic proteins called histones, and architectural proteins such as microtubules and microfilaments, is being considered the primary antioxidant system of the body in some research circles (9). In other words, the body acts as both a storage facility and dissemination service to absorb or donate antioxidant electrons to site of disease or degeneration, in a process facilitated by grounding (9).
Researchers in fact state that damaging oxidant molecules may have evolved as part and parcel of the inflammatory and pathogen-fighting response only because the infinite electron source that is the earth was available to counteract their deleterious effects (9). As articulated in the scientific literature, “Electrons from the earth may in fact be the best antioxidants, with zero negative secondary effects, because our body evolved to use them over eons of physical contact with the ground” (9).
Thus, this substrate of energy, which animates us and governs our finely-orchestrated physiological phenomena, is essential to health. The surface of the earth, therefore, represents an untapped and indispensable therapeutic resource with the potential to improve a myriad of inflammatory maladies. Failing to recharge our bodies with regular contact with the earth, is a certain recipe for degeneration, demise, and debility.
Myriad symptoms and three different sets of classification criteria make Sjögren’s syndrome a challenging diagnosis, according to a presenter at the Congress of Clinical Rheumatology East.
“Sjögren’s is an oft-neglected topic in rheumatology,” Fredrick B. Vivino, MD, MS, of Penn Presbyterian Medical Center, in Philadelphia, said in his presentation.
“Sjögren’s is an oft-neglected topic in rheumatology,” Fredrick B. Vivino, MD, MS, told attendees.
Despite its neglected status, Vivino noted that the disease has meanwhile become the second most common autoimmune disease. As many as 20 million Americans report dry eyes, while some 4.5 million Americans have “clinically significant” dry eyes, according to findings from the Women’s Health Study and Physicians Health Study.
“We have gone from being very rare now to being considered quite common,” Vivino said.
Regarding demographics, because the disease was initially described in Scandinavian women, the “typical patient” has historically been a middle-aged white woman, according to Vivino. However, it can now be seen in younger women and those with different racial and ethnic backgrounds, notably including tennis star Venus Williams.
Vivino stressed that some 80% of patients present with sicca syndrome.
That said, this manifestation is not always present.
“You can diagnose Sjögren’s in the absence of sicca symptoms,” Vivino said. “Please, please keep that in mind.”
Other symptoms at presentation may include seropositive polyarthritis, polymyalgia rheumatica, leukocytoclastic vasculitis, demyelinating disease, peripheral neuropathy, inflammatory myositis, salivary gland swelling or accelerated caries.
In addition, the differential diagnosis can range from chronic sialadenitis to IgG4 syndrome, medication-related dryness to sarcoidosis.
“The most common cause of sicca in this country is medication-related dryness,” Vivino said.
Turning to diagnosis and classification, Vivino first urged rheumatologists to assess patients for the objective presence of salivary gland involvement and proof of autoimmunity. Sialometry or abnormal ultrasound may be used to assess dry mouth and salivary glands.
Vivino then offered a tip for proving autoimmunity: “At the present time, the most reliable way is to test for the presence of anti-SSA, or anti-Ro, antibodies,” he said.
A lip biopsy also may aid in diagnosis. According to Vivino, biopsies should be graded for the presence of lymphoepithelial lesions.
“Lip biopsies are frequently misread,” Vivino said, noting that this occurs when a clinician fails to calculate a focus score, cite QNS/sampling error, measure tissue surface area or describe chronic sialadenitis.
“It behooves us to work with a pathologist,” he said.
According to Vivino, classification of Sjögren’s has been difficult because there are currently three sets of criteria being used. The 2002 American European Consensus Group (AECG) classification criteria still maintain some relevance, as do the 2012 ACR-SICCA criteria and an ACR-EULAR document from 2016, he added.
Vivino acknowledged that with three different classification criteria and such an uncertain array of symptoms, it can be difficult to diagnose Sjögren’s.
“I get confused myself from time to time,” he said. “If you rely strictly on classification criteria, you are going to miss some diagnoses.”
With this in mind, Vivino described the what he called the “physician gold standard” of diagnosis, which he defined as three of the following four criteria: Objective evidence of dry eyes, objective evidence of salivary gland involvement, anti-SSA positivity and/or focal lymphocytic sialadenitis, based on a Focus score greater than 0.25 mm2.
“You need to take a reasonable, common-sense approach to diagnosis,” he said. “If you do that, you will miss very few diagnoses.”
An imbalance in the gut “microbiome” of people with lupus may be driving the chronic autoimmune disease as well as its flare-ups, new research suggests.
The microbiome is the trillions of helpful bacteria that coexist in the human digestive tract and elsewhere in the body.
Comparing gut bacteria from lupus patients with bacteria from their healthy peers, scientists learned those with lupus had about five times more of the bacteria known as Ruminococcus gnavus.
The discovery may lead to better treatments for lupus, which can damage the skin, joints and organs, study author Dr. Gregg Silverman said.
“Current lupus therapies seek to dampen or destroy the immune system,” said Silverman, a professor of medicine and pathology at NYU Langone Health in New York City.
“The idea that we might find in some patients that their disease is being worsened by bacteria in their intestine may mean we [find] much more benign therapeutic approaches,” he added. “This is something I’m excited about because I think it really relates to the health and well-being of patients and people.”
Lupus affects an estimated 5 million people worldwide, according to the Lupus Foundation of America. The cause of the sometimes-fatal disease is unknown, though genetics are believed to play a role. Symptoms can vary and include joint and muscle pain, rashes, hair loss, fatigue and swelling in various body areas.
The gut microbiome is perhaps the most studied of the bacterial communities in the human body. It’s been linked in scientific research to various diseases and immune system function.
For the new study, Silverman and his colleagues analyzed blood and stool samples from 61 women with lupus for bacteria content and immune proteins called antibodies, which develop to fight bacteria and other pathogens. The researchers compared these findings with 17 healthy women of similar ages and racial backgrounds.
In addition to the marked increase in R. gnavus bacteria among lupus patients, the bacteria correlated with a high level of antibodies in these patients, the findings showed.
The results also indicated that disease flare-ups — which can include skin rash, joint pain or even severe kidney problems that require dialysis treatments — were linked to increases in R. gnavus bacteria and antibodies.
Silverman now believes that a “leaky gut” that allows bacteria to escape from the intestines might serve as an immune system trigger of lupus.
“It’s even more challenging now to actually figure out how to use this [information] to make better diagnostic tests and therapies for people” with lupus, Silverman said, adding that specific tests and treatments based on the findings might be available within one to three years.
Dr. David Pisetsky is a professor of medicine at Duke University School of Medicine in North Carolina, and wasn’t involved in the new research. But he said the study provided new knowledge and “is a different way of thinking about the relationship of an autoimmune disease to exposure to bacteria.”
Perhaps antibiotics, which kill bacteria, or probiotics, which promote the growth of certain beneficial bacteria, can be used instead of hard-hitting immune-suppressant drugs to help treat lupus, he said.
“There’s a growing understanding of the importance of the microbiome in human health and disease,” added Pisetsky, who is on the scientific advisory board for the Lupus Research Alliance.
Novel research reveals that blocking exposure to electromagnetic fields (EMF) produces significant symptom changes in 90% of patients with autoimmune disease. No longer can it be ignored that manmade electromagnetic radiation poses innumerable risks to human health
The Ubiquity of Electrosmog
Concerns about electromagnetic fields (EMF) are branded pseudoscientific conspiracy theories and relegated to the realm of tin-hat wearing quackery. However, a recent publication in the peer-reviewed journal Immunologic Research entitled “Electrosmog and Autoimmune Disease,” sheds new light on the validity of concerns about this so-called electrosmog with which we are constantly inundated.
Although we encounter natural microwave electromagnetic radiation in the form of cosmic radiation from outer space, the aurora borealis, and thunderstorms, the vast majority of electrosmog that we encounter is largely manmade (1). These atmospheric phenomena, however, emit electromagnetic radiation at lower radio frequencies and are negligibly weak in comparison to manmade sources, which have increased exponentially due to the emergence of television, cellular phone technologies, and WiFI, all of which utilize microwave frequency bands (1).
According to researchers Marshall and Heil (2017), for instance, “The recent release of WiGig and anti-collision vehicle radars in the 60 GHz region embody a 1000-fold increase in frequency, and photon energy, over the exposures mankind experienced up until the 1950s” (1).
How Electrosmog Interfaces with the Bioelectromagnetic Body
It is intuitive that electrosmog would interact with human biology, since human physiology operates in part via electromagnetic fields. Apart from physical information superhighways such as the blood, nervous, and lymphatic systems, the body uses electromagnetic forms of energy transmission and communication which are several orders of magnitude faster than chemical diffusion (2).
Called biophotonic emission (BPE), these quanta of electromagnetic energy have a visibility one thousand times lower than the sensitivity of our naked eye and are quintessential to cellular metabolism and to the powering of our energy-intensive nervous and immune systems (3). Harbored within our genetic material, biophotons serve as a mode of instantaneous communication from one body part to another and to the extraneous world (4) and their emission is influenced by our global state of health (5). Research even suggests that mental intention and the fabric of our consciousness is mediated by these quantum of light, which operate as highly coherent frequencies and generate an ordered flux of photons (4).
Thus, both the stuff of consciousness and the functioning of our cellular energetics is premised upon electromagnetism, which may be susceptible to distortion by electrosmog. Curtis and Hurtak describe the electromagnetic body as both “an entire body distinct from the chemical body that interpenetrates it” and “a light circulatory system operating on an energetic level in a markedly different manner from that of its molecular counterparts” (2). That there is “an incredible amount of activity at levels of magnification or scale that span more than two-thirds of the 73 known octaves of the electromagnetic spectrum” (6) in the human body is emblematic of our vulnerability to electromagnetic disturbances.
Potential Immune Disturbances due to Electrosmog Exposure
Although current public health laws are predicated on effects of short-term exposure, research suggests that dosage and repetitive exposures likely influence health risk of electrosmog (7). Two thirds of studies examined report ecological effects of electromagnetic radiation, and researchers state that, “current evidence indicates that chronic exposure to electromagnetic radiation, at levels that are found in the environment, may particularly affect the immune, nervous, cardiovascular and reproductive systems” (7).
Although the conventional mantra is that no harm is incurred from low-energy radio waves, low-level exposures to ionizing radiation are known to manifest profound effects upon human physiology (1). Ionizing radiation exposure, which occurs secondary to nuclear energy accidents, for example, produces immunosuppression, so much so that some scientists have even suggested radon exposure as a therapeutic treatment for rheumatoid arthritis due to its inhibition of inflammatory immune messengers such as the adipokine visfatin (8).
There is, however, often a substantial lag time between exposure and the materialization of symptomatology (1). The detriment to immune defense “often does not become apparent until the body catastrophically fails to overcome an acute challenge” (1). In addition, new science is overturning the previous assumption that immunosuppressive effects are exclusive to ionizing radiation exposure.
A research group headed by Lushinov, for example, found that repeated exposures to low-level non-ionizing electromagnetic radiation impaired the immune response in mice, negatively influencing immunogenesis, or the ability of the immune response to respond to an immune-provocating antigenic substance (9). The exposure to low-intensity electromagnetic radiation negatively influenced thymic and splenic cellularity, causing a statistically significant decrease in the immune cells generated by these lymphoid organs (9). The immunocompetence of the Aegean wall lizard was also significantly reduced upon daily exposure to radiofrequency resembling the amount of electrosmog emitted from cordless phones (10).
Moreover, Gapeev and colleagues (2006) elucidated that exposure to low-intensity non-ionizing electromagnetic waves exerted equivalent immunosuppressive effects to a single dose of the nonsteroidal anti-inflammatory drug (NSAID) diclofenac (11). In another experiment, exposure to low-intensity electromagnetic radiation reduce the footpad edema and local hyperthermia, also known as swelling and heat, that accompanied injection of zymosan, an agent that induces acute inflammation (12). This constitutes evidence that electrosmog exposure may impair the normal immune response to potential threats.
Human Proteins are Responsive to Electromagnetic Waves
Biomolecules, which are constantly undergoing molecular collisions and interacting on the scale of picoseconds, are subject to forces exerted by incident electromagnetic fields (1). According to researchers Marshall and Heil, “It seems likely that signals a million times lower than those currently being used in research may be sufficient to elicit a tangible change in human biology” (1).
Induction of Stress Proteins
Electrosmog at both an extremely low-frequency (ELF) or in the radio frequency (RF) range has been found to stimulate a cellular stress response, leading to expression of stress response genes including heat shock protein 70 (HSP70) (13). As a consequence, there is increased production of highly conserved stress proteins, which serve as chaperones by refolding and repairing damaged proteins (13). Heat shock proteins have likewise been observed to up-regulate an immune response, “transferring antigenic peptides to the class I and class II molecules of the major histocompatibility complexes” as well as increasing activity of a class of immune cells which perpetuate an immune reaction, such as macrophages and dendritic cells (14).
Aberrant Anti-Microbial Response
In addition, the function of another human protein, lysozyme, has been shown to be disrupted by electromagnetic radiation (15). Also called muramidase, lysozyme is an antimicrobial enzyme liberated from cytoplasmic granules of immune cells such as granulocytes and macrophages (16). Contained in human secretions such as mucus, tears, saliva, and breast milk, this bacteriolytic element degrades glycosidic bonds in peptidoglycan, a molecule prominent in the cell walls of gram-positive bacteria (17).
Lysozyme is a major contributor to bactericidal activity, facilitating elimination of inhaled airborne microorganisms to prevent their colonization in the respiratory passages, which would interfere with sterile gas exchange (17). Studies have indicated that depletion of lysozyme reduces bacteria-killing ability of human airway sections by approximately fifty percent (18). Animal studies also highlight how lysozyme is especially important in host pulmonary defense, since, “Increased concentration of lysozyme in the airspaces of transgenic mice enhanced bacterial killing whereas lysozyme deficiency resulted in increased bacterial burden and morbidity” (17).
Turton and colleagues (2014) published a study in Nature Communications showing that non-ionizing terahertz electromagnetic radiation altered the binding of lysolyme to its ligand, triacetylchitotriose, which in turn would affect the biological function of lysozyme (15). Although this represents a much higher frequency than normal background electrosmog, the implications are that human immune defenses against pathogen invasion and virulence may be adversely affected due to repeated and cumulative exposures to electrosmog (15).
Derangements in Vitamin D Pathways
Research shows that Vitamin D Receptor (VDR) pathways are susceptible to interference by electrosmog (1). Functionality of the vitamin D receptor, a transcription factor that translocates to the nucleus and influences gene expression when bound to vitamin D, is fundamental for immunomodulation. The cascade of effects that occur upon vitamin D binding to its receptor reinforce gut barrier integrity, establish oral tolerance, and suppress autoimmune responses by enabling the immune system to differentiate self from non-self.
According to researchers, the shape of the VDR molecule transforms with electrosmog exposure within the frequency range of WiFi routers: “Groups of hundreds of atoms which form the helical “backbone” of the VDR…shift together at the lower frequencies present in electrosmog” (1). Sophisticated molecular dynamics software, which illustrates the lock-and-key interaction between the vitamin D receptor and its native ligand, 1,25-dihydroxyvitamin-D (1,25-D), have shown that so-called Lorentz forces act upon charged oxygen atoms in carboxyl groups of the vitamin D receptor (1). These Lorentz forces may either promote or hinder activation of the vitamin D receptor, depending on both the frequency of the “molecular interactions, and that of the impinging electromagnetic waves” (1).
Electrosmog Affects Human Brain Activity and Behavior
As far back as 1987, Bise published a pilot study wherein electrosmog exposure at levels dramatically lower than that observed in urban areas elicited transient changes in human brain waves and behavior (19). He reports, “Constructive and destructive interference patterns from standing waves within the skull possibly interact with the bioelectric generators in the brain, since electroencephalogram wave amplitudes and frequencies increased or decreased respectively at different radio wavelengths” (19).
What’s more, the literature reveals that neuroimaging and electroencephalography studies demonstrate enhanced cortical excitability with EMF exposure, particularly in the front-temporal regions, which is paradoxically correlated with faster reaction times, but may also interfere with sleep (20).
Alarmingly, the patterns observed in human electroencephalograms (EEG) was altered by wave amplitudes as low as -100 dBm (19). Bise was able to induce an immediate frontal headache at a level of -60 dBm (19). Unfortunately, barring use of a Faraday cage, these experiments are impossible to replicate since electrosmog background levels in cities are now 100,000 times stronger at -50 dBm (19).
In a recent case series, patients wore shielding clothing and tenting consisting of silver-coated polyester threads interspersed with bamboo fibers that were partially capable of blocking penetration of microwave electrosmog (1). Due to anecdotal testimonies of improvement, researchers decided to distribute standardized garments that would shield the brain and brain stem in order to systematically analyze the results (1).
In this study, 64 patients with assorted autoimmune diagnoses such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), multiple sclerosis (MS), Sjogren’s syndrome, and celiac disease, many of whom were disabled and house-bound, were recruited (1). Subjects wore the silver-threaded cap for four hours at night and for four hours during the day, and patient-reported outcomes were collected (1). Impressively, 90% of patients indicated a “definite” or “strong” change in their symptomatology, which is at variance with the 3% of the population that is estimated to be sensitive to electrosmog (1).
Some researchers have attributed this so-called electro-hypersensitivity (EHS) or idiopathic environmental intolerance (IEI) to the nocebo effect. However, Dieudonné explores the possibility of a psychosomatic mechanism in the journal Bioelectromagnetics, and concludes, “Overall, symptoms appear before subjects start questioning effects of EMF on their health, which is not consistent with the hypothesis that IEI-EMF originates from nocebo responses to perceived EMF” (21).
In this groundbreaking study, it is also telling that the researchers found the therapeutic efficacy of the silver-coated caps to be so theoretically plausible that they decided the idea of using a control group was unethical. These authors concluded that autoimmune patients exhibit a pronounced susceptibility to electrosmog at levels normally encountered in home and occupational environments, and hypothesized that the exposure may be contributing to their disease etiology (1).
Electrosmog and Mitochondrial Dysfunction
Because electric fields result from voltage differences, whereas magnetic fields from the flow of electric current, EMFs may be capable of disrupting the finely orchestrated proton gradient and flow of electrons within the inner mitochondrial membrane upon which the process of oxidative phosphorylation is contingent (13). Oxygen-dependent aerobic respiration, which relies upon oxidative phosphorylation, is the process that drives production of the cellular energy currency adenosine triphosphate (ATP) in our cellular energy factories, the mitochondria.
These organelles are fundamental to every energy-dependent process in the body but especially quintessential for the energy-demanding nervous system. Thus, EMF-mediated changes in mitochondrial function may affect cognition and even perpetuate development of neurodegenerative diseases such as Alzheimer’s and Parkinson’s in which mitochondrial dysfunction has been demonstrated. In fact, EMF-induced disruption of mitochondria may play a role in many diseases in which mitochondrial collapse is implicated, including psychiatric disorders, autoimmune diseases, migraine headaches, ataxia, stroke, diabetes, heart disease, neuropathic pain, chronic fatigue syndrome, fibromyalgia, and liver disease (22, 23).
It has also been proposed that EMFs can interact directly with electrons in DNA, so it is not a stretch that EMFs could interact with the electron transport chain (ETC) in mitochondria (24). This concept is supported by a study where pulsed electromagnetic radiation (EMR) resulted in alterations in the ETC, leading to adverse metabolic changes, cellular hypoxia, and increased generation of oxidative stress inducing free radicals such as the superoxide anion (25).
Electrosmog and Cancer
Although the undoubtedly industry-influenced mainstream consensus is that EMFs do not play a role in the development of childhood cancers, “Kheifets and Shimkhada [2005] stated that epidemiologic studies of ELF-EMFs and childhood leukemia are difficult to design, conduct, and interpret due to the fact that EMFs are imperceptible, ubiquitous, have multiple sources, and can vary greatly over time and short distances” (13). Also, in an animal study, a correlation between ELF-EMF radiation and development of malignant tumors, specifically gliomas and schwannomas of the heart, was discovered (26).
These findings led the American Academy of Pediatrics (AAP) to revise their criteria for EMF exposure in children, and include recommendations such as using hands-free and wired headsets, holding the phone away from the head, limiting television watching, and texting when possible (13). Currently, a 14-country study called MOBI-Kids is being conducted to examine the carcinogenic effects of RF-EMFs from mobile telephones on the central nervous system in children and adolescents (27).
Further upstream, electrosmog has also been shown to induce DNA strand breakages, such that “Any extensive damage or changes to DNA that need repair may increase the risk of developing cancerous cells” (13). Studies also suggest that electrosmog causes genome-wide alterations in methylation (28), or the attachment of one-carbon tags to DNA sequences which modulate gene expression, affecting everything from neurotransmitter production to detoxification.
Mitigating Electrosmog Exposure
Although more data is needed, the science warrants exercising the precautionary principle and taking simple steps to minimize EMF exposure. To remediate electrosmog, renowned doctor Dietrich Klinghardt recommends removing cordless phones from the house, turning off WiFi, switching off fuses at night, considering an EMF-reducing sleep sanctuary or canopy, and grounding.
Moreover, fundamental to neutralizing the toxic effects of electrosmog is spending time in nature and grounding in order to scavenge free radicals and engender antioxidant effects. Direct contact with the surface of the earth precipitates an influx of electrons, which are absorbed and distributed throughout the ground substance of extracellular tissue as well as intracellular biopolymers, neutralizing oxidative stress in the body (29).
Studies have elucidated that grounding decreases the voltage imposed on the body by a factor of seventy upon exposure to alternating current (AC) electric potential (30). This transfer of electrons that occurs as a result of grounding, therefore, can minimize electrosmog-induced derangements in the electrical activities of our bodies, which is meaningful since researchers state that, “There is no question that the body reacts to the presence of environmental electric fields”
Being “real people sick.” Ugh! Regular illnesses can definitely affect blood sugar and diabetes management. Is there a reason why we can feel so terrible? In this TED-Ed video “The surprising reason you feel awful when you’re sick,” Marco A. Sotomayor explains what’s actually making you feel sick.
“It starts with a tickle in your throat that becomes a cough. Your muscles begin to ache, you grow irritable, and you lose your appetite. It’s official: you’ve got the flu. It’s logical to assume that this miserable medley of symptoms is the result of the infection coursing through your body — but is that really the case?
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