Why Lyme?

has turned into a 1.3b dollar problem

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By David Addona

September 6, 2019

 

Each year there are reportedly 329,000 new Lyme disease cases in the U.S. That’s more than the total cases of breast cancer yet it receives .03% of its funding. While the infectious disease community has yet to develop what you’d consider a handle on the disease, other conditions comparably misunderstood, don’t receive the same pushback in terms of legitimacy.

Novel research, most of which has been funded privately has come to find Neurological disorders like ALS, Parkinson’s and Bell’s palsy have demonstrable links to Lyme. Within the past decade, The International Journal of Infectious Disease performed case studies in which Lyme disease patients have developed what’s called Lyme Cranial Nerve Palsy while being treated with routine Doxycycline. In other words, Borrelia burgdorferi has become much more elaborate in finding ways to survive in the human body. At the same time, it’s collaboratively fortifying its adaptogenic ability to go undetected.

A recent review article published in Current Topics in Medicinal Chemistry references the Halperin study, which found that 50% of ALS patients tested positive for B. burgdorferi, compared with 10.5% of controls. Authors of the review postulate that these mechanisms combine with a genetic predisposition. Thus far, the gene NEK1 has been determined as a factor.

This notion was tested in 2016 when pathologist Dr. Alan B. MacDonald was provided ten diseased MS patient specimens by The Rocky Mountain Multiple Sclerosis Center. Broke by Susan Ferrara with the PCCAG; MacDonald’s analysis concluded that all ten specimens contained evidence of Borrelia pathogens. Two forms of Borrelia were found, including B. burgdorferi, inside parasitic nematode worms. The worm eggs or larvae were located inside brain tissue, as well as spinal fluid. It was also concluded that the initial tick bite actually delivers the nematode into the human body. So there are complex layers in which these pathogens successfully obtain a host.

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Infected nematodes were also found inside tissues of the highly malignant form of brain cancer Glioblastoma multiforme, and Lewy Body dementia which claimed the lives of Ted Kennedy and Robin Williams, respectively. LBD is also responsible for claiming MacDonald’s grandfather, a Harvard Medical School professor. Despite these tissue findings, patients suffering from neurodegenerative symptoms often return normal MRI brain scans. Such scans were documented by infectious disease specialist, Luis A. Marcos in the 2017 Elsevier Case Report. At the same time, a Lyme disease vaccine hasn’t been available since 2002. At that time, the vaccine manufacturer discontinued production citing insufficient consumer demand. The confluence of these circumstances explains precisely why Lyme disease is the most common vector-borne disease in the U.S. Since the Borrelia bacteria has been around for about 15 million years, a better understanding of how it has evolved could play a central role in understanding its overall body of related illnesses.

In line with Madeline Bender’s Sept. 12, 2017, Yale Daily News article; over the summer of 2013, Yale School of Public Health professor, Gisella Caccone, worked to isolate the Lyme bacteria. Her team sequenced 146 Borrelia genomes collected from over 7,000 ticks. Regardless of how accurately DNA-based testing like polymerase chain reaction correlates B. burgdorferi and Neurodegenerative diseases; this study highlights the need to understand ecologically, why the prevalence of these illnesses are surging.

“Now that the researchers have developed an effective technique to isolate bacterial DNA from that of their host, they can apply it to other vector-borne diseases, such as malaria and African sleeping sickness”, Caccone explained. She added that ”While the study did not advance treatment, it may help predict future movement of the disease.” Notably, the researchers found that some strains of the bacteria were conserved even across thousands of miles, suggesting Borrelia can undergo long-range bird migration. This particular finding is significant in understanding that Lyme disease is an ongoing epidemic that has been triggered by human activity.

“This is definitely not the only infectious disease that is re-emerging now because of human-imposed environmental change,” she clarified. “I think it’s important to keep investigating and asking questions about how human health is influenced by changing ecology.”

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So environmentally speaking, we know that habitat disruption is central to the uptick of vector-borne diseases, and that infected arthropod species are especially sensitive to climatic factors. This one-two punch isn’t just throwing off sensitive habitats; it’s throwing off the fine-tuned roles of our immune systems. Since human beings survive by evolving to our environment, disrupting our habitats will, in essence, disrupt our functionality.

In making so much as a dent in this pandemic, it’s essential to understand the complexities of the immune system. Considering just how deep the human footprint has been driven into the earth, the consensus among respected practitioners has naturally called for the Center for Disease Control (CDC) to advance diagnosis and treatment protocols. I recently got to speak with Hillary Thing, LAc, an expert on real-world Lyme detection, at a conference for practitioners in New York City.

Discussed with immediacy was the highly problematic Western Blot test. The Western Blot is how the CDC determines Lyme disease by indirectly detecting antigens, or flagella of Lyme related pathogens. The bone of contention here is that the diagnosis is based on the amount of reactive antibodies, or “bands” within the blood.

According to Thing and those at the forefront of “Lyme Literate” detection, it’s not how many bands—but precisely which ones. “Like a battalion of defense, each antibody has jobs, some more specific than others. For instance, band 23 IGM/IGG has one job. It is specific in fighting Borrelia burgdorferi. Outside of 23, 18 also signifies that Borrelia is present within the body. In total, bands (18, 23, 30, 31, 34, 37, 39, 83 & 93) correlate with Lyme disease and its various forms or co-infections. Therefore, if a patient has any of these antibodies present in their blood and is suffering from Lyme-like symptoms—they should be treated resolutely”, Thing asserted.

There are 21 types of bacteria known to cause Lyme—29 types that cause Rheumatic Fever. Therefore, it’s to the Lyme literate communities benefit to diagnose with urgent sensibility. Raised during Q&A were matters regarding the survival tactics of said pathogens and their ability to evolve. Apparently, one of the ways bacteria thwarts die-off is to become more diverse. Clinical research has brought forward compelling evidence that many pathogens have evolved more within the last thirty years than they have in the previous hundred.

Bacterium is continually developing communication methods like quorum sensing which involve signal molecules called autoinducers. There’s no question that propelling pathogenic research can reveal just where exactly our immune systems are falling short.

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Published on July 2, 2012, in the Journal of Neuroinflammation; Neuroimmune Crosstalk in the Central Nervous System revealed that glial cells can effectively recognize pathogens in both the central nervous system and in peripheral tissues. When glial cells recognize foreign pathogens through the use of peptide signaling, they are able to relay this information to the CNS.

The result, unfortunately, is an increase in depressive symptoms. Moreover, chronic activation of glial cells leads to neuroinflammation and degeneration. Corresponding to Li Tian’s work is Feb 22, 2016’s Annual Review of Neuroscience which confirmed that the pneumogastric nerve, commonly referred to as the “vagus nerve”, connects to the gastrointestinal tract. It also connects to airways and elicits nerve impulses to the brainstem. And it does so as a response to the detection of toxins and pathogens present.

The basis that lymphatic vessels in the brain correspond to iliac nodes in the lower abdomen concedes functional reciprocity. Our understanding of the blood-brain barrier has eradicated the idea that a disease can be located solely in the brain, or, be “all in your head”. That’s just not the way our bodies work. Understanding the extent that our brains—nervous, and immune systems are intertwined shows how depression and other seemingly isolated symptoms are related. Better yet, this understanding reveals symptoms themselves signify disruption within our neuroimmune system, down to a cellular physiological state. Following injury or infection, there is a cascade of inflammatory responses, such as the secretion of chemokines. This couples with the release of neuropeptides and transmitters like substance P or serotonin. Together, this compound neuroimmune response has an amplifying effect on inflammation. Ultimately, this explains the true nature of a chemical imbalance. It also explains why they’re so common.

In short, our bodies are trying to tell us something. The immune system, or better yet, our understanding of it has changed drastically within the last 25 years. Our “gut”, or more aptly described as our enteric nervous system contains more than 100 million neuron receptors. Heralded for its time, and still novel today is Michael Gershon’s 1998 book, The Second Brain. In it, Gershon discusses how scientists at the David Geffen School of Medicine at the University of California, Los Angeles, were shocked to learn that about 90 percent of the fibers in the primary visceral nerve carries information from the gut to the brain and not the other way around. “Some of that info is decidedly unpleasant,” Gershon explained.

In fact, 95 percent of the body’s serotonin is found in the bowels. Consequently, the reliance of drugs like selective serotonin reuptake inhibitors (SSRIs) and biologics not only disrupt the information sent to the brain, in the case of biologics, they also greatly reduce the immune system’s ability to fight infection. In other words, we’re treating the signals of dysfunction, which ultimately compounds the matter. This interference with complex systems we’re just beginning to understand is likely why the number of Americans on antidepressants has increased 64% within the last 20 years.

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This isn’t to say people relying on antidepressants should go off of their medication, instead, it is to point out that what we’re doing is grossly unsustainable, and per the long-term, ineffective.

What’s perhaps most problematic with drugs masking dysfunction is that it makes it more challenging for scientists to gain an understanding of other tick-borne viruses. Case in point, the deadly but thus far, rare “Bourbon virus”, which has been more apt to attach and feed on human cells as of late. Consistent with Megan Molteni’s work in the July 8th, 2019 issue of Wired, the Bourbon virus is a shape-shifter under a microscope and the only pathogen of the genus Thogotovirus to make it to the New World.

“Its nearest evolutionary relatives are viruses found in the bodies of sheep-sucking ticks in Kyrgyzstan and camel-chewing ticks in India, both of which attack neurons and cause brain inflammation.” Understanding what animal populations are going through now suggests what human populations will deal with in the near future. How openly we face our current crises will dictate what impact future crises will have on humanity. This is precisely why supporting advanced diagnosis methods like DNA sequence testing can be elementally transformative in addressing our existing inadequacies.

Developed by Dr. Sin Hang Lee, pathologist, and founder of Milford Molecular Diagnostics, DNA sequence testing is keenly designed to cut out the guesswork that two-tiered serology testing has failed to do. Data on sequence-based testing has shown to drastically curb false negatives—and false positives, alike. Though to the disservice of this vast effort, the CDC has chosen to block its application without producing supportive scientific data. Alternatively, the CDC has chosen to channel public funding to bolster its patented metabolomic method.

This gridlock has forced Lee and his peers to point out the textbook standards and molecular biology principles utilized in direct molecular testing. Released by the Stamford CT based, Moore Communications and Associates; ironically, Lee’s methodology was in fact prompted by Dr. Martin Schriefer of NCEZID (The National Center for Emerging and Zoonotic Infectious Diseases—a specialized division of the CDC), who stated the need for direct molecular detection at an open HHS conference on September 24, 2012. At the time, Dr. Schriefer was directed by the U.S. House of Representatives’ Appropriations Committee bill of September 2009, then reinforced by House Report 115-244.

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As more otherwise enmeshed corporate matters have gained public interest, it’s become increasingly evident to patients that the CDC has a myriad of interests concerning the management of infectious diseases. As with any considerable corporate enterprise, such interests present themselves in order to safeguard assets. Persisting in the realm of contemporary treatment, another dedicated LLMD by the name of Daniel A. Kinderlehrer recently published on the laboratory breakthroughs of Disulfiram. Because of its effectiveness, the antibiotic is undergoing initial clinical testing by Brian A. Fallon, MD, MPH, of Columbia University. Fallon is the director of the Center for Neuroinflammatory Disorders and Biobehavioral Medicine.

Fallon is also the director at the Lyme and Tick-Borne Diseases Research Center. In the form of Antabuse, Disulfiram is typically used to treat alcoholism by worsening hangover symptoms. However, like many pharmaceuticals, its off-label uses are proving to be more purposeful than previously conceived. Initial lab research is privately backed by philanthropist Steven and Alexandra Cohen’s foundation. In fact, inspired by Alexandra’s own struggles with the disease, the couple has committed over $60 million dollars to fund more than 25 Lyme related research projects.

Publishing corresponding studies to Fallon’s is Dr. Ying Zhang of Johns Hopkins University. Together with Dr. Kim Lewis of Northeastern University, their findings focused in-depth on post-treatment Lyme disease. The study revealed that B. burgdorferi can not only survive traditional antibiotic treatment, it also revealed how it manages to do so in vitro, and in mice. Evidently, during treatment, bacterial communities form dormant, antibiotic tolerant cells called persister cells. Cells in what’s referred to as “persister state” are highly immune to antibiotics, which interfere with key molecules. The bacterium effectually put things on hold and go into hiding until the treatment is concluded. At which point, the bacterium effectively resumes. Zhang’s findings affirmed Balaban, Nathalie Q.’s 2013 study, A Problem of Persistence.

Over a hundred years ago, intellectuals scoffed at Béchamp and the very idea that germs could cause disease. Just over 30 years ago, the same occurred when Dr. Barry Marshall proved ulcers were caused by bacteria and not stress or spicy foods. We take little lesson from our not so distant past when we short-change the monumental work doctors like Fallon, Zhang, and Lewis are performing. Lyme’s disregard in view of alternative agendas has made it necessary for tenacious doctors and philanthropists to resolutely persist. The outright willingness to classify 80 auto-immune diseases without associated causes, itself, unveils industry indeed has their hand in the cookie jar. This along with patient fallout has led to the surge of more functional medicine. Like medicine’s past, when available sources run out of road, one’s forced to innovate more conducive pathways.

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In the U.S., the amount of functional medicine practitioners has nearly tripled within the last 20 years. Within the free-market healthcare system, which basis itself on supply and demand; it’s inevitable “the market” adjust to patients’ needs. It’s ironic, however, that those needs are at odds with the bodies put in place to represent them. For all that we don’t know about Lyme, there’s plenty that we do know. Most experienced clinicians will tell you there are no two cases exactly alike. Just as there aren’t two cases of cancer exactly the same. Respectively, it’s understood that each case of cancer is its own. As such, no clear-headed individual would dare argue, “My son survived Leukemia, why can’t yours?” The “My Son Got Lyme Disease. He’s Totally Fine” article is a failure in that it poses one person’s case, regardless of how factual, against hundreds of thousands.

Obviously, not all veterans get PTSD. However, we’ve forged an understand that those without are not the rule, but the exception. We wouldn’t tolerate those exceptions minimizing the rest. Why on earth would we behave differently with another disease? The amount of post-treatment Lyme sufferers each year is roughly 66,000. Does that seem like a small enough minority to minimize? And while we’re playing this frivolous game, what exactly do we suppose would be an appropriate amount? The reason as to why this particular disease has received such pushback is that in solving the riddle of Lyme, we would be solving other riddles along with it. In many ways, Lyme is the confluence of dysfunction. And those solutions would unabashedly undo countless cash-cow procedures for the healthcare industrial complex.

With industry parameters existing precisely within disease management, there is no incentive linked to causation. Lyme, in particular, exists within this cycle of suppression. While relating back the discrepancy of Lyme to cancer funding, I should ironically point out that the body of recent neuroimmune research has also shed some light on how cancer functions. While the complexities of these diseases are categorically different! neither are rooted in the cell. Contrarily, it is the microbiome, or our body of bacteria that determines the disease—not our genes. That same microbiome is what determines how a person with a neuroimmune disease either heals or diminishes. It’s what we do with that information that will broadly determine the same.

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