January 2020 Support Group Meeting
January support group meeting
- January 4, 2020
- 2:30-4:40pm
- East Madison Police Station, 809 S Thompson Dr. Madison, WI 53718
Archive for the ‘Uncategorized’ Category
French and Australian Connections on Lyme, Inflammation and Cancer: Medicine Week 2019, Baden-Baden
https://www.linkedin.com/pulse/french-australian-connections-lyme-inflammation-cancer-yu-md/
French and Australian Connections on Lyme, Inflammation and Cancer: Medicine Week 2019, Baden-Baden
By Dr. Simon Yu, MD
Many of the international speakers covered cutting edge topics of Lyme, parasites, mold, inflammation and chronic infections, and different treatment modalities. Bacteriophage therapy and hemoadsorption therapy were new concepts for me take home to investigate further.
The first speaker, Louis Charles Teulieres, MD from France and England, spoke on bacteriophages in Lyme disease and diagnostics. Bacteriophages are a hot topic in the Lyme community as a means to detect and treat Lyme disease instead of heavily relying on antibiotics. Bacteriophages, a dominant viral life form existing as naked DNA with a protein coat, infect bacteria and “devour” them. They are everywhere: 50 million bacteriophage viruses are found in one milliliter of seawater.
Dr. Teulieres’ main focus: Is there a place for bacteriophages in diagnosis and treatment of Lyme disease? Can this provide an alternative treatment to antibiotics for Lyme disease, and thereby avoid post-antibiotic resistance? His lecture was highly technical, and it is still theoretical to use bacteriophages as a diagnostic tool, or to kill Borrelia Lyme bacteria with a Borrelia-specific virus. Phage Therapy is a novel idea to be tested soon. I have some skepticism about this approach which overlooks hidden dental spirochete and parasite infections, but stay tuned for more research.
Other topics included molds and fungus in chronic inflammation by Dr. Damien Downing of London, a lecture on biofilm by a doctor from Scandinavia, Lyme and co-infections by Prof. Dr. Kenny de Meirleir of Belgium, immune monitoring of hemoadsorption approaches as a new treatment option in antibiotic resistant chronic Lyme infection by Prof. Dr. Marion Schneider of Germany, and patient cases treated with hemoadsorption and extracorporeal hyperthermia by Dr. med. Rainer Mutschler of Germany.
Bacteriophage testing for Lyme disease claims it could detect direct evidence of Borrelia presence, is highly sensitive and specific, could distinguish Lyme from relapsing fever Borrelia strains, could distinguish active and non-active Borrelia presence, and could be developed to have the ability to distinguish different Borrelia sub-types.
On my last day at the Medicine Week, I met Australian researcher Jennie Burke, MSc from Sydney who gave a lecture on, Cancer and Infection. I did not attend her lecture but at the night meeting at the restaurant, she gave me her lecture slides to review.
To my delight, she presented on viral, bacterial and parasite infections as possible causative agents for the development of tumors or opportunistic inhabitants. Her slides covered controversial topics from Virginia Livingston Wheeler, Royal Rife and Dr. Milbank Johnson on BX virus and Rife frequency therapy, Dr. Laszlo K. Csatary on Newcastle virus, and included a list of bacteria and viruses associated with inducing cancer. Her list of cancer types and infections include Gallbladder carcinoma, mucosa-associated lymphoid tissue (MALT) lymphoma, and Ovarian, Colorectal, Lung, Pancreatic, Breast, Prostate, Anal and Oral cancer. She listed the names of the bacterial and viral infections and development of specific cancer types.
Her last slide was: Parasites in Cancer? The antiparasitic mebendazole shows survival benefit in preclinical models of glioblastoma multiforme (brain cancer). Supporting articles include: Mebendazole Monotherapy and Long Term Disease Control in Metastatic Adrenocortical Carcinoma, Mebendazole Inhibits Growth of Human Adrenocortical Carcinoma Cell Lines Implanted in Nude Mice, and Mebendazole Elicits a Potent Antitumor Effect on Human Cancer Cell Lines Both in Vitro and in Vivo.
The development of cancer, infections and environmental toxins are not a new concept, but have been largely sidelined (seduced) by the genetic mutation theory of cancer. It is time to renew infections and environmental toxins, including EMF, as the driving forces of inflammation and immune dysregulation. The end results are the imbalance of Th1, Th2, Th17 and regulatory T immune cells that can trigger autoimmune reactions or development of cancer.
I have written many articles on parasites, fungal infections and cancer connections, presenting cancer as an infectious disease as if cancer is a metabolic parasite. Dr. Tim Guilford and I published, Antiparasitic and Antifungal Medications for Targeting Cancer Cells Literature Review and Case Studies, in PubMed with extensive references. If you are suffering from cancer, get a copy and share with your oncologist. He or she may embrace and try parasite and fungal medications or scorn you and laugh at you. You have nothing to lose by trying.
Listening to French, Australian and other international speakers at Medicine Week was worthwhile, and I learn from going to Baden-Baden every year. Meeting good friends and enjoying good wine, beer, food and Roman Baths give even more incentives to attend, and expand my horizons.
Dr. Simon Yu, M.D. is a Board Certified Internist. He practices Internal Medicine with an emphasis on Integrative Medicine to use the best each has to offer. For more articles and information about integrative medicine, patient success stories, and Dr. Yu’s new book, AcciDental Blow Up in Medicine: Battle Plan for Your Life, visit his website at www.preventionandhealing.com or call Prevention and Healing, Inc., 314-432-7802. You can also attend a free monthly presentation and discussion by on Integrative Medicine at his office on the second Tuesday each month at 6:30 pm. Call to verify the date. Seating is limited, arrive early.
Happy Thanksgiving!
Thankfulness is an act of the will. It is a conscious decision to be thankful despite circumstances.
Dear Lyme Warrior….Help!
https://globallymealliance.org/dear-lyme-warriorhelp-9/
by Jennifer Crystal
Every few months, Jennifer Crystal devotes a column to answering your questions. Here she answers some questions she recently received. Do you have a question for Jennifer? If so, email her at lymewarriorjennifercrystal@gmail.com.
Did your pain move sometimes? My worst pain is near some scar tissue.
Yes! One of the defining features of Lyme pain is that it’s migratory. This distinguishes it from, say, the pain of Rheumatoid Arthritis (RA), which is more symmetrical (both knees instead of just one), and which doesn’t tend to move around like Lyme pain. While RA affects most of the joints, Lyme can affect one, two, or many.
I felt pain mostly in my forearms and shins, but also sometimes in my back, neck, and head. Sometimes my fingers ached so much I couldn’t type, and other days they felt okay. Now that I’m in remission, I know when I’m having a Lyme flare-up because my forearms and shins start to ache. When I’m overtired or I’ve over-exerted myself, I always get a headache on the left side of my head. (This is due to babesia, which eats oxygen in the red blood cells. When I over-exert myself, I don’t get enough oxygen to that side of my brain, causing inflammation and subsequent pain).
Moreover, Lyme loves to hide in scar tissue, so it makes perfect sense that’s where you’re having the worst pain. I had the anterior cruciate ligament of my left knee repaired before I was aware I had Lyme, and it took much longer for that knee to heal than it should have; this is likely because there was Lyme bacteria in the scar tissue. I’ve also had multiple eye surgeries, and my doctor suspects scar tissue over my left eye is why my headaches often start there.
Is the word “cured” ever used with tick-borne illness?
Yes and no. It depends which illness you have, how long you’ve had it, how quickly you got treatment, and how well you’ve responded to treatment. If Lyme is caught early and treated adequately with two to four weeks of antibiotics—and if it is not complicated by co-infections—it can conceivably be cured. However, even in those cases, some 20% of patients still experience ongoing symptoms called Post Treatment Lyme Disease Syndrome (PTLDS), and they can require additional treatment.
My own Lyme is in remission, not cured because I went eight years undiagnosed. By then the bacteria had crossed the blood-brain barrier. Once it’s in the central nervous system, it becomes very difficult to fully eradicate it. I’m probably 80% restored to full health, a percentage that has continually improved (with brief periods of flare-up).
There are others who have had PTLDS who claim to have been cured, but some of these have subsequently relapsed. It really depends on each individual case.
I was originally diagnosed with the co-infection Ehrlichia, and that is now considered to be cured. I no longer test positive for it or show specific symptoms. The co-infection that still gives me the most trouble is babesia. I was not surprised to hear doctors at this year’s ILADS conference say that babesia can be treated to an extent—symptoms can be alleviated and held at bay for a while—but that it often rebounds. Currently, babesia has no cure.
But don’t despair. Researchers are getting closer to using that coveted word “cure” every day. See my “Highlights From ILADS 2019” post that provides information on new drugs like Dapsone and Disulfiram, the latter of which has some patients, as Dr. Kenneth Liegner stated, “enjoying enduring remission,” that is, feeling well for six months or longer. It’s too early to use the word “cure” decisively.
Do you think I’m going down the right path, being treated for tick-borne disease?
I know it can be confusing when so many doctors give you different diagnoses and treatment options. You don’t know who or what to believe, and that is scary. Even two different LLMDs might give you two different protocols (and that’s because they each have a personal opinion on what might work best for you, since there is no single set protocol for treating tick-borne disease).
If you trust the LLMD who has made a clinical diagnosis of Lyme with or without co-infections, and your symptoms corroborate those infections, and/or your blood work confirms those infections, then yes, I absolutely think you are going down the right path. Remember that having Lyme is not a choice.
Once you begin treatment, you’ll know for sure if you’re on the right path. If you do have Lyme, you’ll likely have a Herxheimer reaction (when the antibiotics kill off the Lyme bacteria at a rate faster than your body can eliminate them, making you feel worse before you feel better). That could be a good indication that you should stay the course.
The real question is, do you feel like you are going down the right path? No one knows your body better than you do. You know you are sick. You know what your symptoms are. You know they are not all in your head. If you’ve seen an LLMD and feel in your gut that the doctor is right for you, then trust that feeling, and don’t worry what anyone else says.
Opinions expressed by contributors are their own.
Jennifer Crystal is a writer and educator in Boston. Her memoir One Tick Stopped the Clock is forthcoming. Contact her at lymewarriorjennifercrystal@gmail.com.
Inflammatory Processes Drive Progression of Alzheimer’s and Other Brain Diseases
https://neurosciencenews.com/alzheimers-inflammation-15235/
Inflammatory processes drive progression of Alzheimer’s and other brain diseases
NEUROSCIENCE NEWSInflammation drives the progression of neurodegenerative brain diseases and plays a major role in the accumulation of tau proteins within neurons. An international research team led by the German Center for Neurodegenerative Diseases (DZNE) and the University of Bonn comes to this conclusion in the journal Nature. The findings are based on the analyses of human brain tissue and further lab studies. In the particular case of Alzheimer’s the results reveal a hitherto unknown connection between Amyloid Beta and tau pathology. Furthermore, the results indicate that inflammatory processes represent a potential target for future therapies.
Tau proteins usually stabilize a neuron’s skeleton. However, in Alzheimer’s disease, frontotemporal dementia (FTD), and other “tauopathies” these proteins are chemically altered, they detach from the cytoskeleton and stick together. As a consequence, the cell’s mechanical stability is compromised to such an extent that it dies off. In essence, “tau pathology” gives neurons the deathblow. The current study led by Prof. Michael Heneka, director of the Department of Neurodegenerative Diseases and Gerontopsychiatry at the University of Bonn and a senior researcher at the DZNE, provides new insights into why tau proteins are transformed. As it turns out, inflammatory processes triggered by the brain’s immune system are a driving force.
A Molecular Switch
A particular protein complex, the “NLRP3 inflammasome”, plays a central role for these processes, the researchers report in Nature. Heneka and colleagues already studied this macromolecule, which is located inside the brain’s immune cells, in previous studies. It is a molecular switch that can trigger the release of inflammatory substances. For the current study, the researchers examined tissue samples from the brains of deceased FTD patients, cultured brain cells, and mice that exhibited hallmarks of Alzheimer’s and FTD.
“Our results indicate that the inflammasome and the inflammatory reactions it triggers, play an important role in the emergence of tau pathology”, Heneka said. In particular, the researchers discovered that the inflammasome influences enzymes that induce a “hyperphosphorylation” of tau proteins. This chemical change ultimately causes them to separate from the scaffold of neurons and clump together. “It appears that inflammatory processes mediated by the inflammasome are of central importance for most, if not all, neurodegenerative diseases with tau pathology.”
A Link between Amyloid Beta and Tau
This especially applies to Alzheimer’s disease. Here another molecule comes into play: “amyloid beta” (Amyloid Beta). In Alzheimer’s, this protein also accumulates in the brain. In contrast to tau proteins, this does not happen within the neurons but between them. In addition, deposition of Amyloid Beta starts in early phases of the disease, while aggregation of tau proteins occurs later.
In previous studies, Heneka and colleagues were able to show that the inflammasome can promote the aggregation of Amyloid Beta. Here is where the connection to the recent findings comes in. “Our results support the amyloid cascade hypothesis for the development of Alzheimer’s. According to this hypothesis, deposits of Amyloid Beta ultimately lead to the development of tau pathology and thus to cell death,” said Heneka. “Our current study shows that the inflammasome is the decisive and hitherto missing link in this chain of events, because it bridges the development from Amyloid Beta pathology to tau pathology. It passes the baton, so to speak.” Thus, deposits of Amyloid Beta activate the inflammasome. As a result, formation of further deposits of Amyloid Beta is promoted. On the other hand, chemical changes occur to the tau proteins resulting into their aggregation.
A Possible Starting Point for Therapies
“Inflammatory processes promote the development of Amyloid Beta pathology, and as we have now been able to show, of tau pathology as well. Thus, the inflammasome plays a key role in Alzheimer’s and other brain diseases,” said Heneka, who is involved in the Bonn-based “ImmunoSensation” cluster of excellence and who also teaches at the University of Massachusetts Medical School. With these findings, the neuroscientist sees opportunities for new treatment methods. “The idea of influencing tau pathology is obvious. Future drugs could tackle exactly this aspect by modulating the immune response. With the development of tau pathology, mental abilities decline more and more. Therefore, if tau pathology could be contained, this would be an important step towards a better therapy.”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Source:
DZNE
Media Contacts:
Marcus Neitzert – DZNE
Image Source:
The image is in the public domain.
Original Research: Closed access
“NLRP3 inflammasome activation drives tau pathology”. Christina Ising et al.
Nature doi:10.1038/s41586-019-1769-z.
Abstract
NLRP3 inflammasome activation drives tau pathology
Alzheimer’s disease is characterized by the accumulation of amyloid-beta in plaques, aggregation of hyperphosphorylated tau in neurofibrillary tangles and neuroinflammation, together resulting in neurodegeneration and cognitive decline1. The NLRP3 inflammasome assembles inside of microglia on activation, leading to increased cleavage and activity of caspase-1 and downstream interleukin-1β release2. Although the NLRP3 inflammasome has been shown to be essential for the development and progression of amyloid-beta pathology in mice3, the precise effect on tau pathology remains unknown. Here we show that loss of NLRP3 inflammasome function reduced tau hyperphosphorylation and aggregation by regulating tau kinases and phosphatases. Tau activated the NLRP3 inflammasome and intracerebral injection of fibrillar amyloid-beta-containing brain homogenates induced tau pathology in an NLRP3-dependent manner. These data identify an important role of microglia and NLRP3 inflammasome activation in the pathogenesis of tauopathies and support the amyloid-cascade hypothesis in Alzheimer’s disease, demonstrating that neurofibrillary tangles develop downstream of amyloid-beta-induced microglial activation.
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https://madisonarealymesupportgroup.com/2018/09/11/its-time-to-find-the-alzheimers-germ/
For more on the potential connection between Alzheimer’s and tick borne illness:
https://madisonarealymesupportgroup.com/2016/06/09/alzheimers-byproduct-of-infection/ (Link to Kris Kristofferson’s case. Lyme treatment turned the Alzheimer’s completely around)
https://madisonarealymesupportgroup.com/2017/01/18/a-bug-for-alzheimers/
https://madisonarealymesupportgroup.com/2018/07/28/herpes-viruses-implicated-in-alzheimers-disease/
https://madisonarealymesupportgroup.com/2017/10/14/lost-link-als-lyme/
https://madisonarealymesupportgroup.com/2017/06/10/the-coming-pandemic-of-lyme-dementia/
Madison Area Lyme Support Group 