Why Are Public Health Officials Playing Dumb Over The Alarming Rise Of Paralyzing Polio-Like Infections In American Children This Year?
Public Health Officials Said To Be Clueless Over Outbreak Of Paralytic Polio-Like Infections In Children
November 27, 2018
An alarming rise in the number of cases of a mysterious polio-like illness that produces paralysis in
young children is said to have “health officials scrambling to figure out the cause.”[1] Baffled infectious disease experts are quoted to say: “What we do know is that these patients had fever and respiratory symptoms 3 to 10 days before their limb weakness.”
But the primary culprit, believed to be enterovirus 68, produced no laboratory confirmed cases in 2016. The World Health Organization has been charting acute flaccid paralysis on a worldwide basis for some time now. It is not a new phenomenon. However, acute flaccid paralysis confirmed by viral testing was not even reported in America in the years 2003-2004.[2] Nor was a single case of acute flaccid paralysis reported in the U.S. till the fall of 2014 (120 confirmed cases). Over 150 cases have been reported by mid-November 2018.[3] This outbreak is geographically widespread, reported in 46 states.[4] This suggests contaminated food rather than water may be involved.
Enterovirus-68, which is the enterovirus believed to be triggering the recent outbreak of flaccid paralysis, was first isolated in 1962 from children with respiratory illness and remained in limited circulation in the U.S. for four decades with only 26 cases reported between 1970 and 2005.[5]
Acute flaccid paralysis is defined as sudden paralysis in any part of the body of a child less than 15 years of age, though this paralysis may also occur among adults.[6] Paralysis may be due to infection by the polio virus or non-polio viruses.[7]
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The disturbing photos of young children who can’t move their
limbs has the public on edge. A scientific report published in the
European Journal of Pediatric Neurology is numbingly entitled:
“Enterovirus D68 acute flaccid paresis: destroying young lives.”[8]
With a growing number of distressing news reports, The Centers For
Disease Control has assembled a task force to make it appear it is
dealing with the problem.[9]But precisely what can public health authorities do but wait for a vaccine that can never materialize because there are myriads of enteroviruses that have been identified. As of 2016 there were 110 genetically distinct enteroviruses that infect humans.[10]
There will never be a 110-in-1 shot that inoculates against all enteroviruses. Modern medicine is so overcommitted to vaccines as its sole armament against infectious disease it can’t even concede the medical literature points in a clear but intentionally overlooked direction: nutrition.
The family of viruses involved are known as Picornavidae and include Coxsackie viruses and widely circulating enterovirus 68 and 71 which millions of children are exposed to with only a very few cases gravitating to paralysis.
The public may hope and pray their children never are infected by these enteroviruses. But virtually everyone on the planet is or will be infected at some time or another and will experience a mild fever as memory antibodies are produced against them. Most will develop life-long immunity to this infectious disease.
Enteroviruses, which include the polio virus, are RNA viruses that are parasites that reside inside living cells and replicate rapidly. Upon exposure the innate immune system (first responding white blood cells – monocytes, neutrophils) is alerted and limits the infection.
Enteroviruses are said to be the most common viral agents in humans. The medical literature indicates most enterovirus infections are mild or asymptomatic, but for unexplained reasons a few individuals (mostly children age 6 months to 15 years of age) suffer from nervous system attack of varying degrees of severity.[11]
Because contagious enteroviral infections may produce sores and rashes around the mouth, hands and feet or buttocks, they are also classified as “hand-foot-and-mouth disease.” Personal hygiene (hand washing) is recommended though enteroviruses are better prevented with nutrition.
The provision of supplemental zinc almost immediately calms these symptoms and quickens their disappearance.[12]
These enteroviral infections are seasonal in nature and more common in spring and the fall. Symptoms may last for a few days and include fever, refusal to eat and fatigue. Given that enteroviruses are generally considered to be harmless, how do these horrific cases of paralysis emanate?
Widespread environmental contamination
Contaminated water[13] and food[14] are blamed. But enteroviruses are ubiquitous (found in all) foodstuffs. One study shows infective enteroviruses were found in 79% of crops.[15]
Food and water are just the common vectors – the pathways of transmission. Enteroviruses (Picornaviruses) are the most common infectious agents encountered by mankind.[16] The health status of human populations has been linked with the seasonal load of enteroviruses in water supplies.[17] Because enteroviruses produce symptoms similar to those produced by the influenza virus, most victims initially believe they have the flu.
The virus is shed in stool after infection and often transferred back to infants as mothers change diapers and fecal material is transferred from hand to mouth. Viral shedding from stool can persist for months.[18]
Recurrence of infection can occur as there are a group of viruses, the most common being Coxsackie virus, that are ubiquitous in foods, water and the environment.
Handwashing, which is a commonly advised practice to prevent re-infection from viral shedding in stool, will do nothing to prevent exposure to enteroviruses in food and drinking water.
Beyond polio and paralysis
Enteroviruses can be nasty and life threatening. Enteroviruses cause polio, hand-foot & mouth disease, respiratory illness, gastroenteritis, meningitis, myocarditis (heart), hemorrhagic conjunctivitis (eye bleed), pancreatitis and Type I (childhood onset) diabetes and Guillain-barre syndrome (progressive toe-to-head paralysis).
Turning point: enter arsenic
But why are just a few young children out of millions overcome by this virus?
We begin to learn more from a landmark report that serves as a turning point in the understanding of how to prevent and treat enteroviruses. This telling report was published in 2010 and largely ignored. Researcher Ylva Molin reveals how arsenic, a heavy metal, influences the replication of coxsackie viruses (this virus named after the city in New York where such an enteroviral outbreak occurred).
Wikipedia notes that non-viral causes of polio-like symptoms are observed from chemicals like arsenic.[19]
Ylva Molin, now a senior scientist in microbiology, notes there is no effective antiviral treatment or vaccine for enteroviral infections. Her report identifies arsenic as an aggravation factor in these viral infections. Low-dose arsenic was found to impair innate immunity. Several changes in trace elements (metals) are noted during viral infections.
Coxsackie virus (an enterovirus) changes the balance of trace elements in tissues. The most pronounced change induced by arsenic in animal experiments was arsenic’s ability to decrease blood serum zinc (-64%) and intestinal selenium levels (-30%).[20]
Many viruses mutate extremely rapidly in selenium deficient individuals resulting in greater severity and prolongation of infection. All studies point to selenium deficiency worsening the course of viral infections. Without adequate selenium the body cannot produce selenoproteins which protect against DNA damage. Selenium deficient mice develop more harmful lung inflammation after being infected with influenza virus (vaccination).
Selenium deficiency results in increased vulnerability to enteroviruses like enterovirus-71 that is associated with hand-foot-and-mouth disease.[21]
A report entitled: “Get enough selenium to prevent a viral catastrophe!” is very telling. Where soil selenium levels are extremely low, infectious disease rates rise. This is demonstrated in Keshan County, China where a fatal heart condition arises due to Coxsackie virus infection. Soil selenium levels are extremely low in Keshan, meaning plant foods that deliver selenium to the human body are lacking in that trace mineral. When people in Keshan were given a selenium supplement the incidence of Coxsackie virus-induce heart disease declined by 95%! Selenium makes it easier for the human immune system to eliminate viruses.[22]
When locally produced food does not furnish at least 19.1 micrograms of dietary daily selenium to adult males, Keshan heart disease occurs.
Unrecognized factor: mutations in enteroviruses
Selenium deficiency does more than impair the human immune system from fighting back against enteroviruses. Selenium deficiency makes enteroviruses more virulent and potentially lethal. When selenium deficient mice were genetically bred so they didn’t produce a selenium-derived antioxidant (glutathione peroxidase) and then exposed to influenza virus, the flu virus was much more virulent.[23] The provision of selenium alters the genetic makeup of the infecting Coxsackie virus, converting it from virulence to non-virulence.
Mineral chelation as therapy
Given there is no effective treatment for enteroviruses, the chelation of metals may be considered antiviral therapy. Several trace elements are essential for immune defense, namely zinc (for activation of T cells), selenium (for activation of glutathione peroxidase).
Arsenic adversely affects both selenium and zinc nutriture, the two trace minerals that are most prominent in immune defense.
Widespread arsenic pollution via a weed killer
Arsenic pollutes water supplies everywhere. The U.S. Environmental Protection Agency sets the standard for arsenic in drinking water to 10 parts per billion (or 10 micrograms). A reverse osmosis water filter on your tap water source will eliminate arsenic altogether.
But arsenic is getting into foodstuffs via a stealth man-made source — pesticides. Glyphosate, the most commonly used weed killer used in agriculture, has only recently been found to have significant amounts of hidden arsenic.
No more than traces of glyphosate were ever imagined to get into food stuffs. But a recent study found only 2 of 45 samples of food products made with conventionally grown oats were free of glyphosate.[24]
The Moms Across America website claims glyphosate as Roundup (Monsanto) has a hidden ingredient – arsenic. Arsenic was banned as a pesticide since 1973. Roundup is reported to contain 600-1200 parts per billion of arsenic.[25] Only 0.17 parts per billion has been reported to cause chronic poisoning.
NOT glyphosate
What pesticide makers have done is nothing short of sleight of hand. They list the main ingredient in their weed killers as glyphosate which does not kills weeds at all, then hide the really toxic ingredients in “formulants” that are never tested for toxicity.
Published scientific reports say glyphosate is NOT the major toxic compound in herbicides, petroleum compounds such as POEA and heavy metals like arsenic at levels that exceed well above admissible ones in drinking water are. DEFARGE
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There are also inert (biologically inactive) ingredients in
pesticides that are not included in pesticide labels. The most toxic
substance found in these pesticides is not glyphosate but POEAs
(polyethoxylated alkylamines), and along with isobutane and petroleum
distillate in glyphosate pesticides may induce DNA damage. However
these so-called adjuvants are characterized as inert ingredients. POE
is said to be the primary toxic principle toxin in human cells exposed
to pesticides[26] being 100 times more toxic than glyphosate.[27] POEA persists in the soil past the season it was administered.Some 10-20 percent of glyphosate-based herbicides are unidentified adjuvants or formulants in their products. The toxic properties and hormone altering properties of glyphosate are largely produced by the POEA formulant alone. Heavy metals including arsenic are also found within glyphosate herbicides. This is new data that was not evaluated by regulatory agencies and it appears there is no longer sufficient data to ensure safety of glyphosate products.[28]
The US maximum contaminant level of glyphosate is 700 micrograms/liter, high than for other pesticides, whereas the EU tolerable level is ~0.1 micrograms/liter.
Non-glyphosate toxins in weed killers
Photos of plants subjected to glyphosate alone provide observable evidence that glyphosate does not demonstrate herbicidal activity.
In the photo above C = control (no herbicide, water only);
G = glyphosate only; R = glyphosate + formulants.
Source: Toxicity of formulants and heavy metals in glyphosate-based herbicides and other pesticides. Toxicology Reports 5: 156-63, 2018.
Beyond paralysis
The potential harm from glyphosate exposure extends beyond paralysis among young children.
The mineral chelating properties of glyphosate are suspected of contributing or inducing to insidious kidney failure among workers in sugar cane crops where glyphosate is flooded onto the fields to ripen the cane. Heavy metals are evident in urine samples of affected field workers. The more glyphosate that is used the greater the excretion of heavy metals among people living in area of cane fields. Glyphosate has been shown to be toxic to kidneys in low doses.[29]
Glyphosate alone does not cause an epidemic of chronic kidney disease but it acquires that ability to destroy renal tissues when it forms complexes with minerals in hard water.
Glyphosate is a mineral chelator
The globally used pesticide glyphosate is of interest here because it has only been recently revealed that it is a mineral chelator.
An untold property of glyphosate is its mineral chelating (key-lay-ting) properties. By withholding minerals from plants, they die off. This makes glyphosate a multimodal weed killer. By altering the availability of toxic heavy metals (copper, lead, iron, cadmium, arsenic, etc.) that are now bound to the soil instead of uptake by plants. Glyphosate also inhibits a key enzyme needed for plant growth (5-enolpyruvylshikimate-3-phosphate synthase). Prior herbicides were fat-soluble and were stored in human fatty tissue. Glyphosate as a water-soluble plant toxin was advertised as a much safer alternative.
There are fears that glyphosate not only strips the body of essential minerals but also disrupts hormone levels and deleteriously affects gut bacteria.
After years of use, there is concern that soil will be undersupplied with minerals needed for plant growth. In this manner plants may lose some of their natural resistance against disease and affect human and animal health as well.
The chelating properties of glyphosate were not by accident. Patents were filed for glyphosate as a mineral chelator. By virtue of glyphosate’s ability to bind to minerals it can remobilize metals for update into soil organisms. One study found glyphosate relieved the toxicity of copper in soil.[30]
Diabetes and enteroviruses
The public health threat posed by enteroviruses is more horrific than realized. Enterovirus infection is also associated with childhood onset (Type I) diabetes. The Coxsackie enterovirus in drinking water supplies is believed to play a causal role in Type I diabetes.[31] It should be noted that water supplies are often contaminated with natural sources of arsenic. Chronic arsenic consumption from drinking water has been found to increase (almost double) the risk for adult-onset (Type II) diabetes.[32]
The reported seasonal onset of Type I childhood diabetes matches the seasonal occurrence of enteroviral infections and the pre-harvest use of glyphosate pesticides.
ALS (Amyotrophic lateral sclerosis
Add ALS (aka Lou Gehrig’s disease) to the list of maladies associated with hidden enteroviruses in the spinal cord. The first report linking enteroviruses with an ALS-like disease was published back in 1967.[33] Only recently have researchers observed that entero-virus pathology remarkably resembles ALS.[34] Given ALS is another devastating disease for which there is no effective cure, the insights in this paper regarding heavy metals like arsenic, reduced immunity and exposure to pesticides should be instructive towards discovery of a cure.
Is a vaccine on the horizon?
A vaccine against enteroviruses (Coxsackievirus B) has been tested in animals.[35]
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However, a vaccine may never materialize. A live-attenuated
strain of enterovirus-71 inoculation of monkeys led to production of
antibodies that demonstrated reactively with many enterovirus strains
but also led to neurologic symptoms and entered the spinal cord.[36]Of acute interest, non-polio enteroviruses reduce the antibody activation of oral poliovirus vaccines.[37]
Call for re-evaluation of glyphosate
Glyphosate was approved for use by health authorities but new data suggests a reevaluation of its safety because of the following revelations.[38]
- The half-life (degradation rate) is longer than previously recognized. Studies show glyphosate may increase in soil up to 7 years[39] or even 22 years.[40]
- Estimates of tolerable daily intake are based on outdated science.
- Its endocrine gland disruptive properties need to be reviewed.
- Exposure to glyphosate in early life may not emanate into disease till many decades later.
- Glyphosate also unfavorably alter gut bacteria.
- Glyphosate may interfere with normal sexual development.
- Glyphosate interferes with the susceptibility of bacteria to antibiotics.
- Glyphosate is on a watch list for non-Hodgkins lymphoma which was doubled in the U.S. between 1975 and 2006, the era of glyphosate adoption as a weed killer.
- Glyphosate is now used to ripen or dry crops late in the growing season.
- Glyphosate is now ubiquitously found in processes foods.
- Glyphosate’s molecule structure is similar to glutamate, a nerve transmitter in the brain when overstimulated induces excitotoxicity to brain cells.
We should not lose sight of the fact, prior to glyphosate, DDT was commonly used as a pesticide. It was Jim West who called public attention to the linkage between polio and pesticides in 2003. His charts provide undeniable evidence pesticides, in particular arsenic-based weed killers as well as DDT played a strong role in the polio epidemics of old. DDT was banned in in U.S. in 1972.[41]
Natural Antidotes to enteroviruses
Researchers note, while there are millions of citations at the National Library of Medicine under the search term “nutrition and infection,” “no one even thought to consider the effects of host nutritional status on the genetic makeup of an infecting pathogen” (like Coxsackie enteroviruses). Scholarly investigations were confined to the ability of nutrients to active immunity, not upon their ability to influence the virulence of viruses themselves.[42]
Most enteroviral infections produce only minor fever and sufficient memory antibodies are produced against them. But for immune compromised individuals, what appears to be the flu can break into the nervous system and leave very young children paralyzed.
Given that out-of-control enteroviral infections may emanate from poor nutrition, it is a wonder why drugs or vaccines are being considered at all to quell the horrific outbreaks of flaccid enteroviral infection that seasonally kill or paralyze young children.
Modern medicine casts a blind eye at nutritional therapy. Our children pay a price for this. Don’t expect doctors to be informed enough to provide guidance or to embrace much of what you have read here.
A sufficient body of knowledge exists that natural molecules can effectively prevent or quell active enteroviral infections. A recent review of natural anti-enterovirus 71 agents identified 71 different botanical molecules that have been shown to quell enterovirus-71.[43]
Here are other natural remedies against enteroviruses.
Lactoferrin
One such remedy is lactoferrin, an iron-binding protein that is produced in the body during infection. It also binds to copper, manganese, zinc and other metals. White blood cells known as neutrophils secrete lactoferrin. Lactoferrin is in mother’s milk and in colostrum. Iron serves as a growth factor for enteroviruses. Therefore, lactoferrin is categorically a strong antiviral agent. Lactoferrin may bind to zinc to inhibit viral replication. Lactoferrin-enriched milk has been reported to block enterovirus-71 infection. Since enteroviruses attack the mucosal wall of the intestines and lactoferrin binds to viral particles, it has been called “an important brick in the mucosal wall against viral attacks.” Lactoferrin can be purchased without prescription. Lactoferrin inhibits viral adhesion and entry into host cells.[44]
Probiotics
In a lab dish study, a commercially available probiotic (Lactobacillus reuteri) that impairs entry of viruses into host cells. It is effective against Coxsackie viruses. It has safely been used for over a decade.[45] Also Lactobacillus plantarum has recently been reported to exhibit preventive effects against Coxsackie B4 virus.[46]
Luteolin
Luteolin is a molecule found in small amounts in celery, thyme and green peppers. Luteolin exhibited the most potent inhibition of viruses compared to quercetin and other molecules.[47]
Niacinamide
Nicotinamide (niacinamide, vitamin B3) protects insulin-making islet cells and should be considered for inclusion in any nutrient fortification for subjects with onset of Type 1 diabetes as well as other enteroviral infections.[48]
Resveratrol
Resveratrol (rez-vair-ah-trol), known as a red wine molecule, inhibits enterovirus-71.[49] Resveratrol is widely known as an activator of the Sirtuin1 survival gene. Sirtuin1 gene protein inhibits the replication of enterovirus-71.[50]
Advice how to deal with enteroviral infections at home
Few if any healthy readers are at meaningful risk for any of the syndromes associated with enteroviruses with the exception of hand-foot-mouth disease. Authoritative advice is given to parents whose children may develop any of the many disorders associated with enterovirus. The common symptoms of hand-foot-mouth disease are (1) moderate to mild fever; (2) loss of appetite; (3) rash on hands and feet; sort throat; (4) fatigue and headaches.
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If these symptoms occur, isolate your child from others in the family including exclusive use of a bathroom in the home to prevent transmission to others. While hand washing is a must, even antiseptic wipes at the bedside are a good idea. Avoid use of aspirin for fever or aches as it induces a deficiency of vitamin C which may produce the potentially deadly Reye’s Syndrome after a bout with a viral infection.[51]
Consumption of organic foods and or washing fruits and vegetables makes sense.
Nutritional support should be emphasized, centered around supplementation with selenium, zinc, vitamin D, vitamin C, vitamin A[52], lysine, as well as resveratrol, elderberry syrup, lactoferrin and probiotics. Given that vitamin C has been shown to inactivate enteroviruses[53], repeated dosing throughout waking hours will help achieve optimal blood levels. Fresh-crushed garlic is also documented to help quell Coxsackie enteroviruses.[54] Children with paralysis are likely to have lost their appetite for food but will probably be able to down a few vitamin pills to aid in their quick recovery. Obviously, provision of vitamin pills to children would be wise prevention.
Summary: the environmental recipe for acute flaccid enterovirus infections with paralysis of limbs depends upon a triangulation of circumstances: (1) infection by an enterovirus; (2) consumption of arsenic that disarms the immune response due to depletion of selenium and zinc; and (3) contact or consumption of a toxin such as glyphosate and its accompanying formulants.
References
[1] CDC probe continues as cases of acute flaccid myelitis rise. Infectious Disease Advisor, Nov. 15, 2018.
[2] Craig M, Pediatric viral infections: enteroviruses and CMV, 2004, online at http://www.virologyresearch.unsw.edu.au/virology/wp-content/uploads/2013/08/VIM04-Maria-Craig.pdf
[3] Branswell, H., CDC investigating burst of possible new cases of polio-like paralysis, as mystery persists. Stat News, Nov. 15, 2018.
[4] AFM Investigation. Centers for Disease Control & Prevention, Nov. 20, 2018.
[5] Khetsuriani N, et al, Enterovirus Surveillance – United States, 1970-2005. MMWR, 55: SS08), Sept. 15, 2006.
[6] Kaushik R, et al, Acute flaccid paralysis in adults: our experience. Journal Emergencies, Trauma & Shock, 7 (3), 149-54, 2014.
[7] Acute flaccid paralysis (AFP) surveillance: the surveillance strategy for poliomyelitis eradication. World Health Organization, India. At http://www.searo.who.int/india/topics/poliomyelitis/acute_flaccid_paralysis_surveillance.pdf?ua=1
[8] Eunson P, Enterovirus D68 acute flaccid paresis- destroying young lives. European Journal Pediatric Neurology 21 (6): 803, 2017.
[9] Soucheray S, CDC creates AFM task force as confirmed cases rise to 109. Center for Infectious Disease Research & Policy?. Nov. 20, 2018.
[10] Lugo D, Krogstad P, Enteroviruses in the early 21st century: new manifestations and challenges. Current Opinion Pediatrics 28 (1): 107-113, 2016.
[11] Mao, Q, et al, EV-A71 vaccine licensure: a first step for multivalent enterovirus vaccine to control HFMD and other severe diseases. Emerging Microbes & Infections, 5 (7), e75, 2016.
[12] Gnanaraj J, Kumar B, Quick case: Hand, foot mouth disease in a remote area in northeast. MD Current, India, undated.
[13] Iaconelli M, One-year surveillance of human enteric viruses in raw treated wastewaters, downstream river waters, and drinking waters. Food Environmental Virology, 9 (1): 79-86, 2017.
[14] Shukla S, Prevalence and evaluation strategies for viral contamination in food products: risk to human health- a review. Critical Reviews Food Science Nutrition, 58 (3): 405-19, 2018.
[15] Prez VE, et al, Tracking enteric viruses in green vegetables from central Argentina: potential association with viral contamination of irrigation waters. Science Total Environment 637-38: 665-67, 2018.
[16] Anastasina M, et al, Human picornaviruses associated with neurological diseases and their neutralization by antibodies. Journal General Virology 98(6): 1145-1158, 2017.
[17] Prevost B, et al, Large scale survey of enteric viruses in river and waste water underlies the health status of the local population. Environment International 79: 42-50, 2015.
[18] Bennett NJ, Steele RW, Pediatric enteroviral infections workup. Medscape June 16, 2017.
[19] Polio-like syndrome. Wikipedia. Oct 13, 2018.
[20] Molin Y, Arsenic influences virus replication in experimental Coxsackie B3 infection. Uppsala Dissertations 513, 2010.
[21] Guangzhou G, et al, Blood selenium of low-level associated with development of hand-foot-mouth-disease. Journal Animal Veterinary Advances 11 (3): 381-85, 2012.
[22] Get enough selenium to prevent a viral catastrophe. Nutrisphere, March 14, 2017.
[23] Beck MA, Levander OA, Handy J, Selenium deficiency and viral infection. Journal Nutrition 133 (5): 1463S-67S, 2003.
[24] Temkin A, Breakfast with a dose of Roundup? Environmental Working Group, Aug. 15, 2018.
[25] Honeycutt Z, Arsenic and heavy metals found in herbicide sprayed on food crops. www.momsacrossamerica.com. Jan 8, 2018.
[26] Mesnage R, Bernay B, Seralini GE, Ethoxylated adjuvants of glyphosate-based herbicides are active principles of human cells toxicity. Toxicology 313 (2-3): 122-28, 2013.
[27] Marrs C, Inert ingredients in glyphosate herbicides are toxic too. HormonesMatter.com, April 24, 2013.
[28] Defarge N, et al, Toxicity of formulants and heavy metals in glyphosate-based herbicides and other pesticides. Toxicology Reports 5: 156-63, 2018.
[29] Jayasumana C, Gunatilake S, Sirbaddana S, Simultaneous exposure to multiple heavy metals and glyphosate may contribute to Sir Lankan agricultural nephropathy. BMC Nephrology, 16: 103, 2015.
[30] Mertens M, et al, Glyphosate – a chelating agent – relevant for ecological risk assessment? Environmental Science & Pollution Research 25:5298-5317, 2018.
[31] El-Senousy WM, et al, Coxsackie B4 as a causative agent of diabetes mellitus Type I: is there a role of inefficiently treated drinking water and sewage in virus spreading? Food & Environmental Virology 10 (1): 89-98, 2018.
[32] Islam R, et al, Association between type 2 diabetes and chronic arsenic exposure in drinking water: a cross sectional study in Bangladesh. Environmental Health 11:38, 2012.
[33] Modestova NV, et al, On the role of enteric viruses in the pathology of the nervous system. Zhurnal nevropatologii i psikhiatrii imeni S.S. Korsakova 67 (2): 176-80, 1967.
[34] Xue YC, et al, Enteroviral infection: the forgotten link to amyotrophic lateral sclerosis. Frontiers Molecular Neuroscience 11: 63, 2018.
[35] Hyoty H, Leon F, Knip M, Developing a vaccine for Type I diabetes by targeting coxsackievirus B. Expert Review Vaccines, Nov 19, 2018.
[36] Arita M, et al, An attenuated strain of enterovirus 71 belonging to genotype a showed a broad spectrum of antigenicity with attenuated neurovirulence in cynomolgus monkeys. Journal Virology 81 (17): 9386-95, 2007.
[37] Praharaj I, et al, Influence of non-polio enteroviruses and the bacterial gut microbiota on oral poliovirus vaccine response: a study from south India. Journal Infectious Diseases, Sept. 24, 2018.
[38] Myers, JP, et al, Concerns over use of glyphosate-based herbicides and risks associated with exposures: a consensus statement. Environmental Health 15: 19, 2016.
[39] Eberbach P, Applying non-steady-state compartmental analysis to investigate the simultaneous degradation of soluble and sorbed glyphosate (N-phosphonomethyl)glycine) in four soils. Pesticide Science 52 (3), 1999.,
[40] Nomura NS, Hilton HW, The adsorption and degradation of glyphosate in five Hawaiian sugarcane soils. Weed Research 17 (2): 1977.
[41] National Pesticide Information Center, DDT Fact Sheet, 1999.
[42] Lavender OA, Beck MA, Selenium and viral virulence. British Medical Bulletin, 55 (3): 528-33, 1999.
[43] Wang L, Anti-enterovirus 71 agents of natural products. Molecules 20 (9), 16320-16333, 2015.
[44] Berlutti F, et al, Antiviral properties of lactoferrin – a natural immunity molecule. Molecules 16 (8): 6992-7018, 2011.
[45] Ang LYE, Antiviral activity of Lactobacillus reuteri protects against Coxsackie A and Enterovirus 71 infection in human skeletal muscle and colon cells lines. Virology Journal 13: 111, 2016.
[46] Arena MP, et al, Inhibition of Coxsackievirus B4 by Lactobacillus plantarum. Microbiological Research 210: 59-64, 2018.
[47] Xu L, et al, Identification of luteolin as enterovirus 71 and Coxsackievirus A16 inhibitors through reporter viruses and cell viability-based screening. Viruses 6 (7): 2778-95, 2014.
[48] Moell A, et al, Antiviral effect of nicotinamide on enterovirus-infected human islets in vitro: effect on virus replication and chemokine secretion. Journal Medical Virology 81 (6): 1082-87, 2009.
[49] Zhang L, et al, Resveratrol inhibits enterovirus 71 replication and pro-inflammatory cytokine secretion in rhabdosarcoma sells through blocking IKKs/NFkB signaling pathway. PLoS One 10 (2): e0116879, 2015.
[50] Han Y, et al, SIRT1 inhibits EV71 genome replication and RNA translation by interfering with the viral polymerase and 5’UTR RNA. Journal Cell Science 129 (24): 4534-4547, 2016.
[51] Sardi B, Why Reye’s Syndrome (aspirin-related deaths among small children who have viral infections) prevailed from 1950-1980 and then suddenly disappeared. Knowledge of Health, Sept 18, 2011.
[52] Chen S, et al, Influence of vitamin A status on the antiviral immunity of children with hand, foot and mouth disease. Clinical Nutrition 31 (4): 543-48, 2012.
[53] Saki RJ, Cliver DO, Inactivation of enteroviruses by ascorbic acid and sodium bisulfite. Applied Environmental Microbiology 36 (1): 68-75, 1978.
[54] Tsai Y, et al, Antiviral properties of garlic: in vitro effects on influenza B, herpes simplex and Coxsackie viruses. Planta Medica 5: 460-61, 1985.
Bill Sardi [send him mail] is a frequent writer on health and political topics. His health writings can be found at www.knowledgeofhealth.com, billsardiblog.com and resveratrolnews.com.
Copyright © 2018 Bill Sardi, writing from La Verne, California. This article has been written exclusively for www.LewRockwell.com and other parties who wish to refer to it should link rather than post at other URLs.
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