Archive for the ‘Parasites’ Category

Risky Business: Linking T. gondii & Entrepreneurship Behaviors

http://rspb.royalsocietypublishing.org/content/285/1883/20180822

Risky business: linking Toxoplasma gondii infection and entrepreneurship behaviours across individuals and countries

Stefanie K. Johnson, Markus A. Fitza, Daniel A. Lerner, Dana M. Calhoun, Marissa A. Beldon, Elsa T. Chan, Pieter T. J. Johnson
Published 25 July 2018.DOI: 10.1098/rspb.2018.0822

Abstract

Disciplines such as business and economics often rely on the assumption of rationality when explaining complex human behaviours. However, growing evidence suggests that behaviour may concurrently be influenced by infectious microorganisms. The protozoan Toxoplasma gondii infects an estimated 2 billion people worldwide and has been linked to behavioural alterations in humans and other vertebrates. Here we integrate primary data from college students and business professionals with national-level information on cultural attitudes towards business to test the hypothesis that T. gondii infection influences individual- as well as societal-scale entrepreneurship activities. Using a saliva-based assay, we found that students (n = 1495) who tested IgG positive for T. gondii exposure were 1.4× more likely to major in business and 1.7× more likely to have an emphasis in ‘management and entrepreneurship’ over other business-related emphases. Among professionals attending entrepreneurship events, T. gondii-positive individuals were 1.8× more likely to have started their own business compared with other attendees (n = 197). Finally, after synthesizing and combining country-level databases on T. gondii infection from the past 25 years with the Global Entrepreneurship Monitor of entrepreneurial activity, we found that infection prevalence was a consistent, positive predictor of entrepreneurial activity and intentions at the national scale, regardless of whether previously identified economic covariates were included. Nations with higher infection also had a lower fraction of respondents citing ‘fear of failure’ in inhibiting new business ventures. While correlational, these results highlight the linkage between parasitic infection and complex human behaviours, including those relevant to business, entrepreneurship and economic productivity.

________________

**Comment**

I’ve always been fascinated with parasites.  Call me crazy – maybe I have them….

The take home here is that parasites can affect behavior.  This is important for Lyme/MSIDS patients to know as a tick’s gut is a literal garbage can full of bizarre and complex creatures that feast on the human body, wreaking all manner of havoc.

In Lyme circles, it won’t take long before you hear patients stating that they aren’t feeling well and then within the same breath, state it’s due to a full-moon.

For a number of reasons, Lyme/MSIDS patients can be coinfected with T. gondii.  While food, congenital, blood transfusions, and organ transplants are the common route of transmission, sexual transmission is theorized.  Also, people can get it from cleaning a cat’s litterbox and then not washing their hands well.  If you go to the following link, you will read of a case of a person with Lyme and Toxoplasmosis:  https://madisonarealymesupportgroup.com/2016/05/21/toxoplasmosis/  This article will also reveal T. gondii is responsible for about 1/5 of schizophrenia cases.  Women carrying IgG antibodies when giving birth have a greater risk for self-harm.  The article also gives testing and treatment options.  

It’s a common parasite:  https://madisonarealymesupportgroup.com/2018/06/20/brazil-569-confirmed-cases-of-toxoplasmosis-of-which-50-are-pregnant-women/

And lastly, I’ll never forget this information on how parasites affect human behavior by Dr. Klinghardt, which I found here:  http://www.betterhealthguy.com/a-deep-look-beyond-lyme

  • Parasite patients often express the psyche of the parasites – sticky, clingy, impossible to tolerate – but a wonderful human being is behind all of that.

  • We are all a composite of many personalities. Chronic infections outnumber our own cells by 10:1. We are 90% “other” and 10% “us”. Our consciousness is a composite of 90% microbes and 10% us.

  • Our thinking, feeling, creativity, and expression are 90% from the microbes within us. Patients often think, crave, and behave as if they are the parasite.

  • Our thinking is shaded by the microbes thinking through us. The food choices, behavioral choices, and who we like is the thinking of the microbes within us expressing themselves.

  • Patients will reject all treatments that affect the issue that requires treating.

  • Patients will not guide themselves to health when the microbes have taken over.

With this information in mind, it’s quite clear how Lyme/MSIDS is such a complex disease as many are dealing not only with Lyme but other coinfections including parasites which are either directly transmitted by a tick or activated due to a dysfunctional immune system.

This article has a lot of great info regarding parasites:  https://madisonarealymesupportgroup.com/2017/10/03/removing-parasites-to-fix-lyme-chronic-illnesses-dr-jay-davidson/

as well as this one:  http://drallisonhofmann.com/wp-content/uploads/2015/11/TownsendLetter-Parasitosis.pdf

Please consider parasites and discuss with your medical practitioner.

Category:

Lyme, Parasites, Psychological Aspects, research, Testing, Ticks, Toxoplasmosis, Transmission, Treatment

What the Mystery of the Tick-Borne Meat Allergy Could Reveal

https://www.nytimes.com/2018/07/24/magazine/what-the-mystery-of-the-tick-borne-meat-allergy-could-reveal.html

What the Mystery of the Tick-Borne Meat Allergy Could Reveal

Unraveling why tick bites are suddenly causing a strange reaction in some people who eat meat could help scientists better understand how all allergies work.

By Moises Velasquez-Manoff

One spring evening in 2016, Lee Niegelsky’s underarm began to itch. An investment manager, he was doing housework around his condo, and he thought he’d been bitten by a chigger. But within 15 minutes, hives had erupted all over his body. He responded with what he calls a “typical man reaction” — if the hives didn’t clear up by the next day, he would have them checked. Fifteen minutes later, the itch had become unbearable. He needed help right away.

His wife wasn’t home, so he drove himself to the university hospital emergency room near where he lived in Chapel Hill, N.C. As he explained his symptoms at the check-in counter, he began to feel faint, then fell to one knee. An orderly offered a wheelchair. He sat down — and promptly lost consciousness.  (See link for article)

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**Comment**

I find it interesting that no one is mentioning the fact ticks have been tweaked in a lab for biowarfare purposes.  

https://madisonarealymesupportgroup.com/2018/03/07/hantavirus-tularemia-warnings-issued-in-san-diego-county/  Tularemia, brucella, certain Rickettsia’s, numerous viruses, some chlamydia’s, and of course mycoplasma have all been weaponized.  https://madisonarealymesupportgroup.com/2015/08/12/connecting-dots-mycoplasma/

http://www.immed.org/infectious%20disease%20reports/InfectDiseaseReport06.11.09update/PHA_Nicolson_0709_v4.07.pdf

“According to Dr. Nicolson, some of the experiments used Mycoplasma while others utilized various “cocktails of microbial agents” such as Mycoplasma, Brucella, and DNA viruses such as Parvovirus B19. This project later become the topic of a book by Dr. Nicolson entitled Project Day Lily.

Dr. Nicolson believes that Mycoplasma fermentans is a naturally occurring microbe. However, some of the strains that exist today have been weaponized. Dr. Nicolson’s research found unusual genes in M. fermentans incognitus that were consistent with a weaponized form of the organism. Weaponzing of an organism is done in an attempt to make a germ more pathogenic, immunosuppressive, resistant to heat and dryness, and to increase its survival rate such that the germ could be used in various types of weapons. Genes which were part of the HIV‐1 envelope gene were found in these Mycoplasma. This means that the infection may not give someone HIV, but that it may result in some of the debilitating symptoms of the HIV disease.”

Regarding the weaponization of tick pathogens:  https://www.lymedisease.org/lymepolicywonk-questioning-governments-role-lyme-disease-make-conspiracy-theorist/  (Go here to read excerpts of an interview with a biologist who acknowledged doing biowarfare work on ticks and mosquitoes.  He admits every time he has a strange illness his physician says it’s probably a rickettsia – an idiopathic condition that never tests positive but symptoms indicate it.)

‘The interview suggests to me that the reason we have such a large problem with our tick population today may be related to military experiments in the 50s. They were part of a biological warfare effort against the Russians. One goal was to figure out how to get ticks to reproduce quickly and abundantly, as well as how to distribute ticks to targeted areas.”

For a lengthy but informative read on the Lyme-Biowarfare connections:  CitizensAlert_Bob13  (Scroll to page 44 to see an executive summary.  Please notice the names of Steere, Barbour, Shapiro, Klempner, and Wormser, the first four are affiliated with the CDC Epidemic Intelligence Service (EIS).  Wormser, lead author of the fraudulent Lyme treatment guidelines, lectures as an expert on biowarefare agents and treatments).  The author of the pdf believes borrelia (Lyme) has been bioweaponized due to (excerpt from pdf footnote):

226 An article was put out by the Associated Press mentioning the study of Lyme disease at a new biowarfare lab at the University of Texas, San Antonio. The article was quickly retracted and mention of Lyme disease was scrubbed from the article. Here is the text of the original article: “A new research lab for bioterrorism opened Monday at the University of Texas at San Antonio. The $10.6 million Margaret Batts Tobin Laboratory Building will provide a 22,000-square-foot facility to study such diseases as anthrax, tularemia, cholera, lyme disease, desert valley fever and other parasitic and fungal diseases. The Centers for Disease Control and Prevention identified these diseases as potential bioterrorism agents.” MSNBC, 11/21/2005. For a comparison of the censored and uncensored articles, see: http://members.iconn.net/~marlae/lyme/featurearticle02.htm

So you tell me.  Could all this lab tweaking have something to do with tick borne illness and allergies?

Category:

Activism, Alpha Gal Meat Allergy, Malaria, Parasites, research, Testing, Ticks

Herpes Viruses Implicated in Alzheimer’s Disease

https://www.the-scientist.com/news-opinion/herpes-viruses-implicated-in-alzheimer-s-disease-64246#.W1VYqg-Tels.linkedin

Herpes Viruses Implicated in Alzheimer’s Disease

SAM GANDY, ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI

Herpes Viruses Implicated in Alzheimer’s Disease

A new study shows that the brains of Alzheimer’s disease patients have a greater viral load, while another study in mice shows infection leads to amyloid-β build up.

Jun 21, 2018, Anna Azvolinsky

 

The brains of Alzheimer’s disease patients have an abnormal build up of amyloid-β proteins and tau tangles, which, according to many researchers, drives the ultimately fatal cognitive disease. This theory is being challenged by a newer one, which posits that microbes may trigger Alzheimer’s pathology.

Two new studies, using different approaches, further bolster this pathogen theory. Analyzing the transcriptomes of post-mortem brain samples from patients with Alzheimer’s disease, one group of researchers finds that two strains of human herpesvirus are significantly more abundant than in the brains of people of the same age without Alzheimer’s disease. Gene networks in the brains of Alzheimer’s patients with these strains are also rewired such that disease-related genes are differentially expressed compared to controls.

In the other study, another team of investigators observed in mouse models and in a three-dimensional human neuronal cell culture that a Herpseviridae infection could seed amyloid-β plaques. 

“These two papers add to a weight of evidence that viruses—and pathogens in general—must now be seriously considered as causal agents in Alzheimer’s disease,” Chris Carter, who studies the genetics and epidemiology of Alzheimer’s and other neurological disorders at Polygenic Pathways in the U.K., tells The Scientist.

Over three decades, there have been accumulating data from human studies suggesting that certain microbes, namely, viruses bacteria and fungi, may trigger or promote Alzheimer’s pathology in the aging brain. 

See “Do Microbes Trigger Alzheimer’s Disease?”

The Mount Sinai group initially set out to mine their RNA and DNA sequencing data from Alzheimer’s brain samples for drug targets. Then they found these viral sequences that were difficult to ignore. “I recently gave a talk that I titled, ‘I went looking for drugs but all I found was these viruses,’” study coauthor Joel Dudley, a genomics researcher at the Icahn School of Medicine at Mount Sinai, tells The Scientist.

In their study of elderly human brains, Dudley and the team from Mount Sinai sequenced more than 1,400 post-mortem brain samples, finding the first evidence that human herpesviruses 6A (HHV-6A) and 7 (HHV-7) are in greater abundance in regions of the brain including the superior temporal gyrus, anterior prefrontal cortex, and dorsolateral prefrontal cortex.

These data suggest that multiple pathogens, and not just these viruses, likely contribute to Alzheimer’s disease. 

—Chris Carter, Polygenic Pathways

Using RNA and DNA sequencing data, the team computationally generated regulatory network models that implicated the presence these viruses in altering the activity of genes linked to Alzheimer’s risk.

The researchers turned to one of the microRNAs, miR-155, found in their analysis to be suppressed by HHV-6A in the human samples, to see what the functional consequence is of this interaction. They homed in on miR-155 because it was a novel microRNA and because it had been previously linked to herpes viruses. When they knocked out the gene for miR-155 in a mouse model of Alzheimer’s disease, the animals’ brains had larger amyloid plaques and higher levels of amyloid-β compared to the mouse model with a wildtype MIR155 gene.

“Conceivably, the viral proteins are acting as transcription factors that control expression of Alzheimer’s risk genes,” coauthor Sam Gandy, a professor of neurology who specializes in Alzheimer’s disease at Mount Sinai, writes in an email to The Scientist. “Perhaps this viral dysregulation of Alzheimer’s genes that we see promotes the Alzheimer’s pathology of amyloid beta aggregation, inflammation and tau tangles,” he says.

The results, published today (June 21) in Neuron, could pave the way to new intervention strategies. “If established that these viruses indeed play a role in the development of Alzheimer’s, retroviral agents should be tested as a potential therapy,” says Dudley.

In the other study, available as a preprint on the Cell website and in Neuron July 11, Rudolph Tanzi and Robert Moir, both researchers at Harvard Medical School and Massachusetts General Hospital, and their colleagues tested how amyloid-β in the brain—which these labs previously found to be an antimicrobial—reacts to herpes simplex virus 1 (HSV1), HHV6A, and HHV6B. These strains all tend to integrate into the genomes of neurons. They found that in a culture of human neuronal cells, amyloid-β could prevent HSV1 infection and can bind and aggregate the HSV1 and HHV6 viruses. Mice infected with HSV1—which can cause encephalitis—that also had genetically elevated amyloid-β expression were protected against encephalitis, but also had increased amyloid deposits.

“These studies further add to the steadily increasing number of papers that support a microbial role in Alzheimer’s disease,” Ruth Itzhaki, a molecular neurobiologist at the University of Manchester in the U.K. who studies the link between viruses and the development of Alzheimer’s disease, writes in an email to The Scientist.

A recent epidemiology study adds real-world credence to the microbial link to Alzheimer’s. A population study in Taiwan examined more than 33,000 individuals and found that those with a herpes simplex virus infection had a 2.5-fold greater risk of developing Alzheimer’s disease. The study authors found that in those people treated with antiherpes medications, the 2.5-fold risk dropped back down to baseline. 

“The conclusion you can draw is that the antiherpes medication reduced the risk of Alzheimer’s by keeping the herpes infection in check,” says Moir.

Itzhaki agrees. This study and two others, also from Taiwan, appear to link HSV1 causally to Alzheimer’s disease, she writes. “Despite various shortcomings, these Taiwan studies are the essential first steps to a proof that a microbe could be the cause of a non-infectious disease, in this case, Alzheimer’s.” Itzhaki and a colleague wrote about these studies recently in a commentary, which aimed to interpret the “important and surprising Taiwan data” on the effectiveness of the antiviral treatment, Itzhaki tells The Scientist.

Carter cautions that the new reports should not be interpreted to mean that there is likely a single, unique Alzheimer’s pathogen, if there is one at all. “These data suggest that multiple pathogens, and not just these viruses, likely contribute to Alzheimer’s disease. It is also likely that the pathogens may vary between Alzheimer’s patients.”

The Mount Sinai team will now be verifying whether HHV6 and HHV7 are actually integrated into the genomes of Alzheimer’s patients’ brains and testing for the presence of HHV6 and HHV7 in the bloodstream and central nervous system of Alzheimer’s patients. They would like to do a study comparing living patients and controls to see if the link they observed between the viruses’ presence and changes in gene regulation related to Alzheimer’s holds up.

Tanzi’s and Moir’s labs are focusing on the role of the brain microbiome in Alzheimer’s disease. Comparing the brains of older and younger individuals, including those with Alzheimer’s, their preliminary evidence shows that the brain microbiome—which contains hundreds of bacterial and fungal species—is shifted and linked to pro-inflammatory activity. “It’s analogous to what happens with the gut microbiome in individuals with irritable bowel syndrome,” says Moir. “Our model right now is that it’s not just a single microbe, but a disturbance in the brain microbiome that can lead to Alzheimer’s disease.”

B. Readhead et al., “Multi-scale analysis of independent Alzheimer’s cohorts finds disruption of molecular, genetic, and clinical networks by human herpesvirus,” Neuron, doi.org/10.1016/j.neuron.2018.05.023, 2018.

W.A. Eimer et al. “Alzheimer’s disease-associated β-amyloid is rapidly seeded by herpesviridae to protect against brain infection,” Neuron, in press, July 12, 2018.

Correction (June 21): We removed two sentences in paragraph seven. One noted the prevalence of virus in diseased brains, but did not note that the prevalence is the same in control brains. The other sentence misstated the regions of the brain where the viruses were in greater abundance compared to control brains and stated these brain regions were linked to Alzheimer’s disease. The Scientist regrets the error.

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**Comment**

  1.  Lyme/MSIDS patients often have viral involvement – particularly herpes strains
  2. The role of bacteria, viruses, and fungus is important and likely includes the very things Lyme/MSIDS patients have and are being treated for.
  3. This article points out another reason to take treatment for Lyme/MSIDS seriously.  If left unchecked, Lyme/MSIDS can possibly be a perfect storm for Alzheimer’s later.

For more:  https://madisonarealymesupportgroup.com/2017/01/18/a-bug-for-alzheimers/

https://madisonarealymesupportgroup.com/2016/06/09/alzheimers-byproduct-of-infection/

https://madisonarealymesupportgroup.com/2016/11/17/antibiotics-and-alzheimers/

https://madisonarealymesupportgroup.com/2016/06/03/borrelia-hiding-in-worms-causing-chronic-brain-diseases/

https://madisonarealymesupportgroup.com/2018/03/25/a-brief-history-of-neuroborreliosis-research-dementia-an-inside-look-at-two-researchers/

https://madisonarealymesupportgroup.com/2017/06/10/the-coming-pandemic-of-lyme-dementia/

https://madisonarealymesupportgroup.com/2016/11/17/alzheimers-lyme/

Dr. David Baewer discusses arboviruses & Lyme:  https://madisonarealymesupportgroup.com/2016/06/07/dr-david-baewer-coppe-labs/ Coppe Labs, in Wisconsin, provides advanced testing for leukotropic herpesviruses: EBV, CMV, HHV-6A and HHV-6B, as well as tick-borne pathogens, and their tests distinguish between latent and active infections.

 

 

Category:

Alzheimer's, Inflammation, Lyme, Parasites, Psychological Aspects, research, Treatment, Viruses

Tickborne Diseases – Confronting a Growing Threat

https://www.nejm.org/doi/full/10.1056/NEJMp1807870

Tickborne Diseases — Confronting a Growing Threat

Catharine I. Paules, M.D., Hilary D. Marston, M.D., M.P.H., Marshall E. Bloom, M.D., and Anthony S. Fauci, M.D.

July 25, 2018, at NEJM.org.

Every spring, public health officials prepare for an upsurge in vectorborne diseases. As mosquito-borne illnesses have notoriously surged in the Americas, the U.S. incidence of tickborne infections has risen insidiously, triggering heightened attention from clinicians and researchers.

nejmp1807870_f1

Common Ticks Associated with Lyme Disease in North America.

According to the Centers for Disease Control and Prevention (CDC), the number of reported cases of tickborne disease has more than doubled over the past 13 years.1 Bacteria cause most tickborne diseases in the United States, and Lyme disease accounts for 82% of reported cases, although other bacteria (including Ehrlichia chaffeensis, Anaplasma phagocytophilum, and Rickettsia rickettsii) and parasites (such as Babesia microti) also cause substantial morbidity and mortality. In 1982, Willy Burgdorfer, a microbiologist at the Rocky Mountain Laboratories of the National Institute of Allergy and Infectious Diseases, identified the causative organism of Lyme disease, a spirochete eponymously named Borrelia burgdorferi. B. burgdorferi (which causes disease in North America and Europe) and B. afzelii and B. garinii (found in Europe and Asia) are the most common agents of Lyme disease. The recently identified B. mayonii has been described as a cause of Lyme disease in the upper midwestern United States. Spirochetes that cause Lyme disease are carried by hard-bodied ticks (see graphic), notably Ixodes scapularis in the northeastern United States, I. pacificus in western states, I. ricinus in Europe, and I. persulcatus in eastern Europe and Asia. B. miyamotoi, a borrelia spirochete found in Europe, North America, and Asia, more closely related to the agents of tickborne relapsing fever, is also transmitted by I. scapularis and should be considered in the differential diagnosis of febrile illness occurring after a tick bite.

Patterns of spirochete enzootic transmission are geographically influenced and involve both small-mammal reservoir hosts, such as white-footed mice, and larger animals, such as white-tailed deer, which are critical for adult tick feeding. The rising incidence and expanding distribution of Lyme disease in the United States are probably multifactorial, but increased density and range of the tick vectors play a key role. The geographic range of I. scapularis is apparently increasing: by 2015, it had been detected in nearly 50% more U.S counties than in 1996.

Lyme disease’s clinical manifestations range from relatively mild, nonspecific findings and classic erythema migrans rash in early disease to more severe manifestations, including neurologic disease and carditis (often with heart block) in early disseminated disease, and arthritis, which may occur many months after infection (late disease). Although most cases are successfully treated with antibiotics, 10 to 20% of patients report lingering symptoms after receiving appropriate therapy.2 Despite more than four decades of research, gaps remain in our understanding of Lyme disease pathogenesis, particularly its role in these less well-defined, post-treatment symptoms.

Meanwhile, tickborne viral infections are also on the rise and could cause serious illness and death.1 One example is Powassan virus (POWV), the only known North American tickborne encephalitis-causing flavivirus.3 POWV was recognized as a human pathogen in 1958 after being isolated from the brain of a child who died of encephalitis in Powassan, Ontario. People infected with POWV often have a febrile illness that can be followed by progressive and severe neurologic manifestations, resulting in death in 10 to 15% of cases and long-term sequelae in 50 to 70% of survivors.3 An antigenically similar virus, POWV lineage II, or deer tick virus, was discovered in New England in 1997. Both POWV subtypes are linked to human disease, but their distinct enzootic cycles may affect their likelihood of causing such disease. Lineage II seems to be maintained in an enzootic cycle between I. scapularis and white-footed mice — which may portend increased human transmission, because I. scapularis is the primary vector of other serious pathogens, including B. burgdorferi. Whereas only 20 U.S. cases of POWV infection were reported before 2006,3 99 were reported between 2006 and 2016. Other tickborne encephalitis flaviviruses cause thousands of cases of neuroinvasive illness in Europe and Asia each year, despite the availability of effective vaccines in those regions. The increase in POWV cases coupled with the apparent expansion of the I. scapularis range highlight the need for increased attention to this emerging virus.

The public health burden of tickborne pathogens is considerably underestimated. For example, the CDC reports approximately 30,000 cases of Lyme disease per year but estimates that the true incidence is 10 times that number.1 Multiple factors contribute to this discrepancy, including limitations in surveillance and reporting systems and constraints imposed by available diagnostics, which rely heavily on serologic assays.4 Diagnostic utility is affected by variability among laboratories, timing of specimen collection, suboptimal sensitivity during early infection, imperfect use of diagnostics (particularly in persons with low probability of disease), inability of a single test to identify coinfections in patients with acute infection, and the cumbersome nature of some assays. Current diagnostics also have difficulty distinguishing acute from past infection — a serious challenge in diseases characterized by nonspecific clinical findings. Moreover, tests may remain positive even after resolution of infection, leading to diagnostic uncertainty during subsequent unrelated illnesses. For less common tickborne pathogens such as POWV, serologic testing can be performed only in specialized laboratories, and currently available tests fail to identify novel tickborne organisms.
Such limitations have led researchers to explore new technologies. For example, one of the multiplex serologic platforms that have been developed can detect antibodies to more than 170,000 distinct epitopes, allowing researchers to distinguish eight tickborne pathogens.4 In addition to its utility in screening simultaneously for multiple pathogens, this assay offers enhanced pathogen detection, particularly in specimens collected during early disease. Further studies are needed to determine such assays’ applicability in clinical practice.

Nonserologic platform technologies may also improve diagnostic capabilities, particularly in identifying emerging pathogens. Two previously unknown tickborne RNA viruses, Heartland virus and Bourbon virus, were discovered by researchers using next-generation sequencing to help link organisms with sets of unexplained clinical symptoms. The development and widespread implementation of next-generation diagnostics will be critical to understanding the driving factors behind epidemiologic trends and the full clinical scope of tickborne disease. In addition, sensitive, specific and, where possible, point-of-care assays will facilitate appropriate clinical care for infected persons, guide long-term preventive efforts, and aid in testing of new therapeutics and vaccines.

In the United States, prevention and management of tickborne diseases include measures to reduce tick exposure, such as avoiding or controlling the vector itself, plus prompt, evidence-based treatment of infections. Although effective therapies are available for common tickborne bacteria and parasites, there are none for tickborne viruses such as POWV.

The biggest gap, however, is in vaccines: there are no licensed vaccines for humans targeting any U.S. tickborne pathogen. One vaccine that was previously marketed to prevent Lyme disease, LYMErix, generated an immune response against the OspA lipoprotein of B. burgdorferi, and antibodies consumed by the tick during a blood meal targeted the spirochete in the vector.5 Nonetheless, the manufacturer withdrew LYMErix from the market for a combination of reasons, including falling sales, liability concerns, and reports suggesting it might be linked to autoimmune arthritis, although studies supported the vaccine’s safety. Similar concerns will probably affect development of other Lyme disease vaccines.5

Historically, infectious-disease vaccines have targeted specific pathogens, but another strategy would be to target the vector.5 This approach could reduce transmission of multiple pathogens simultaneously by exploiting a common variable, such as vector salivary components. Phase 1 clinical trials are under way to evaluate mosquito salivary-protein–based vaccines in healthy volunteers living in areas where most mosquito-borne diseases are not endemic. Since tick saliva also contains proteins conserved among various tick species, this approach is being explored for multiple tickborne diseases.5

The burden of tickborne diseases seems likely to continue to grow substantially. Prevention and management are hampered by suboptimal diagnostics, lack of treatment options for emerging viruses, and a paucity of vaccines. If public health and biomedical research professionals accelerate their efforts to address this threat, we may be able to fill these gaps. Meanwhile, clinicians should advise patients to use insect repellent and wear long pants when walking in the woods or tending their gardens — and check themselves for ticks when they are done.
________________

**Comment**

While this article repeats much of the same verbiage that’s been repeated for years, particularly the vaccine push, they are ignoring the following:

  1. Many TBI’s are congenitally transmitted:  https://madisonarealymesupportgroup.com/2018/06/19/33-years-of-documentation-of-maternal-child-transmission-of-lyme-disease-and-congenital-lyme-borreliosis-a-review/, https://madisonarealymesupportgroup.com/2018/07/24/congenital-transmission-of-lyme-myth-or-reality/, https://madisonarealymesupportgroup.com/2018/02/26/transplacental-transmission-fetal-damage-with-lyme-disease/
  2. There is a real probability of sexual transmission:  https://madisonarealymesupportgroup.com/2018/02/06/lyme-in-the-southern-hemisphere-sexual-transmission/, https://madisonarealymesupportgroup.com/2017/02/24/pcos-lyme-my-story/
  3. While they mention Ehrlichia, Anaplasma, Rickettsia, and Babesia, there are many other players that are hardly getting a byline.  For a list to date:  https://madisonarealymesupportgroup.com/2017/07/01/one-tick-bite-could-put-you-at-risk-for-at-least-6-different-diseases/.  This is an important issue because to date the medical world is looking at this complex illness as a one pathogen one drug illness when nothing could be further from the truth.  No one has done any research on the complexity of being infected with more than one pathogen.  It will reveal the CDC’s guidelines of 21 days of doxy to be utter stupidity.
  4. Also, worth mentioning is that only a few of these are reportable illnesses so there is absolutely no data on how prevalent any of this is.  Surveillance is a real problem.
  5. Regarding what ticks are where….this ancient verbiage needs to change.  Ticks are moving everywhere.  This is on record in numerous places:  https://madisonarealymesupportgroup.com/2018/07/16/ticks-that-carry-lyme-disease-are-spreading-fast/, https://madisonarealymesupportgroup.com/2018/07/10/we-have-no-idea-how-bad-the-us-tick-problem-is/, https://madisonarealymesupportgroup.com/2018/07/22/citizen-scientists-help-track-tick-borne-illness-exposure/
  6. No tick is a good tick.  They all need blood meals and have the potential to transmit disease.  
  7. This article is silent about the Asian Longhorned tick that propagates itself by cloning and can drain cattle of their blood.  Found in six states so far it was recently found on a child in New Jersey:  https://www.northjersey.com/story/news/environment/2018/07/24/bergen-county-nj-child-may-first-carrying-longhorned-tick-us/825744002/.  Word in the tick world is it had NOT bitten the child and tested negative for pathogens.  What is concerning is that it is known to transmit SFTS virus and Japanese spotted fever in Asia. This story is a reminder that this tick is NOT just a livestock problem and that a normal child going about a normal day with NO contact with livestock had this tick on her.  Another clear reminder that it is foolish to put any of this in a box.
  8. They need to emphasize that the “classic erythema migrans rash” while indicative of Lyme, is unseen or variable in many patients.
  9. Constraints in testing is a true problem but an even bigger problem is untrained and uneducated medical professionals.  This stuff may never test clearly.  Get over it.  Get trained to know what to look for!
  10. The Lyme vaccine was a bust.  It still is.  Unless safety concerns are dealt with we want nothing to do with any vaccine.
  11. All I know is that mosquitoes and Zika get more attention that this modern day 21st century plague that is creeping everywhere and is a true pandemic.  It still isn’t being seriously dealt with or researched.  What research is being done is same – o – same -o stuff we already know.  Study the tough stuff – the unanswered questions or things that are just repeated as a mantra for decades.
We need answers out here not repeated gibberish that isn’t helping patients.
Afterthought:

The one thing I didn’t deal with that I will point out now is this regurgitated number in the NEJM article of 10-20% of patients moving on to chronic/persistent Lyme. The following informative article written by Lorraine Johnson points out this number to be considerably higher which corresponds to my experience as a patient advocate: https://madisonarealymesupportgroup.com/2018/07/22/lyme-costs-may-exceed-75-billion-per-year/. Excerpt below:

Besides the staggering financial cost to this 21st century plague, this paper, based on estimates of treatment failure rates associated with early and late Lyme, estimates that 35-50% of those who contract Lyme will develop persistent or chronic disease.

Let that sink in.

And in the Hopkins study found 63% developed late/chronic Lyme symptoms.

For some time I’ve been rankled by the repeated CDC statement that only 10-20% of patents go on to develop chronic symptoms. This mantra in turn is then repeated by everyone else.

While still an estimate, I’d say 35 to over 60% is a tad higher than 10-20%, wouldn’t you? It also better reflects the patient group I deal with on a daily basis. I can tell you this – it’s a far greater number than imagined and is only going to worsen.

 

 

Category:

Anaplasmosis, Babesia, Borrelia Miyamotoi (Relapsing Fever Group), Lyme, Lyme Vaccine, Parasites, Testing, Ticks, Treatment, vaccines, Viruses

Recover From Brain Fog & Lyme Disease Naturally

https://www.linkedin.com/pulse/recover-from-brain-fog-lyme-disease-naturally-gary-blier/

Recover From Brain Fog & Lyme Disease Naturally

Published on June 26, 2018
Gary Blier
Founder, Advanced Cell Training

When most people think of Lyme disease, it conjures up thoughts of rashes, flu-like symptoms, and joint pain. However, there are a significant number of Lyme sufferers who also experience brain fog: agonizing neurological symptoms that leave them feeling drained, irritable, confused, and cognitively lagging.

Brain fog is one of the most common psychiatric manifestations of Lyme Disease. In fact, it’s estimated that 70% of individuals affected by Lyme show signs of cognitive decline or memory loss.

While you may be familiar with brain fog within the Lyme community, you may not be aware of what it is or why it happens. We’ll break it all down for you in this article and provide you with natural solutions you can carry out at home to lift the fog that robs you of a clear mind.

What is Brain Fog?

Brain fog is a term given by those whose brain function is underperforming compared to a normal, healthy brain. It can range from a mild case of “cloudiness” to a more severe case that makes it difficult to perform basic tasks.

Brain fog symptoms include:

Memory loss
Slowed processing
Difficulty thinking or making decisions
Poor concentration
Mood swings
Confusion
Sleep disturbances
Decreased problem-solving abilities
Easily overwhelmed
Low energy or fatigue
Headaches
Depersonalization or dissociation (i.e., loss of emotional connection to others and life)
Other brain fog indicators may include feeling fuzzy-headed, unmotivated, melancholy, or irrational for no apparent reason. It’s also not uncommon for anxiety and depression to accompany brain fog, especially in cases of prolonged illness.

Additionally, brain fog symptoms can wax and wane during periods of high stress, exposure to electromagnetic frequencies and overly stimulating environments, hormonal changes, and during a herxheimer reaction. Symptoms can even intensify with certain moon cycles.

Your Brain on Lyme

Scientists are still trying to understand Lyme disease and how it affects the brain, but several studies have already concluded that Lyme bacteria can impact every aspect of the brain. Medical experts also agree that Lyme and coinfections cause the brain to swell, which can result in neurological or neuropsychiatric symptoms such as brain fog.

One of the most common causes of brain fog are the Lyme pathogens themselves, otherwise referred to as spirochetes. These corkscrew-shaped bacteria deeply embed themselves inside tissues, neurons, and cells. They can cross over the blood-brain barrier and wreak havoc on brain receptors and neural pathways.

When these pathogens die off, they excrete harmful endotoxins and exotoxins that inhibit brain function. If you do not detox properly, these toxins can accumulate and cause brain fog or damage brain tissue. The very presence of such toxins trigger the immune system to go into hyperdrive, releasing more cytokines into the blood, fueling inflammation within the brain and body. Cytokines are small proteins that are instrumental in cell signaling.

To overcome Lyme disease and brain fog, it’s crucial to address all underlying inflammation by making modifications to one’s diet and lifestyle.

Natural Brain Fog Recovery Tips

Get on the road to recovery from Lyme brain fog by taking inventory of the following areas:

Restful Sleep

One of the most significant neurological challenges for people with Lyme is insomnia. More than just a frustrating symptom, disturbed sleep patterns can interfere with healing by damaging the immune system, allowing toxins or pathogens to take root in the body. Insufficient sleep can also raise cytokine chemicals and quinolinic acid in the body that can lead to inflammation and worsen neurological symptoms.

Getting adequate sleep is key to Lyme recovery. Remember, it’s not just about the hours you clock every night, but also the quality of sleep that matters. Your brain and immune system do most of their healing when you are in a deep sleep, so it’s advised to get sleep around 10:00 pm and wake after about 7-8 hours of good sleep.

Need extra help in this department? Ask a medical practitioner about checking your hormones or thyroid levels to see what could be preventing you from getting enough zzz’s.

Anti-Inflammatory Diet

To support your brain health, try an anti-inflammatory diet to give your brain and body the nutrients it needs to heal. Buy organic as often as possible because toxic GMOs and pesticides can cause inflammation and put unnecessary stress on your body.

Eliminate these common offenders from your diet: caffeine, alcohol, refined carbohydrates, gluten, and sugar. All of these are enemies of brain fog and can impair brain function. It’s also best to avoid these substances until after your Lyme recovery.

Click here to read a great article on the top 15 anti-inflammatory foods that can transform your health:  https://draxe.com/anti-inflammatory-foods/

Also, cut out neuro-inflammatory saturated fats and instead up your intake of good or monounsaturated fats. Olive oil, nuts, avocado, and some types of fish have been shown to enhance memory and cognitive function, according to Harvard Medical School.

De-Stress Your Brain

High levels of cortisol, the body’s “stress hormone” have been linked to brain fog. Chronically elevated cortisol can disrupt your symphony of hormones that work intrinsically to keep your body in check. When one hormone falls too low, another one overcompensates to restore harmony.

Routinely check your cortisol levels (preferably via a saliva test) to ensure your levels are in balance. Actively pursue activities that reduce stress and declutter your mind, whether it be meditation, prayer, music, or your favorite hobby. Give yourself permission to unplug from the grid and relax.

Detox, Detox, Detox

Brain fog is often a sign of built-up toxins–Lyme, mold, parasites, or yeast–in the blood and intestines. Consider infrared sauna sessions, or doing light exercise or yoga to stimulate your lymphatic system. Get those toxins moving out of your body!

You may also speak to your healthcare providers about supplements you can take to support your detox pathways. Bentonite clay, activated charcoal, and juice cleanses are generally safe options for cleaning out the sludge.

Another way to help flush toxins out is to stay well-hydrated throughout the day. Multiply your body weight by 67%. The resulting number is the number of ounces of water you should drink daily. For example, a 100-pound person would need 67 ounces of water. Divide that by 8 – the number of ounces in a glass of water – and the result is roughly 8 glasses of water per day. Most of us fall far short of this amount.

Self-Healing for Lyme Disease and Brain Fog

You might also need extra support recovering from Lyme disease and brain fog. Advanced Cell Training (ACT) offers a self-healing program that enables your body’s own awesome ability to kill microorganisms – even in the brain. With ACT, you can train your own immune system to respond appropriately to spirochetes, parasites, and coinfections. This simple training process has helped thousands over the last 20 years overcome health issues. Basically, we point out where your body is going wrong and show it how to self-correct and get things back on track.

For more on ACT:  https://advancedcelltraining.com

 

Category:

Activism, Detoxing, diet and nutrition, Inflammation, Lyme, Parasites, Psychological Aspects, Treatment