Shorts

Jule Klotter

EMF Immunosuppression

Electromagnetic fields (EMFs) can stimulate or inhibit the immune system, depending upon the exposure quality, duration, frequency, power density, and the state of the cell or organism. P.R. Doyon and O. Johansson present a possible explanation for EMF immune suppression found in multiple laboratory and epidemiological studies in their 2017 Medical Hypotheses article. Federal regulations only look at the thermal effects of EMF. As a result, non-thermal effects, which have been documented for decades, are largely ignored. For example, Doyon and Johansson cite research by K.S. Nageswari and colleagues who, back in the 1980s, exposed rabbits to chronic low-power microwave radiation (2.1 GHz @ 5 mW/cm² for 3 hours daily, 6 days a week for 3 months). Nageswari et al, according to Doyon and Johansson, reported “significant suppression of T-lymphocyte numbers; lymphoid cell depletion in lymph node, spleen, and appendix; recurrent infections; an increased susceptibility to bacterial infection; an increase in the number of large leukocytes; a decrease in the number of small leukocytes, neutrophils, and erythrocytes; [and] leukocytosis” in the exposed animals. Studies involving people exposed to various EMFs during work also show decreases in total lymphocytes and in T-lymphocytes (T8, CD4, and CD3), as well as other markers of immune function.

Doyon and Johansson hypothesize that EMF exposure that leads to immune suppression is due to calcineurin inhibition. Calcineurin is an enzyme involved in numerous cellular development and cell cycle progression pathways. It also activates T-lymphocytes. High production of reactive oxygen species (i.e., nitric oxide, superoxide, and hydrogen peroxide), leading to oxidative stress, is known to inhibit calcineurin. Radio frequency electromagnetic fields (RF EMF) (e.g., from WiFi, cell phones, smart meters, television and radio transmission) are known to increase oxidative stress. Doyon and Johansson cite a 2016 review by I. Yakymenko and colleagues that found 93 out of 100 peer-reviewed studies found oxidative stress in biological systems exposed to low-intensity RF EMF.

EMFs—depending on the frequency, power density, and modulation—open voltage-gated calcium channels (VGCCs) in cell outer membranes, causing a “pathological” flow of extracellular calcium ions into the cell. The calcium ions stimulate the enzyme nitric oxide syntase and affect superoxide dismutase, causing a buildup of reactive oxygen species and oxidative stress that inhibits calcineurin and, thereby, suppressed the immune system.

Pharmaceutical calcineurin inhibitors, such as cyclosporine, pimecrolimus, and tacrolimus, suppress the immune system in order to prevent organ rejection in transplant recipients. Doyon and Johansson point out that opportunistic infections (i.e., fungal, viral, atypical bacterial, and parasitic) are a major side effect of immune suppressing drugs. They say:

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The same opportunistic infections induced as side effects in transplant recipients taking immunosuppressant calcineurin inhibitors to prevent organ rejection – reactivated viral (EBV, CMB, coxsackie, etc.), candida, mold, bacterial (mycoplasma), and parasitic (toxoplasmosis) infections – have also been uncovered in a number of what have been described as neuro-immune dysfunction syndromes….eg, CFS, ASD, ADHD, and Alzheimer’s disease.

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Doyon and Johansson say that two research avenues need to be conducted to prove or negate their hypothesis. First, researchers need to see whether EMFs decrease calcineurin levels in immune cells like they do in muscle and bone cells. Second, experiments (not epidemiology) need to show whether long-term low-level EMF exposure causes immunosuppression and increased opportunistic infections. Given the push for 5G technology and the increase in WiFi devices, identifying the parameters (frequencies, etc.) that suppress the immune system seems urgent, to me.

Whether or not the hypothesis offered by Doyon and Johansson proves to be totally accurate, decreasing EMF exposure is prudent advice for anyone who is dealing with chronic infectious disease.

Doyon PR, Johansson O. Electromagnetic fields may act via calcineurin inhibition to suppress immunity, thereby increasing risk for opportunistic infection: Conceivable mechanisms of action. Medical Hypotheses. 2017;106:71-87.

Ozone Without Borders

In response to his experience during the 2014 Ebola outbreak in Sierra Leone, Robert Jay Rowen, MD, has co-founded Ozone Without Borders (https://ozonewithoutborders.ngo ; www.ozonewithoutborders.com). This non-profit humanitarian international organization aims to unify the bio-oxidative therapy community and encourage the use of oxygen therapies and related non-pharmaceutical treatments internationally.

Medical ozone has been used to treat infectious, immunological, and circulatory conditions for about 100 years. Like the ozone naturally generated by immune cells, medical ozone kills pathogens. It also inactivates many viruses, preventing their entry into cells where they reproduce. In addition to fighting pathogens, medical ozone modulates the immune system, balancing inflammatory/anti-inflammatory cytokines; elevates antioxidant enzymes such as SOD; increases glutathione; increases red blood cell flexibility; and improves oxygen delivery to tissue.

When the Ebola crisis made headlines in 2014, Dr. Rowen and Dr. Howard Robins took 10 ozone generators, donated by manufacturer Longevity Resources, Inc. (Vancouver, BC), and buffered vitamin C and Thiodox, donated by Allergy Research Group (California) to Sierra Leone with the intention of training medical personnel to treat Ebola patients. Overall, about 60% of the people infected with Ebola die. During the 2014 outbreak, conventional treatment consisted of an extremely expensive, experimental drug called ZMapp. Pharmaceutical makers were also trying to develop a vaccine. Ozone therapy cost about $5 per person.

During staff training at the Freetown Hastings Ebola Center, Sierra Leone’s Minister of Health called the clinic and ordered the training to stop. Despite the health ministry’s ban, five people were treated with ozone at the clinic, using a protocol developed by Rowen and Robins. Four were health care workers at the clinic, and the fifth was the female companion of a physician who had died from the disease. Rowen, Robins, and Sierra Leone colleagues described these cases in a 2016 article, published in the African Journal of Infectious Diseases. Four patients, three of whom tested positive for Ebola virus, had symptoms. The five received direct intravenous gas administration, rectal gas administration, and/or ozonized water along with vitamin C and glutathione as support. Although treatment was given for up to 10 days, the authors were surprised at how quickly symptoms resolved: “within a few days and with limited treatments.” Recovery began with the first treatment.

Death from Ebola is actually due to a cytokine storm, the immune system’s hyperactive response to the virus’ rapid reproduction. It is the cytokine storm that damages the vascular system and tissues, resulting in hemorrhage and organ failure. Ozone oxidizes sulfhydryl groups, found on the lipid envelope glycoproteins of some viruses such as cytomegalovirus; sulfhydryl groups are the means by which the virus enters cells to replicate. Oxidation of the sulfhydryl groups prevents the virus from entering a cell; consequently, it cannot reproduce. The authors believe that this is how ozone therapy inactivates Ebola virus. In addition, ozone, especially with high-dose vitamin C, modulates the damaging high levels of NO, TNF-alpha, and inflammatory cytokines that occurs with Ebola virus disease.

Survival rates at the Freetown Hastings Ebola Center was 40%, yet all five of the ozone-treated patients survived. The authors note that all five were in early stages of the disease; the effect on critically ill patients is unknown.

Case reports have historically been the basis for defining possible research topics. Given the severity of this infection, wouldn’t it make sense to follow up? Even though ozone, vitamin C, and glutathione will never cost what a new drug will?

Fassa P. American Doctor Kicked out of Africa for Healing Ebola with Ozone Therapy Instrumental in Creating Internation “Ozone Without Borders.” Health Impact News. April 23, 2018.

Rowen RJ, et al. Rapid Resolution of Hemorrhagic Fever (Ebola) in Sierra Leone with Ozone Therapy. Afr J Infect Dis. 2016;10(1):49-54.

Herbicides and Antibiotic Resistance

The overuse of antibiotics in agriculture is not the only factor causing pathogens’ resistance to antibiotics. Other chemicals, including herbicides, can induce antibiotic resistance. In a 2015 study, Brigitta Kurenbach and colleagues tested pathogen response to antibiotics after herbicide exposure. They exposed colonies of Escherichia coli and Salmonella enterica serova Typhimurium to one of three common herbicides and to combinations of the herbicides: Kamba (active ingredient dicamba), 2,4-D, or Roundup (active ingredient glyphosate). They then measured the bacterial response to five different types of antibiotics: ampicillin, ciprofloxacin, chloramphenicol, kanamycin, and tetracycline.

The authors found that the magnitude of response varied by bacterial species, antibiotic, and herbicide. The salmonella bacterium become more resistant to ampicillin, ciprofloxacin, chloramphenicol, and tetracycline but more susceptible to kanamycin after being exposed to non-lethal doses of 2,4-D or dicamba. Roundup significantly increased the salmonella’s tolerance to kanamycin and ciprofloxacin but had no effect on or increased salmonella’s susceptibility to ampicillin, chloramphenicol, and tetracycline. E. coli had a similar response to Kamba and 2,4-D except it did not show more tolerance to ampicillin. While Roundup also increased E. coli’s tolerance to kanamycin and ciprofloxacin, it had no effect or increased susceptibility to ampicillin, chloramphenicol, and tetracycline. The authors noted that all herbicide exposures to both species increased resistance to ciprofloxacin.

When herbicides that caused similar changes were combined, the effect increased. While the amount of herbicide needed to cause a maximum response was above residue limits allowed under international trading laws, the amount needed to cause a detectable change was lower than the label-specified herbicide application rate.

The observed antibiotic responses to the bacteria in this study has real world consequences. The minimum concentration of an antibiotic in an agar plate at which no growth was observed when about 10⁸ CFUs of bacterium was applied to the plate surface (MIC) increased three-fold or more with some herbicides. Kurenbach et al cite a 2013 study in which a majority of hospitalized patients did not get high enough doses to affect cipro-susceptible strains of E. coli, Klebsiella ispp., Enterobacteriaceae, Proteus spp., and Pseudomonas aeruginosa: “A 2-fold change in the MIC of infecting strains…was enough to cause 21% of patients to get a lower-than-target dose of the antibiotic, and when the MIC reached a 4-fold increase…75% of patients failed to received the target dose.”

Kurenbach and colleagues state: “This increasingly chemically potent world necessitates a rethinking of how we measure and regulate exposures to common products. Testing each compound in isolation and only for severe effects on microbes, as is done during risk evaluation of herbicides, may underestimate its role in the emergence of antibiotic resistance phenotypes.”

Kurenbach B, et al. Sublethal Exposure to Commercial Formulations of the Herbicides Dicamba, 2,4-Dichlorophenoxyacetic Acid, and Glyphosate Cause Changes in Antibiotic Susceptibility in Escherichia coli and Salmonella enterica serovar Typhimurium. mBio. March/April 2015; 6(2).

Roundworms (Toxocara)

Roundworms, parasites that live in the intestines of cats and dogs, made headlines in the New York Times earlier this year. Toxocariasis is one of the most overlooked but prevalent parasitic infections. Areas with a large number of stray animals or where pets do not get regular veterinary care and worming have higher levels of roundworm eggs in the soil. Once in the soil, these eggs, containing infective third-stage larvae, can be ingested by humans or other non-host animals via contaminated food, water, soil, utensils, or unwashed hands. A 2018 review, led by Guangxu Ma, explains that, once ingested, the larvae do not mature in non-host animals or humans; but they do enter the circulatory system through the small intestinal wall. Once in circulation, the larvae travel to the lungs, liver, muscles, and central nervous system where they can remain for years. While asymptomatic infection is common and usually self-limiting, roundworm infection can produce a diverse—and sometime serious—range of symptoms. The most common clinical signs include coughing, wheezing, myalgia, itching, rashes, panniculitis, and vasculitis. Ma et al say that lymphadenopathy, granulomatous hepatitis, myocarditis, nephritis, and arthritis have also been observed. Infection of the eye is common in children, ages 3-16 years, impairing sight and causing chronic inflammation of the inner eye and retina. ELISA and immunoblot testing criteria are available for toxocariasis, but the tests will not determine whether the infection is still active.

Albendazole is the preferred anthelmintic for acute toxocariasis because it, like the larvae, distributes throughout the body once metabolized. Prevention consists of thorough hand-washing, preventing children from eating possibly contaminated dirt, and avoiding raw or undercooked meat of any kind. Cows, sheep, chicken, and rabbits—like humans—can be infected with roundworm eggs. Prevention strategies are particularly important in areas of high poverty or areas that have a large number of stray dogs.

Beil L. The Parasite on the Playground. The New York Times. January 16, 2018.

Ma G et al. Human toxocariasis. Lancet Infect Dis. 2018;18:e14-24.