Archive for the ‘Parasites’ Category

Co-Infection Patterns in Wisconsin Black Legged Ticks Show Associations Between Viral, Eukaryotic & Bacterial Microorganisms

Co-Infection Patterns in Individual Ixodes scapularis Ticks Reveal Associations between Viral, Eukaryotic and Bacterial Microorganisms.

Cross ST, et al. Viruses. 2018.


Ixodes scapularis ticks harbor a variety of microorganisms, including eukaryotes, bacteria and viruses. Some of these can be transmitted to and cause disease in humans and other vertebrates. Others are not pathogenic, but may impact the ability of the tick to harbor and transmit pathogens. A growing number of studies have examined the influence of bacteria on tick vector competence but the influence of the tick virome remains less clear, despite a surge in the discovery of tick-associated viruses.

In this study, we performed shotgun RNA sequencing on 112 individual adult I. scapularis collected in Wisconsin, USA. We characterized the abundance, prevalence and co-infection rates of viruses, bacteria and eukaryotic microorganisms.

We identified pairs of tick-infecting microorganisms whose observed co-infection rates were higher or lower than would be expected, or whose RNA levels were positively correlated in co-infected ticks. Many of these co-occurrence and correlation relationships involved two bunyaviruses, South Bay virus and blacklegged tick phlebovirus-1. These viruses were also the most prevalent microorganisms in the ticks we sampled, and had the highest average RNA levels.

Evidence of associations between microbes included a positive correlation between RNA levels of South Bay virus and Borrelia burgdorferi, the Lyme disease agent. These findings contribute to the rationale for experimental studies on the impact of viruses on tick biology and vector competence.


**Eukaryotes are protozoans or parasites which includes worms (nematodes/helminths)**

Mainstream medicine has yet to take into account the synergistic effect of all of the pathogens found within a tick upon human suffering.  So far they continue to believe this is a one pathogen/one disease/one drug paradigm, hence the mono-therapy of doxycycline as their answer to this 21st century plague.

Until this changes, we are doomed.

Dr. Jay Davidson – Video on Nematodes in the Eye  Video here Approx. 15 Min.

Parasites in the eyeballs and parasites from Rats!…/67/wr/mm6730a4.htm…

The top link shows Dr. Jay Davidson talking about rat lungworm, hookworm, Strongyloides, and nematodes in the eye. Believe it or not, this particular eye parasite affects 12 million people worldwide.

He also gives a preview of a parasite symptom checklist.

For more on parasites:


Risky Business: Linking T. gondii & Entrepreneurship Behaviors

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


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.



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:  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:

And lastly, I’ll never forget this information on how parasites affect human behavior by Dr. Klinghardt, which I found here:

  • 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:

as well as this one:

Please consider parasites and discuss with your medical practitioner.

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


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.

When he came to, he was on the floor. He had rolled out of the wheelchair and hit his head. A gaggle of worried-looking medical staff stood over him. They asked if he was on drugs. Did he have heart problems? His blood pressure was extremely low, probably the reason he had passed out. Niegelsky, who was 58, told them that he was healthy and drug-free and had no heart condition.

“I could see the concern on their faces in a way that did not help my confidence level at all,” Niegelsky says.

He felt as if insects were biting every inch of his hands, armpits and groin. A doctor asked if he had any food allergies. The hives and the low blood pressure suggested anaphylaxis, a severe allergic reaction. Again the answer was no, but Niegelsky did recall that he had a very bad allergic reaction a month earlier to a tick bite he got at a concert.


The E.R. doctor ordered two shots of epinephrine, a form of adrenaline that dampens the allergic reaction; the hives and itching began to subside about 25 minutes later. Now the doctor asked Niegelsky what he’d eaten that day. A hamburger for lunch, Niegelsky told him. In his recollection, the doctor’s eyes widened, and he said,

“I think we know what you have” — a condition called mammalian-meat allergy.

Meat allergy was first observed in the 1990s and formally described in 2009, which makes it a relatively recent arrival to the compendium of allergic conditions. Its most curious quality may be that it is seemingly triggered by a tick bite. In America, the culprit, called the lone-star tick — females have a distinctive white splotch on their backs — is common in the warm and humid Southeast, where most cases of meat allergy have been diagnosed. Niegelsky had in fact heard about the allergy from friends. He remembers shaking his head and thinking that it sounded “made up.” He understood now, in a visceral way, how real it was. That bite from a month ago had primed his body for today’s hives and plummeting blood pressure.

Until meat allergy was recognized, the prevailing medical wisdom held that an allergic reaction to meat from mammals was extremely unusual. Unlike that from shellfish, say, meat from mammals was thought by some allergists to be too similar to human flesh for the immune system to attack it with the full fury of the allergic arsenal. In this and other respects, meat allergy is upending longstanding assumptions about how allergies work. Its existence suggests that other allergies could be initiated by arthropod bites or unexpected exposures. It also raises the possibility that other symptoms often reported by patients that clinicians might dismiss because they don’t fit into established frameworks — gluten intolerance, for example, or mucus production after drinking milk — could, similarly, be conditions that scientists simply don’t understand yet.
Mammalian-meat allergy “really has the potential to revolutionize our understanding of food allergy, because it doesn’t fall under the umbrella of our paradigm,” Dr. Maya R. Jerath, a professor of medicine at Washington University School of Medicine, in St. Louis, told me. “Maybe our paradigm is wrong.”
The meat-allergy story begins somewhat obliquely, with a new drug for metastatic colon cancer called cetuximab. In 2006, Thomas Platts-Mills, an allergist at the University of Virginia School of Medicine, received a phone call from a colleague. Oncologists testing cetuximab were baffled to find that nearly one in four patients had severe anaphylactic reactions to the drug. A few patients even died. The caller urged Platts-Mills to look into the mystery. He agreed and began by comparing the blood from those who had an allergic response to cetuximab with the blood from those who didn’t. The patients who reacted, he discovered, had allergic antibodies to a complex sugar called galactose-alpha-1,3-galactose, or alpha-gal for short. Most mammals produce alpha-gal; it’s a component of their cell membranes. The exceptions are African and Asian apes and monkeys. As primates of African origin, we do not produce alpha-gal, either. That makes the human immune system unusual: It can learn to see alpha-gal, present in the beef and pork and other mammalian meat we eat, as foreign and threatening, thereby allowing for an allergic response. Cetuximab contained alpha-gal, it turned out; the sugar came from the genetically modified mice used to manufacture the drug.
While Platts-Mills had identified the molecule in the drug causing these severe allergic reactions, he didn’t yet know why those patients were allergic to it. How had their immune systems become sensitized to it? Humans aren’t born allergic to anything; allergy is like a bad habit the immune system needs to learn. Many scientists suspect that our allergic machinery — the swelling of tissues, mucus production, the coughing and sneezing — served an important purpose in our evolutionary past. It probably helped us to fight off parasites. But in allergic disorders, the body unleashes this ancient anti-parasite response inappropriately against molecules that aren’t obviously dangerous (beyond their role in causing a reaction) — against cat dander or pollens or peanuts. The mystery of any allergy is how and why the immune system is first led to make this mistake.
What had primed the patients to be allergic to the alpha-gal sugar? The oncologists did have one clue: They noticed that allergic patients tended to come from the Southeast. Initially Platts-Mills thought that maybe intestinal parasites or even a mold from the region was sensitizing patients to alpha-gal. But a technician in his lab pointed out that the geographical distribution of cases matched the reported distribution of a tick-borne disease called Rocky Mountain spotted fever.
That got Platts-Mills thinking about ticks.
At the same time, he was seeing a growing number of patients in his allergy clinic, many of them hunters and outdoorsy types, complaining about what was apparently a strange reaction to eating meat. They suffered stomach pains and rashes hours later. When Platts-Mills analyzed their blood, he found that, like the cancer patients who had an allergic reaction to cetuximab, they also had allergic antibodies for alpha-gal. And when he and his colleague Scott P. Commins surveyed the patients, they found that more than 80 percent of them reported having had strong reactions to tick bites.
Independent of the research Platts-Mills was doing, in 2007 an Australian allergist named Sheryl van Nunen described 24 cases of meat allergy associated with tick bites. Colleagues were skeptical of her claims, she told me. They didn’t think an allergy to meat from mammals was very likely. And she hadn’t identified what the immune system was specifically attacking, the molecule in meat that was attracting the onslaught. That discovery fell to Platts-Mills, Commins and their colleagues. They posited that alpha-gal was the allergen that made people sick hours after eating hamburgers (or, in Australia, kangaroo steaks). And they proposed tick bites as the trigger. Ticks could explain the two seemingly disparate phenomena: why people who reacted to cetuximab came from the Southeast and why most cases of meat allergy occurred in the same region. The Southeastern lone-star tick was exposing and thus sensitizing people to the sugar through its bites. Some subset of the ectoparasite’s victims would thereafter react to alpha-gal whenever they encountered it, including in meat and cetuximab.
Platts-Mills still lacked definitive proof that a tick bite initiated the allergy. He hadn’t conducted an experiment in which, for example, he deliberately induced meat allergy in human volunteers. But one day in August 2007, he took a hike in the nearby Blue Ridge Mountains. When he got home, he discovered hundreds of larval-stage ticks feeding on his ankles. (He spent the evening removing them with a knife and Scotch tape.) Platts-Mills doesn’t eat red meat often — he had a heart attack in 2005 — but a few months after that hike, on a trip to Europe, he ate two lamb chops and had a glass of red wine.
“Six hours later I was in a hotel, covered in hives, itching like crazy and laughing at myself,” he told me. By then, he thought he knew what was happening: The ticks had made him allergic to those chops.
In 2013, on a hike and a picnic with some friends in the Blue Ridge Mountains, Platts-Mills was again swarmed by larval ticks. By this time he was already monitoring his alpha-gal antibody levels, so he was able to compare how much antibody he had circulating before and after these ticks fed on him. Post-picnic, the allergic antibodies directed at alpha-gal in his bloodstream surged more than tenfold, direct evidence that tick bites had provoked the allergic response to alpha-gal. It seemed he had cracked the case, and others around the world took note. Sheryl van Nunen, now at the University of Sydney, told me this understanding of the precise cause of mammalian-meat allergy makes it unique.
“This is really allergy in a kit — how to get it and how to lose it,” van Nunen said. “There’s really nothing else like it.”
Until meat allergy was recognized, the prevailing medical wisdom held that an allergic reaction to meat from mammals was extremely unusual.  CreditPhoto Illustration by Daan Brand

Mammalian-meat allergy differs from most other food allergies in several important ways. One is the delayed reaction; it’s not uncommon for sufferers to wake up in the middle of the night, hours after a steak dinner, covered with hives and struggling to breathe. By contrast, those with food allergies to peanuts usually develop symptoms within minutes after ingesting the offending food. And whereas in most cases of allergy, the immune system pursues a protein, meat allergy is set off by a sugar.

Another unusual aspect of meat allergy is that it can emerge after a lifetime spent eating meat without problems. In other food allergies, scientists think that children’s immune systems may never learn to tolerate the food in the first place. But in meat allergy, the tick seems to break an already established tolerance, causing the immune system to attack what it previously ignored. One way to understand how the parasite pulls this off is to consider its bite as a kind of inadvertent vaccine. A vaccine teaches an immune system to pursue a pathogen it otherwise wouldn’t by exposing it to weakened versions of that pathogen — an attenuated measles virus, say — or bits and pieces of dead pathogen. Vaccines also often contain a substance called an adjuvant, which is designed to spur the immune system into action.

In similar fashion, when the lone-star tick feeds, alpha-gal leaks from its mouth into the wound, exposing the victim’s immune system to the sugar, prompting the immune system to remember and pursue alpha-gal. But exposure to alpha-gal alone probably doesn’t achieve this feat. Commins, who is at the University of North Carolina, at Chapel Hill, has identified a candidate, an enzyme in the tick’s saliva called dipeptidyl-peptidase that works as an adjuvant. It’s also common in bee and wasp venom. This enzyme, Commins argues, is what tells your immune system to see alpha-gal as the type of threat that warrants the itching and swelling of the allergic response.

Once sensitized, some victims find that they can no longer tolerate beef, pork, lamb — even milk or butter, foodstuffs with only very small amounts of alpha-gal. Several factors can also affect the severity of the allergic reaction, or if there is an allergic reaction at all. Grilled meat is less allergenic than other methods of preparation that preserve more of its fat. Fatty meat leads to more alpha-gal crossing a person’s gut barrier into his or her circulatory system, triggering a stronger immune reaction than leaner cuts. A study of German patients also found that alcohol imbibed with meat can push people toward an allergic reaction, as can exercise; both actions make the gut more permeable, exposing the immune system to more alpha-gal.

As it happens, an immune response to alpha-gal is also what drives, in part, the rejection of tissue transplanted from animals to people.

Scientists have developed genetically modified pigs meant to supply parts that can be grafted onto human bodies without eliciting an anti-alpha-gal immune reaction. Now, as awareness of the meat allergy spreads, there has been talk of using such alpha-gal-free pigs for food — pork chops your doctor can prescribe if you find yourself allergic to meat.

A recent study by scientists at the National Institutes of Health, which included Commins and Platts-Mills as co-authors, linked allergic sensitization to alpha-gal with a greater risk of arterial plaques, a hallmark of heart disease. It’s unclear whether having alpha-gal antibodies specifically increases your risk of developing plaques or whether some other factor increases a person’s risk of heart disease and sensitization to alpha-gal. But if it turns out that meat allergy pushes people toward cardiac arrest, it would imply that encounters with the lone-star tick contribute to the leading cause of death in the United States.

The big, unanswered question is why meat allergy is on the rise today. Commins estimates that at least 5,000 cases have been diagnosed in the United States, and many more probably remain undiagnosed. In some tick-heavy regions, the prevalence of meat allergy is estimated to be at least 1 percent of the population. Ticks are not new. Neither is the human consumption of meat. Why the sudden problem for so many? One possibility is that the ticks have changed somehow.

Maybe they’ve acquired a pathogen we don’t understand yet, and this infection is causing the allergy. Or perhaps, Commins says, changes to the insect’s microbiome, the collection of symbiotic microbes that it carries in its body, have somehow made its bites more allergenic.

The idea is plausible and could nicely explain how an arachnid that has been around for a long time could begin causing a new set of complications. Scientists have long debated where the alpha-gal in the tick originates: Does it come from the blood a tick sucks from other mammals and then regurgitates as it feeds on people, or does it come from the tick itself? Shahid Karim, a vector biologist at the University of Southern Mississippi, in Hattiesburg, told me that the answer might be neither; the sugar probably comes from the microbes that the tick carries within it. So it’s entirely possible, he said, that changes in its microbiome could, by increasing the amount of alpha-gal humans are exposed to in tick bites, make the lone-star tick more likely to induce meat allergy.

What such an account fails to address, however, is why the meat allergy has increased in other parts of the world, like Australia and Europe. (Van Nunen says that in the tick country around Sydney, people are now more likely to carry EpiPens, which contain a shot of adrenaline, for meat allergy than for better-known peanut allergies.) Other tick species are linked with meat allergy in those regions, not the lone-star tick. And it seems very unlikely that the microbiomes of all these ticks on different continents have changed in similar ways at the same time.

“I don’t for the life of me have a unifying hypothesis for why it’s happening everywhere,” Commins told me, although he added that pesticides could be one factor changing tick microbiomes globally.

It may simply be that an increase in the number of ticks has turned a problem once so rare that it went scientifically unnoticed into an observable epidemic.

“I think we’ve got far more tick bites today than people had as recently as 35 years ago,” Platts-Mills told me. He lays the blame for the growing spread of ticks on newly abundant deer.

In Virginia, he thinks new laws requiring dogs to remain on leashes have emboldened deer, which then bring ticks closer to people. People aren’t necessarily venturing deeper into the forests than in the past, he says. More than half the patients he sees with the allergy were bitten on their own lawns.

His leash theory is anecdotal, but it’s certainly true that the current ecological state of Eastern forests is probably encouraging ticks to multiply. After having been cleared in the Colonial era, the forests have partly grown back. Deer and turkey, which the lone-star tick likes to feed on, are abundant again. They thrive in the new-growth forests, now fragmented by roads and suburbs. Large predators are mostly absent. And the rise of tick-borne disease generally has been linked with the decline (or absence) of predators that eat the animals ticks feed on. In Australia, for example, van Nunen points to the eradication of foxes, an introduced species there, as one factor in the increase of ticks and the rise of meat allergy.

We might label this the disturbed ecosystem theory of meat allergy. Forests ecosystems have recovered partially — lots of animal hosts for ticks but not enough predators to keep those hosts in check — and this imbalance has fostered an exponential growth in the number of ticks. In some ways, this is the most probable explanation for the rise of meat allergy. Climate change may be aiding the lone-star tick’s move northward too, Rick Ostfeld, a disease ecologist at the Cary Institute of Ecosystem Studies, told me. Hundreds of cases of meat allergy have been diagnosed on Long Island in recent years, which wasn’t part of the tick’s range in recent history. The tick has been spotted as far north as Maine.

But what’s happening in the American East can’t account for the full extent of the phenomenon elsewhere in the world. In Northern Europe, ticks are proliferating as forests recover and the climate becomes warmer. But in Spain and Southern Europe, the rising incidence of meat allergy has not been accompanied by an increase in tick numbers, according to José de la Fuente, a professor at the Institute of Game and Wildlife Research in Ciudad Real, Spain. For him, the mystery of meat allergy is captured in one question: If a tick bites two genetically similar people, why might only one develop the meat allergy?

Onyinye Iweala, an assistant professor who works with Scott Commins’s lab at the University of North Carolina, echoes this uncertainty. Why are some people sensitized to alpha-gal — meaning they have allergic antibodies directed at the sugar in their blood stream — but never have an allergic reaction to it? This can happen in all allergies. You can have antibodies to, say, cat dander, yet never wheeze or sneeze around cats. Iweala suspects that sensitization to alpha-gal isn’t new. What’s changing is the proportion of people who, after sensitization, proceed to overt allergy. Something else in the environment, she told me, is likely pushing people toward full-blown meat allergy. Perhaps shifts in the microbes that live within us have somehow made us more easily sensitized by tick bite. As a model of how this might work, Iweala points to intriguing research on the interaction between malaria and the human microbiome that centers on alpha-gal.

OUR DISTANT ANCESTORS once made alpha-gal. Understanding why humans don’t could shed light on the meat-allergy mystery. Like other mammals, South American monkeys produce alpha-gal. Only Old World monkeys and apes (and humans) have lost the ability to make the sugar. Hence scientists deduce that the change most likely happened after New and Old World primates diverged from each other around 40 million years ago. One explanation for the disappearance of alpha-gal is that it was driven by some catastrophe, a deadly infection that afflicted Old World primates, perhaps, and as a result maybe these distant relatives of ours stopped being able to produce the sugar because doing so conferred an evolutionary advantage. The mutation that eliminated alpha-gal could have improved a primate’s ability to fight off an infection by enabling its immune system to more easily distinguish between its own body and some pathogen with alpha-gal.

What could this pathogen have been? In the late 2000s, Miguel Soares, a scientist at the Instituto Gulbenkian de Ciência in Oeiras, Portugal, began to suspect the plasmodium parasite that causes malaria. Because the protozoan is so deadly and has historically been so widespread in warmer climes, geneticists often say that malaria has been the single greatest force shaping the human genome in our recent evolutionary history. The parasite remains a leading cause of death in the developing world. And it’s coated in alpha-gal.

Soares and his colleagues investigated a rural Malian population that was naturally exposed to malaria. As it happens, humans produce some antibodies to alpha-gal all the time. They’re not allergic antibodies like those responsible for Lee Niegelsky’s anaphylactic experience, but antimicrobial ones that give rise to a different, less drastic immune response. Between 1 and 5 percent of all the antibodies circulating in any person, a remarkably large quantity, are directed at alpha-gal, Soares estimates. The target of these antibodies is not the alpha-gal in the steak you may have eaten for dinner but the alpha-gal that leaks into circulation from the microbes dwelling in your gut. There are natural variations in the amount of these antibodies any individual produces; some people make more, some less. Soares wanted to know if this variability influenced the villagers’ susceptibility to malaria.

What he discovered may yet change how malaria is combated. Villagers who produced the greatest quantity of alpha-gal antibodies, he found, weren’t immune to infection by the parasite, but they were less likely to be infected after exposure.

What was different about those with more alpha-gal antibodies? They had more gut microbes that produced the sugar, Soares speculated. By priming their immune response against alpha-gal, these individuals’ microbiomes probably helped shield them against malaria. Soares showed as much using mice. Rodents colonized by a strain of E. coli found in the human microbiome that contains alpha-gal produced antibodies to the sugar and were protected from malaria. Rodents that harbored an E. coli strain that didn’t produce the sugar, on the other hand, were not protected. (Other scientists later observed a connection between resistance to malaria and the composition of Malian villagers’ microbiomes.) This research highlights one reason we probably have a few pounds of microbes in us: Friendly microbes can help protect us against unfriendly ones.

Soares is currently working on a vaccine to spur the immune system to attack alpha-gal more actively, thereby conferring greater protection against malaria. His findings also raise the prospect, at least theoretically, of an antimalarial probiotic. In the context of meat allergy, his work underscores the fact that our microbes may affect how we respond to alpha-gal from other sources, including, perhaps, tick bites.

How might this work? You can envision antibodies as arrows that have Velcro on the front instead of arrowheads. Depending on their targets, that Velcro sticks only to a particular substance, like alpha-gal or peanut protein. The back end of the arrow displays a signal that tells the immune system what to do. Allergic antibodies, called immunoglobulin-E, or IgE for short, call for an allergic response. But the antibodies that humans typically have in circulation directed at alpha-gal are antimicrobial antibodies like IgM and IgG, not allergic ones.

A question central to the meat-allergy mystery is how, if we’re always exposed to alpha-gal from our gut microbes, and we’re constantly mounting a nonallergic response against it, the lone-star tick prompts what’s called “class switching,” spurring the immune system to pump out allergic antibodies instead of antimicrobial ones?

The microbes we host may, by stimulating the immune system and guiding its response to alpha-gal, make this class switching more or less likely, Onyinye Iweala told me. But scientists don’t yet know how the relationship works. Perhaps if your microbiota have more species that produce alpha-gal, these microbes stimulate your immune system in a way that protects you from allergic sensitization to the sugar when a tick bites. Or maybe the relationship works the other way around: If you host fewer alpha-gal-producing species and your immune system is less exposed to alpha-gal on a daily basis, that relative lack of stimulation might prevent alpha-gal allergy from developing when you’re bitten by a tick. These interactions can be tested — as Iweala is doing — with mice that, like humans, don’t produce alpha-gal.

What scientists do know is that if you treat a baboon with antibiotics, reducing the amount of alpha-gal-producing microbes in its gut, and thus lessening the stimulation they provide, the quantity of alpha-gal antibodies in its bloodstream also declines. This suggests that altering a primate’s gut microbes may change its immune response to alpha-gal. People living in developed countries, where most cases of meat allergy have been diagnosed, have been doing something very similar to themselves. “We keep changing the microbiome with antibiotics and what we eat,” Iweala says. By tweaking the microbes that live inside us, we may have inadvertently changed how our immune system responds to alpha-gal, making us more vulnerable to tick-induced meat allergy. It’s also possible, however, that the microbes that determine the general tone of our immune function have shifted, altering how we respond to all potential allergens, not just alpha-gal.

Since at least the late 20th century, and probably earlier, we’ve been living in the midst of what’s often called the allergy epidemic, an era that has seen an increase in the prevalence and severity of food allergies generally and, before that, a rise in the prevalence of respiratory allergies and asthma. The forces driving this trend may help account for meat allergy as well. A leading explanation holds that we develop more allergies now because our immune systems have become more sensitive to what they encounter, not because they are exposed to more pollens or allergenic foods than in the past. The reason the modern immune system errs this way, the thinking goes, is that it’s not receiving the right kind of education.

The news media have taken to calling this explanation the “hygiene hypothesis,” which is unfortunate and misleading; personal hygiene has little to do with what’s at issue. More accurate terms coined by researchers include the microbial-deprivation hypothesis, the disappearing-microbiota hypothesis and even the “old friends” hypothesis (the implication being that we’ve lost contact with once-ever-present friendly organisms).

Whatever you call it, the idea is that the rising tide of allergic diseases comes from changes to the type and quantity of microbes we encounter in our environment, particularly in our early life, as well as from changes to the microbes that live on and in us. Improved sanitation, antibiotics and the junk-food-ification of our diet, among other factors, may have shifted our microbial communities, giving us an immune system that’s overly jumpy, unable to reliably distinguish friend from foe and prone to diseases of overreaction, like allergies.

Studies on populations that have bucked the increase in allergies support the idea. Nearly 20 years of research on European children who grow up on farms with animals, for example, indicates that they are less likely to have respiratory allergies, asthma and eczema compared with other children in the same rural areas. The abundant microbial stimulation of the farm environment, scientists have proposed, tunes farming children’s immune system in a way that prevents allergic disease. The cowshed has thus become a stand-in for premodern conditions and the immune system that that environment produces — lightly stimulated but less likely to react to allergens — a model of how the human immune system might have worked in a more microbially enriched past.

So here is the question as it relates to meat allergy: If a lone-star tick bit a Bavarian farm-raised child, would she be less likely to develop an allergy to alpha-gal compared with her nonfarming counterparts? Put another way, if the tick bit someone 150 years ago when the whole world was more like a cowshed, would that person be less or more likely to develop a food allergy than someone from modern-day Chapel Hill?

It’s pure speculation at this point, but gradual, intergenerational changes to our microbes may have altered our immunological tenor, shifting it from cool, calm and collected toward restless and irritable and increasing the odds of developing allergy from a tick bite. Today we may encounter more ticks than in times past, but they may also be interacting with an immune system that’s more sensitive to their bites than ever before. “It’s the ‘perfect storm,’ as you would say in America,” Sheryl van Nunen told me.

For Lee Niegelsky, who had eaten hamburgers his entire life, the allergy forced him to constantly scrutinize his diet. You don’t realize how many foods have meat-derived products in them, he told me — especially in the South, where pork fat and bacon are widely used as flavoring — until you have to avoid meat for fear of passing out. Not long ago, for example, he fell ill after eating clam chowder, which he attributes to meat broth that he suspects was in the soup.

The good news is that, provided you’re not bitten by a tick again, sometimes the meat allergy fades on its own. A year after his visit to the emergency room, under Scott Commin’s supervision, Niegelsky began introducing small amounts of lean meat into his diet. The idea is to test the possibility that his allergic alpha-gal antibodies have subsided to the point that his immune system no longer attacks the sugar. It took Niegelsky about a week to muster the courage to take his first bite of pork tenderloin. He waited anxiously for six hours. When nothing happened, he moved on to steak.

Moises Velasquez-Manoff is a contributing Op-Ed writer for The Times and the author of ‘‘An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases.’’ He last wrote for the magazine about carbon farming.



I find it interesting that no one is mentioning the fact ticks have been tweaked in a lab for biowarfare purposes.  Tularemia, brucella, certain Rickettsia’s, numerous viruses, some chlamydia’s, and of course mycoplasma have all been weaponized.

“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:  (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:

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

Herpes Viruses Implicated in Alzheimer’s Disease

Herpes Viruses Implicated in Alzheimer’s Disease


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,”, 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.



  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:

Dr. David Baewer discusses arboviruses & Lyme: 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.



Tickborne Diseases – Confronting a Growing Threat

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

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.


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.


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:
  2. There is a real probability of sexual transmission:
  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:  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:
  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:  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.

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: 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.



Recover From Brain Fog & Lyme Disease Naturally

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
Sleep disturbances
Decreased problem-solving abilities
Easily overwhelmed
Low energy or fatigue
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:

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: