The 2016 ILADS Annual event "Lyme Disease - An Evolving Paradigm for Chronic Illness" was held in Philadelphia on November 3-6, 2016.  This was my 11th ILADS annual event.  When I first went in 2006, it was rather small - maybe 100 people or so.  This year, I was told there were over 800 people and that some were turned away as they could not accommodate more.  

While I am excited to see the growth, we probably need 80,000 doctors at these events to handle the size of the problem that exists with Lyme disease.  Nonetheless, it was another superb event all around, and I am grateful for ILADS and the important work they do to advocate on behalf of those struggling with Lyme and to move the treatment of Lyme disease forward.   

Disclaimer: Nothing in this text is intended to serve as medical advice. All medical decisions should be made only with the guidance of your own personal licensed medical authority.

Disclaimer: This information was taken as notes during the conference and may not represent the exact statements of the speakers. Errors and/or omissions may be present.

Note: As this information may be updated as any errors are found, I kindly request that you link to this single source of information rather than copying the content below. If any updates or corrections are made, this will help to ensure that anyone reading this is getting the most current and accurate information. 

Brian J. Balin PhD spoke on "The Role of Infection as a Trigger for Alzheimer's Disease Neurodegeneration" and shared:

  • Genetics are not the key issue.
  • 2.5-5% of the issue is genetic. 95-98% of the issue is not due to genetics.
  • APOE4 is a genetic risk factor for Alzheimer's.
  • Chlamydia pneumoniae has an association with APOE4 when expressed in the body.
  • Sense of smell is impacted very early.
  • Neurofibrillary tangles and beta amyloid are involved.
  • Tangles can be seen in chronic encephalitis or CTE (chronic traumatic encephalopathy).
  • Many blame amyloid for the disease; it is not specific to genetic mutations but related to damage to the nervous system.
  • Damage to the nervous system can be related to infections.
  • Amyloid is not specific to Alzheimer's and can be seen in other conditions such as HIV.
  • He presented a correlation between various diseases and their associated infectious etiologies:
    • Cervical, head, and neck cancer: HPV
    • Hodgkin's disease, Burkitt's Lymphoma: EBV
    • Liver cancer and chronic hepatitis: Hep B and Hep C
    • Lymphoma: Kaposi Herpes Virus 8
    • Gastric lymphoma, carcinoma, and peptic ulcers: H. Pylori
    • Neurosyphilis: Treponema pallidum
    • Lyme disease: Borrelia burgdorferi
    • Rheumatic fever, post-strep Glomerulonephritis: Group A Strep
    • Reactive Arthritis: Chlamydia trachomatis
    • Guillain-Barre Syndrome: Campylobacter jejuni
    • Adult T-cell Leukemia: HTLV-1
  • To ignore that Lyme disease can be chronic is ignorant and foolish.
  • Genes are only part of the story; we need to understand the epigenetic influences which are tremendous.
  • Proposed infections that could be involved in Alzheimer's include: Chlamydia pneumoniae, Borrelia, HSV-1, H. Pylori, Candida.
  • HSV stays in the trigeminal ganglia; there is a pathway to olfaction (sense of smell). Herpes encephalitis impacts the temporal lobe. There is a pathway into the brain.
  • H. Pylori is higher in Parkinson's and a potential factor in Alzheimer's.
  • Candida can be found in the brains of Alzheimer's.
  • Tryptophan breakdown leads to quinolinic acid which can damage brain cells. Chlamydia pneumonia requires tryptophan.
  • APOE4 brains have higher Chlamydia pneumoniae and HSV-1.
  • Chlamydia pneumoniae may be involved in insulin resistance and diabetes.
  • Borrelia burgdorferi is believed to be involved in Alzheimer's.
  • 30-40% of the time amyloid is found in HIV that leads to dementia.
  • Aging leads to immunocompromise; oxidative stress damages neurons.
  • In mice, introducing infections such as Chlamydia pneumoniae intranasally leads to finding the infection in the brain and amyloid.
  • Beta-amyloid has anti-infective properties. It may be the response to infection.
  • Neuroinflammation is the key to damage. 

Ying Zhang MD, PhD spoke on "Targeting Borrelia Persisters for More Effective Treatment of Lyme Disease" and shared:

  • Their work so far is in vitro (out of the body).
  • There are the spirochete, round body, and micro-colony forms of Borrelia.
  • With Lyme, you get something unexpected at every turn.
  • Current antibiotics do not work well for late-stage Lyme.
  • The causes of Post Treatment Lyme Disease Syndrome (PTLDS) are unclear: host response to antigenic debris, autoimmune, damage to tissues from infection, co-infections, persisters not killed by current Lyme antibiotics.
  • There is no FDA treatment for PTLDS.
  • Persisters have been demonstrated in mice, dogs, and monkeys after antibiotic treatment.
  • The microbes become viable, but not culturable.
  • Current antibiotics are good for Borrelia that are growing, but not for persisters. Doxycycline and Amoxicillin are good only for "growing" Borrelia.
  • The top drugs for stationary Borrelia (persisters) include: Daptomycin, Clofazimine, Cefoperazone, and Carbomycin.
  • Tetracycline is better than Doxycycline.
  • Cefuoxime is slightly better than Ceftriaxone.
  • The best combination was Daptomycin, Doxycycline, and Ceftin; with no pulsing of these medications.
  • Artemisinin has been one of the options that has shown some promise.
  • Daptomycin is available only as an IV.  An oral regimen is needed that works equally well.
  • They need to move from in vitro to in vivo and start clinical trials.
  • If we can find a therapy to cure PTLDS, that will be the response to the critics.
  • Persister drugs are needed.

Theoharis Theoharides, MD, PhD spoke on "Mast Cell Activation" and shared:

  • Mast cells are critical in terms of inflammation; including inflammation of the brain.
  • Mast cells are important in Lyme in terms of the symptoms that are produced.
  • Mast cells are important in the neurological symptoms of Lyme.
  • Mast cells are involved in many diseases, including Lyme.
  • Does Borrelia create the symptoms or does it activate something else that creates the symptoms?
  • Mast cells release histamine and other substances; can release every single interleukin.
  • They are important for setting up inflammatory reactions.
  • Mast cells increase blood-brain barrier permeability which leads to inflammation of the brain.
  • They can impact the hypothalamus and HPAT axis.
  • MCAS (Mast Cell Activation Syndrome) now has its own insurance code.
  • Mast cells can respond to substance P and not necessarily an allergen. This leads to more substance P and a viscous cycle ensues.
  • Borrelia could trigger mast cells.
  • You have to stop the overdrive.
  • Flavanoids may block inflammatory reactions; luteolin being a key one.
  • Luteolin reduces oxidative stress, inhibits inflammation, inhibits MCAS, inhibits microglial activation, inhibits neurotoxicity, is a weak metal chelator, increases memory, prevents autism in mice, improves attention and sociability in ADD.
  • Another flavanoid Tetramethoxyluteolin has 4 methyl groups and is a better inhibitor of mast cells. It is better absorbed, decreased metabolism, methyl donor, no phenol intolerances. There is a topical preparation at http://www.gentlederm.com.
  • Erythema migrans is mast cells.
  • http://www.mastcellmaster.com 

Robert Rowen, MD spoke on "Ozone Therapy - Its Use in Infectious Diseases: From Lyme to Ebola and Back" and shared:

  • Ozonides are not free radicals but are messengers.
  • Ozone reduces inflammation; the expression of COX-2 goes down.
  • Under a microscope, one sees rouleaux before and dispersion after ozone therapy.
  • Viruses have two key structures that lead to cell entry; they have to enter the cell.
  • One study showed that 95% of Polio virus was eliminated with ozone. Oxidized CMV was unable to enter cells.
  • Human cells can repair from exposure to ozone; bacteria and viruses cannot.
  • They had resolution of Ebola in Sierra Leone with ozone therapy. If you can oxidize the virus, you can fix the patient; even with Ebola. 5 of 5 recoveries in those treated with ozone in a condition with a 60% mortality rate.
  • Ozone shoots a hole in a bacterial cell like a bullet and it dies instantly. Acts like a bullet through the heart.
  • Ozone is much more effective at killing organisms than bleach; 1000 times.
  • Antibodies generate ozone to attack invaders.
  • Ozone stimulates cytokines and interferons.
  • Ozone increases anti-cancer and anti-allergy enzymes.
  • SOD stimulates telomerase; ozone increases SOD.
  • IV gas can be hard on the veins.
  • There is no such thing as autoimmune disease; it is due to stealth pathogens.
  • With a 10 pass ozone session, each pass is 10-15 minutes; can do 10 passes in as little as 40 minutes.
  • Brain fog clears in a single session in many people.
  • Dr. Robins uses ozone, probiotics, and Vitamin C.
  • Dr. Rowen finds 9 of 10 patients do very well with ozone.
  • They were doing a single pass ozone twice weekly for 3-6 weeks and now do a 10-pass once per week.
  • Why is there no Herx after ozone? There can be occasionally, but ozone is oxidizing the toxins as well which turns them into carbon dioxide and water.
  • There is no problem with gut flora; even with rectal ozone.
  • Two people out of tens of thousands may have an allergy to ozone.
  • Oregano, Carnivora, and Berberine may be helpful for patients; bases on muscle testing. Spleen is always an issue for those patients.
  • Inflammation is the result of lower oxygen and lower circulation.

I had an opportunity to talk with Steve Fry, MD and catch up on some of his latest work and learned:

  • People that have oestoarthritis seem to often have a fungus called Saccharomyces cerevisiae. Given potential relation, he does not use Saccharomyces boulardii as a beneficial yeast in patients.
  • What was Protomyxzoa rheumatica and thought to be a protozoa is now believed to be Funneliformis mosseae which is more of a fungal organism.
  • In some patients blood, they observe Hydrurus foetidus, which is a type of algae.

Kristen Reynolds, MD spoke on "Small Intestinal Bacterial Overgrowth (SIBO): An Integrative Approach" and shared:

  • Her daughter had GI issue and abdominal pain after antibiotics for a Strep infection.
  • There are 10 times as many bacterial cells as human cells.
  • 200 times as much DNA in our microbiome than our own DNA.
  • 70-80% of the immune system and 95% of our serotonin is in the gut.
  • SIBO is when bacteria from the large intestine moves back into the small intestine where there should be minimal.
  • Anaerobes such as E. Coli, Enterococcus, Klebsiella, and Proteus may be present.
  • Methanogens such as Methanobrevibacter smithii may be present and can cause constipation.
  • SIBO is present in 78% of patients with IBS.
  • Rifaximin is an RX medication often used for SIBO and is more effective with three times daily dosing as compared to twice daily.
  • SIBO is present in 67% of patients with IBS.
  • The small intestine is normally protected from bacterial overgrowth via gastric acid, the intestinal mucosa, and motility.
  • Gastric acid may be compromised as proton-pump inhibitors have been found in water.
  • The intestinal mucosa includes the gut immune system, enzymes and bile acids, and commensal bacteria.
  • Motility is the gross anatomic structures such as the ileocecal valve, adhesions, strictures, diverticuli.
  • Migrating motor complex cleans out the small intestines between meals. Can be impacted by infections, Clostridia, Parasites, Lyme, hypothyroidism, Scleroderma, Diabetes, Ehlers-Danlos, opiates, antibiotics, and stress.
  • Campylobacter, E. Coli, Shigella, Salmonella and others may create Cytolethal Distending Toxin (CDT) that the body creates an antibody to and this inhibits the MMC and slows motility.
  • Starches and certain fibers feed the bacteria and lead to a fermentation process. This results in pain and bloating.
  • There is blood testing available for anti-CDT and anti-viniculin which may be helpful in SIBO cases. They look at an autoimmune component with SIBO.
  • Symptoms of SIBO include: bloating, nausea, vomiting, weight loss, depression, acne, fatigue, joint pain, and malnutrition.
  • Syndromes associated with SIBO include Fibromyalgia, Chronic Fatigue Syndrome, restless legs, rosacea, IBD, interstitial cystitis, arthralgia, chronic prostatitis, pelvic pain syndrome, Parkinson's, and fatigue.
  • Diagnosis is done using glucose or lactulose (fermentable carbs) and then measuring either hydrogen or methane.
  • If hydrogen >= 20ppm or there is a rise of 12ppm or methane is >= 3ppm with constipation or >= 12ppm, this is considered positive.
  • Lactulose testing is better as it gets to the end of the small intestine where glucose does not.
  • Hydrogen sulfide may be part of a clinical diagnosis - may look for a flat-line breath test or if the patient has rotten egg smelling gas.
  • A 36 hour restrictive diet with no breads, fibers, potatoes, and starches is implemented and a 12 hour water fast is done before the testing.
  • Treatment is with RX options or herbs, healing using the 5Rs, and prevention with dietary changes and supporting motility.
  • May be a killing phase, a 3 month prevention phase, and then a healing phase.
  • Antimicrobials, diet, supplements, manual therapy may all be used.
  • RX treatment is with Rifaximin; Neomycin is added when methane is present.
  • Rifaximin is used three times daily for two weeks.
  • Rifaximin may be used with guar gum at 5 grams daily; this is a prebiotic.
  • Herbs may include neem, peppermint, berberine, wormwood, oregano, allicin.
  • There is a commercial product with Quebracho, Conker Tree, and Peppermint that may be used. At ILADS, they cannot say the name of commercial products, but this appears to be Atrantil. Enteric coated peppermint oil may be used. Homeopathics may be helpful.
  • With neem, allicilin may be added if the patient was methane positive.
  • There is an Elemental Diet which helps to feed the person and starve the bacteria. There is a meal replacement product which tastes bad but works. Information on the homemade elemental diet can be found at http://www.siboinfo.com.
  • Prokinetic medications support motility and may include low dose erythromycin, LDN, and Prucalapride. Herbal options may include ginger, 5-HTP, and a combination of 9 herbs from Germany. Again, this was not mentioned by name but appears to be Iberogast.
  • Diets may be used to prevent a recurrence - SCD, GAPS, FODMAP, SIBO diets, and others.
  • FODMAPs are Fermentable Oligosaccharides, Disaccharides, Monosaccharides and Polyols and are short-chain carbs that are not well-absorbed in the small intestine and are easily fermentable. A diet low in FODMAPs is often used.
  • Recurrence rate is about 44%.
  • Prevention includes stopping acid blockers, SIBO Diet, hydrochloric acid, correcting the ileocecal valve, resolving sympathetic dominance.
  • Ozone can be helpful for SIBO.
  • It is not clear how well probiotics work.

Kent Holtorf, MD spoke on "Innovative "Alternative" Therapies for Chronic Lyme Disease" and shared:

  • There is no autoimmunity; it is all chronic infections.
  • LDN can help to address the balance of Th1 and Th2 in the immune system.
  • Low dose heparin can be helpful in some that fail conventional treatment.
  • Doctors don't look at underlying causes. If you find Lyme (a cause), then you no longer have "Chronic Fatigue Syndrome".
  • A small amount of an organism can stimulate huge amounts of cytokines and toxins.
  • Most people that have Lyme are asymptomatic.
  • Antibiotics are unlikely to fix Lyme disease.
  • There is a Th1 to Th2 shift in the body. Th1 addresses inside the cells; Th2 outside. Thus when Th1 is low and Th2 is high, we cannot fight intracellular infections.
  • Is Babesia a cause of hypertension and Diabetes? Treating it often leads to blood pressure and Diabetes improvements.
  • Coagulation issues are common with Babesia. Oxygen getting to the cells goes from 2 seconds to 15 minutes.
  • Adrenal problems are often not the adrenals themselves, but more of a brain problem with the hypothalamus and pituitary.
  • Babesia is one of the biggest problems; it is hard to detect and treat.
  • Borrelia may need 12-24 hours to double. Strep and staph need 20 minutes. It is 35-75x slower at replicating than other bacteria. This means you would need antibiotics for 1.5 to 3 years to have the same curative potential.
  • Immune modulators include LDI, peptides (thymosin alpha-1/Thymosin B4/BPC 157), Heparin, LDN, IVIG, ozone, UVBI, transfer factors, mushrooms, Isoprinosine, bee venom, allergy elimination, and more.
  • LDN reduces inflammation, resets Th1/Th2 balance (shifts Th2 to Th1), promotes healing, reduces thyroid resistance where thyroid does not go into the cells, promotes weight loss.
  • National Academy of Hypothyroidism can be found at https://www.nahypothyroidism.org/
  • LDN reduces Fibromyalgia symptoms by 28.8%. In study with Dr. Horowitz and 1000 MSIDS patients, 75% had less fatigue and pain.
  • TA1 thymic peptide may stimulate the immune system, reduce proinflammatory cytokines, improve immune balance, and shift Th2 to Th1. Results in improved healing, defense to infection, microcirculation, stress tolerance, viral inhibition, cancer defense, antioxidant, and reduced inflammation.
  • BPC-157 is one of the best options for leaky gut. Wound healing including tendon/ligaments/muscles.
  • Follistatin helps with weight issues and is a myostatin inhibitor.
  • VEGF may go up with Bartonella, but Lyme can also suppress it.
  • ECP goes up with Babesia; may need to treat and then test again to see it rising.
  • 41kda on Western Blot - have yet to see one on Quest test that did not end up having Lyme; especially when it is IgM.
  • 60-90% of Chronic Fatigue Syndrome, Fibromyalgia, Gulf-War Syndrome, and Lyme have an abnormal activation of the coagulation system (hypercoagulation).
  • Pulse oximeter testing may show 99 or 100 but if you blow out all your air, hold your breath, it should go down, but it doesn't in these conditions.
  • CVID, common variable immune deficiency, goes away after you treat the infections.

Kenneth Bock, MD spoke on "Autoimmune Encephalopathy: The Emerging Role of Neuroinflammation in Neuropsychiatric Disorders" and shared:

  • You may see a disorder that appears to be entirely psychiatric and it isn't psychiatric.
  • The nervous system and immune system are complex and amazing that they work as well as they do.
  • There is a bi-directional relationship between the nervous system and the immune system.
  • The gut-brain axis is bi-directional.
  • The importance of an in-tact mucosal barrier to prevent the movement of larger particles beyond the gut is key.
  • 75% of the immune system is under the GI mucosa.
  • Immune tolerance is centered around the gut.
  • We don't want the immune system reacting to everything.  
  • Host bacteria vitally regulate microglia maturation and function; comes back to microbiome.
  • Triad of immune, gut, and brain constantly talking to one another.
  • Gliadin, casein, and other sensitive foods can lead to immune dysregulation and increased intestinal permeability.
  • Blood brain barrier can be disrupted by heavy metals.
  • Copper, manganese, and iron are important, but manganese can be toxic. Manganese can be a neurodevelopmental toxicant.
  • PCBs disrupt the integrity of the blood brain barrier.
  • Environmental toxicants contribute to the disruption of these key relationships in the body.
  • Pollution can increase inflammatory mediators, increase oxidative stress, neuroinflammation, and neurodegeneration.
  • Ecephalitis is a severe inflammatory disorder of the brain with many causes and a complex differential diagnosis. It can be autoimmune or infectious.
  • Psychiatric issues can be autoimmune or infectious.
  • Most autoimmune disease, if not all, has an underlying infection.
  • PANDAS may be helped with antibiotics, IVIG, and plasmapheresis.
  • It is not just strep and thus now is called PANS as it can be initiated by viruses, Mycoplasma, Lyme, Bartonella and others. 

Kristine Gedroic, MD spoke on "Regulation of the Microbiome: Mold, Phospholipids and Their Effect on Vagal Bi-Directional Signaling" and shared:

  • Patients challenge us to rise to new levels of understanding.
  • She uses very little antibiotics and can get most people through chronic Lyme in about six months.
  • Her interest is in the microbiome.
  • Geography, age, diet, breast fed vs. formula, vertical transmission, and medications all impact the microbiome.
  • Biofilms are microcolonies of sessile microorganisms attached to the mucosa or growing in the mucous layers in healthy and diseased individuals.
  • The gut biofilm = the microbiome.
  • There is an upper and lower microbiome in the gut in terms of the layers where microbes may reside. Bacteria are in the upper microbiome. These are responsive to antibiotics, ozone, and other therapies. The lower layer is fungus, parasites, and heavy metals.
  • The pathology of the patient could be in the upper or lower microbiome. Most patients need support in both.  
  • Phosphatidylcholine (PC) is a polyunsaturated fatty acid with a positive head and a negative tail.
  • Active colitis responds to treatment with PC.
  • PC is anti-inflammatory and downregulates TNF-alpha.
  • If you are not producing enough bile salts, patients lose their trigger to secrete PC. They use bile salts with all of their patients.
  • Dendritic cells turn into regulatory or stimulatory / pro-inflammatory dendritic cells.
  • In Naviaux's work with cell-danger response (CDR), heavy metals, BPA, plasticizers are electrophiles.
  • His most recent paper "Metabolic Features of Chronic Fatigue Syndrome" discusses a hypometabolic state like hibernation. CDR is inflammatory. Patients may be living at a lower metabolic rate to preserve over a period of time. 
  • Fumonisins from Fusarium can be found on corn. Low levels of molds come from grains such as corn and oats. In CFS, almost all have an element of mycotoxicosis. There is a big problem with molds out there that we all have to think about.
  • Patients that have mold issues may not be able to deal with folic acid in any form.
  • Treatment works to restore phospholipid balance, regulate lipid rafts, and reduce pathogenic biofilms.
  • PC comprises 90% of the intestinal mucosa and is vital for the microbiome.
  • IV Butyrate has become a top therapy. It may be reducing pathology associated with fungi and viruses.
  • Patients should not take lots of antioxidants. We need oxidation of very long chain fats.
  • Molds have profound effects on mitochondria, increase anxiety, and lead to mental symptoms.
  • A balanced microbiome is key to regulating the immune system. An imbalanced microbiome leads to dysregulation of the Vitamin D Receptor.
  • We need to keep our cell membranes healthy with phospholipids and oils.
  • Diet is important and impacts the microbiome.

Ritchie Shoemaker, MD spoke on "Advances in Diagnosis and Treatment of the Chronic Inflammatory Aspects of Post Lyme Syndrome: From CNS Volumetrics to Transcriptomics" and shared:

  • We need to look at inflammation and gene regulation.
  • Regulation of regulation of gene transcription is the future.
  • Mold is NOT Candida; that is a yeast.
  • There is not much difference in CIRS symptoms between post Lyme and mold.
  • If you see 10 Lyme patients a day, 7 or 8 of them have mold as a problem. Not paying attention to it is failing your duty.
  • Mycotoxins are only 1% of the problem with exposure to water-damaged buildings.
  • Horizontal gene transfer and MARCoNS resistance has been confined to antifungal users. He suggested that we should stop the use of antifungals.
  • Differential gene activation persists until there is definitive regulation of the regulatory genes.
  • There are 30 different entities that lead to illness via inflammation resulting from water-damaged buildings.
  • Actinomyces is giant and a new lab is coming online soon in San Antonio.
  • Post Lyme Syndrome is a CIRS; do the labs.
  • There is a connection between leaky gut and MSH.
  • MMP9 is a Th1 response.
  • C4a is huge.
  • Antibiotics feed biofilm formers and lead to more bacterial resistance factors; MARCoNS.
  • Pulmonary hypertension is seen in 40-50% of CIRS patients.
  • Low VO2 Max is observed in 80% of CIRS patients.
  • The ERMI has been superseded by the HERTSMI-2.
  • Symptoms can be analyzed with cluster analysis. If there are 8 or more of 13 clusters, this points to a CIRS patient.
  • In terms of HLA, 21% have predisposition to post Lyme; 24% to water-damaged buildings.
  • MARCoNS makes a palytoxin.
  • Cholestyramine and Welchol are used as binders. Nothing else works; he has tried them all.
  • VIP is a fabulous tool.
  • Testing that thinks that mycotoxins are the problem is ignoring the data.
  • NeuroQuant has been avialable since 2006. It is an MRI of the brain and reliably separates Lyme from mold.
  • There are patterns with NeuroQuant that are unique to mold, Lyme, PTSD, etc.
  • Atrophy can be reversed with VIP.
  • The right side thalamus is huge in Lyme patients.
  • Gene activity is plastic and correctable.
  • NeuroQuant and transcriptomics will supplant guessing.

There was a panel discussion where I learned:

  • MARCoNS are slow growers.
  • For PANDAS, Dr. Bock may use Augmentin, Ceftin, Omnicef, and Zithromax. Doxycycline and Minocycline are good for Mycoplasma but not Strep. Considers antivirals and probiotics as well.
  • Dr. Gedroic mentioned that she has seen nasal ozone helpful in PANDAS.
  • Dr. Bock mentioned the use of sinus nebulizers with Amphotericin-B and similar solutions.
  • Dr. Andrew Heyman mentioned that low cortisol may be a compensatory change or an immune threat may be present. Administering cortisol could be a disserivce to patients.
  • Dr. Gedroic mentioned that oral PC helps to recover mitochondria. The IVs affect the outer cell membrane and clears epigenetic effects of outer membrane assaults; also modulate the biofilm of the microbiome.
  • Dr. Shoemaker mentioned that the NeuroQuant pattern in PTSD is a small amygdala, small hippocampus, and small thalamus.
  • CortechsLabs.com has a locator for places that can do the NeuroQuant.
  • Dr. Ehrlich did not see spirochetes in his brain research of patients with Alzheimers. 

Konstance K. Knox, PhD spoke on "Zika, West Nile, and Powassan: New Concerns for Old Viruses" and shared:

  • Once an insect is infected with an arbovirus, it remains infected for life.
  • The principle vector of arbovirus is the mosquito and the tick.
  • Humans are dead-end hosts for the virus from the mosquito; once we are infected it is not transmitted from us back to another mosquito.
  • Arboviruses are a broad group of viruses that contain three families including Flaviviridae, Togaviridae, and Bunyaviridae. Some of the better known Flaviviridae include Dengue (mosquito), Tick-Borne Encephalitis (ticks), Powassan (ticks), St. Louis Encephalitis, Zika (mosquito), Yellow Fever (mosquito), Hepatitis C, West Nile (mosquito). Totaviridae include Chikungunya (mosquito), Eastern/Western/Ross River Encephalitis, Rubella. Bunyaviridae include Hantaan, Heartland (ticks), California Encephalitis, Rift Valley/Crimean-Congo Hemorrhagic Fevers, LaCross Encephalitis.
  • Mosquitoes kill more humans than humans kill humans.
  • The Aedes mosquito prefers to dine on humans.
  • 200 Arboviruses cause human disease with the majority being in the Flavivirus family.
  • Powassan needs to be considered more in tick-borne illnesses in the US.
  • Flaviruses have 10 genes where Herpes viruses have 100-200 genes.
  • There are neurotropic (West Nile, Zika) and hemorrhagic (Yellow Fever, Dengue) Flaviviruses. Neurotropic have more headaches; like neurons. Hemorrhagic lead to anorexia and nausea and like the liver.
  • West Nile comes from the Culex mosquito which prefers to dine on birds; not humans.
  • 80% have few or no symptoms with West Nile. Has a 2-15 day incubation. 20% get fever. Headaches, muscle pain, nausea, vomiting, loss of appetite, rash. Less than 1% are severe with neurological symptoms,. encephalitis, meningitis, poliomyelitis. Those at risk are the young, elderly, those with immune dysfunction, and those on immunosuppressive drugs. There is a 10.5% rate of birth defects when West Nile is contracted during pregnancy.
  • Zika is due to the global spread of the Aedes aegypti mosquito that loves humans. It was introduced into South America in 2014 from sporting events. Thousands of children have been born with the devastating effects of Zika. It is relatively mild in adults. We do not have the mosquito in the US that carries Zika; we have the Culex which were still negative for Zika after feeding on infected mice.
  • Tick Borne Flaviviruses - Tick Borne Encephalitis Virus (TBEV) is a serious problem in Europe. In the US, we have the Powassan virus. Deer Tick Virus and Powassan are lineages of TBEV. May be transmitted by unpasteurized milk. Takes only 15 minutes to acquire from a tick. Powassan and Deer Tick Virus do not commonly lead to neuro-invasive disease, but when they do, 10% of neuro-invasive cases are fatal.
  • In 106 atients with suspected acute tick-borne disease and recent tick exposure, 10.4% were positive for Powassan in one study.
  • 37-40% of ticks in Northern Wisconsin were positive for Borrelia with 4-5% positive for Powassan.
  • In another study, 11 Powassan positive samples had a co-infection rate of 81.8% woth Borrelia. Of 55 Lyme positive samples, 16.4% had co-infecton with Powassan. This is very close to the 20% of Lyme treated patients that suffer Post Treatment Lyme Disease Syndrome.

Rick Sponaugle, MD spoke on "PET Brain Imaging in Lyme Disease and Mold Toxic Patients: Correlation of Neurological Symptoms with Specific Brain Regions" and shared:

  • His daughter had every tick-borne infection imaginable and was bedridden after 2 years of conventional treatment.
  • Trichothecene is a lipophilic toxin that destroys cell membranes. It also downregulates dopamine.
  • Trichothecene is the culprit in the majority of Lyme disease patients he sees.
  • Trichothecene shuts down CD4/CD8 ratios if the patient is in the wrong building and has the wrong genetics.
  • He uses Great Plains testing for benzene metabolites to see if industrial toxicity is a factor. Benzene is a common denominator.
  • 90% of his patients are severe and 83% are women.
  • The majority of patients have immune dysregulation much worse than HIV patients.
  • Lipophilic toxins go right through the skin; bathing may be a source of toxins.
  • A lot of Houston patients are the result of air from oil refineries; it is worse than LA or NYC.
  • Sushi is a cause oa parasitic worms. Don't let dogs kiss you; they pass worms.
  • Uses glutathione, alpha-lipoic acid, phosphatidylcholine.
  • He discussed a case study where they used IV Amino Acids, detoxification, Patricia Kane's protocol, Vancomycin, Rocephin, Amphotericin, parasite treatment, cryptolepis, and more.
  • For Protomyxzoa, they may add Cryptolepis or Mepron.
  • He closely follows brain scans with treatment.
  • An ERMI is only good if it is positive; it means nothing if it is negative.
  • Stachybotrys is a silent killer that does not smell.

Richard Horowitz, MD spoke on "Update in the Management of Lyme and Associated Diseases" and shared:

  • They have been exploring treatment with Mycobacterium and persister drugs.
  • Climate change impacts diseases showing up in ticks, fleas, and mosquitoes.
  • Lyme is not the only persistent infection.
  • Bartonella is a persister.
  • Coinfections are the rule; up to 8 different types of organisms identified with 36 different pathogens total in the same tick with most being intracellular.
  • 15 different new species of Borrelia identified in the past 20 years; essentially 1 per year. Borrelia miyamotoi and Borrelia mayonii among the more recent.
  • Not all Borrelia can be picked up with ELISA and Western Blot testing.
  • Babesia has been found in up to 40% of ticks in some studies. 
  • Parasites supress immunity and shift us towards autoimmune reactions. This makes it more difficult to get rid of other parasites.
  • Filarial worms were found in MS and Alzheimer's by Alan Macdonald.
  • Co-infected patients are much sicker; Babesia makes people much sicker.
  • Bartonella, Mycoplasma, and Chlamydia pneumoniae increase neurological symptoms.
  • Borrelia, Bartonella, Babesia, and Mycoplasma may all persist.
  • Borrelia goes into the eyes, ligaments, and joints where the blood supply is not very good; this allows them to persist.
  • Multiple intracellular infections drive the inflammatory response.
  • Immune evasion occurs via pathogens changing outer surface proteins.
  • Organisms in biofilm communities may exchange genes.
  • Biofilm microcolonies are very difficult to eradicate. Antibodies cannot find the infections, persisters are shielded from the immune system, and antibiotics cannot get to the microbes.
  • Porphyromonas gingivalis is found in Alzheimer's plaques.
  • Pesticides have been found in the brains of those with Alzheimer's. Brain cells with pesticides form amyloid.
  • Inflammation and environmental toxins form amyloid.
  • Flagyl and Tinidazole help in treating persistent Lyme, but they are not enough.
  • You have to treat the cell wall, cystic, and intracellular forms as as well as biofilms.
  • Serrapeptase, Stevia, and Lauricidin may be useful for biofilms.
  • Biofilms and persisters are likely the explanation for relapse.
  • Persisters exist in TB and syphilis. The idea that Lyme does this is newer.
  • Recently published paper "The Use of Dapsone as a Novel “Persister” Drug in the Treatment of Chronic Lyme Disease/Post Treatment Lyme Disease Syndrome"
  • Dapsone may be used with Rifampin and Clofazimine which are leprosy persister drugs.
  • Rifampin alone has an effect against biofilms per research done by Dr. Eva Sapi.
  • Bactrim is effective for Lyme persisters; helps with Lyme, Babesia, and Bartonella, but now also with persisters.
  • Dapsone may be used for Toxoplasmosis and Malaria prophylaxis. Used for autoimmune disease.
  • He had 400 people on Dapsone at his office; a large number of people that failed every prior treatment are improving.
  • Dapsone helps resistant Babesia.
  • The side effects include Herxheimer reactions, anemia, rashes, and methemoglobinemia.
  • Herxes are severe. LDN may help; glutathione helps as one of the options to shutdown NFkb.
  • Infections and toxins create oxidative stress and NFkb; have to shut it down. Alkalize, drainage remedies, Sarsaparilla, slow ramp. Higher doses are more effective.
  • There can be a 3g drop in hemoglobin with Dapsone.
  • Dapsone interferes with folic acid. May need Leucovorin or methylfolate.
  • Do not put iron deficient women on Dapsone.
  • Cannot use Dapsone if G6PD deficient.
  • Can have rashes. Dapsone is a sulfa drug; though most tolerate. May need H1/H2 blockers like Zyrtec/Zantac.
  • Methemoglobinemia - 6-10% may feel fatigue, shortness of breath, headaches. > 10% may have blue hands and lips. May need folic acid and glutathione. May need to increase antioxidants; curcumin, green tea, sulphoraphane, ALA, NAC, liposomal glutathione.
  • One should not use ozone while on Dapsone.
  • Consider Dapsone when there is persistent Lyme, multiple intracellular infections, parasitic infections, and when the severity of the symptoms warrant aggressive IV therapy. Cannot have history of sulfa senstivity, be anemic, or have G6PD deficiency.
  • For Babesia, the patient should have failed every therapy you have given them.
  • Babesia herbals include Cryptolepis, Artemisinin, and Neem.
  • Doxycycline, Rifampin, and Dapsone lowered biofilms by 50% in 3 days in Dr. Eva Sapi's research.
  • 2 of 3 patients that failed traditional antibiotic treatment are responding to Dapsone.

 
Disclaimer: While I attempted to accurately represent the statements of the various speakers, it is possible that the above contains errors or inaccuracies. If you have any corrections to the content listed above, please Contact Me.   


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  BetterHealthGuy.com is intended to share my personal experience in recovering from my own chronic illness.  Information presented is based on my journey working with my doctors and other practitioners as well as things I have learned from conferences and other helpful resources.  As always, any medical decisions should be made only with the guidance of your own personal medical authority.  Everyone is unique and what may be right for me may not be right for others.