Archive for the ‘Lyme’ Category

A New Look At Chronic Lyme

https://experiencelife.lifetime.life/article/a-new-look-at-chronic-lyme/

image compilation lyme disease
(See link for article)
SUMMARY:
  • Weintrub highlights Jennifer Crystal’s story which mimics many other patients
  • Unfortunately, the article regurgitates the notion that only up to 20% experience chronic symptoms when the number is more like 60%
  • Weintraub explains that historically LLMD’s used high doses of antibiotics/antimalarials in harsh regimens lasting months or years but due to grueling side effects have adopted a multi-pronged approach that combines the judicious use of drugs which includes natural therapies
  • The article also erroneously blames rising temperatures for tick expansion when independent research has shown this to be false
  • The reason infections are reported in every state but Hawaii and Oklahoma has to do with migrating birds, reptiles, and mammals – including humans.
  • Weintraub explains the difference between the “two types” of Lyme disease: the acute, straight-forward cases, and those who remain sick after standard treatment, who are typically diagnosed late, and who have more than one infection – which research confirms who are as impaired as those with congestive heart failure and sicker than type 2 diabetics, and who have a striking degree of neuro-inflammation
  • Unfortunately, this second group which suffers greatly with chronic infections is still gas-lit by physicians who would rather label them with chronic fatigue or fibromyalgia and give them “scattershot” treatment
  • The article then goes into the big problem with faulty Lyme testing which can not register antibodies for 6 weeks, miss a significant subset of people who will always remain seronegative, that can not register certain strains of borrelia, or pick up the organism which lies dormant within tissues.
  • Despite a CDC disclaimer, many doctors still rely on the faulty CDC surveillance case definition which requires a positive test or the EM rash, when many will never test positive and many never get a rash.
  • I was thankful for Dr. Maloney who states an early course of antibiotics does NOT eliminate the risk for chronic Lyme
  • The article then delves into the fact many patients are infected with way more than just Lyme
  • Researchers that previously doubted that Bartonella could be spread by ticks are changing their position as there is now strong circumstantial evidence
  • The article points out that research has identified “persister cells” which are antibiotic tolerate and generally unresponsive to drugs as well as biofilms which work to protect infectious organisms, also making it hard to eliminate them
  • Stanford researchers have exposed persister forms (in vitro) to more than 4,000 drugs to observe effectiveness which has resulted in the use of disulfiram/Antabuse, an old drug for use for alcoholism but is potent against Lyme disease (but can cause severe side-effects in some)
  • Dr. Zhang has tested lyme-containing biofilms (in vitro) using antibiotics and herbs and has found that Japanese knotweed, black walnut, sweet wormwood, and Ghanaian quinine are all effective against Lyme disease.
  • Dr. Horowitz has found that a 2-month course of dapsone combined with biofilm buster rifampin has helped almost half of his chronically ill patients return to health. One patient accidentally took quadruple the dose for 4 days which put her into full remission – another example of how dosage matters.  A few other patients used this approach with similar success leading Horowitz away from long-term antibiotics to hitting hard for several days 3-4 times a year
  • Dr. Kinderlehrer reports that a formerly straightforward infection has morphed into body-wide instability: extreme sensitivities to foods, mold, chemicals, activation of mast cells, and dangerous allergic reactions, which can trigger brain fog, mood problems, pain syndromes, and profound fatigue.
  • A suppressed immune system can reactivate other infections like EBV
  • Integrative doctor Erica Lehman’s experience has taught her to recognize the different between those with neurologic disease versus illness that hits the gut, endodrine system, joint tissues, etc.
  • Many of the doctors who specialize in chronic Lyme do so because they have gone through it themselves

I highly, highly recommend Weintraub’s 2008 book “Cure Unknown: Inside the Lyme Epidemic.”  Although it was written 14 years ago, it remains one of the most thorough, accurate accounts of the Lyme debacle and clearly demonstrates that little has changed.

She also wrote about Dr. Masters the Rebel for Lyme Patients Who Took on the CDC Single-handedly  and broke it down into four parts in Psychology Today and which I summarize in the link. This history must not be lost. 

We must remember the fraud and corruption behind & in the world of Lyme/MSIDS.

Infectious Agents and Alzheimer’s Disease

https://www.imrpress.com/journal/JIN/21/2/10.31083/j.jin2102073

Infectious agents and Alzheimer’s disease

Show More
 
*Correspondence: dorszewskaj@yahoo.com; jolanta.dorszewska@ump.edu.pl (Jolanta Dorszewska)
Academic Editor: Rafael Franco
J. Integr. Neurosci. 2022, 21(2), 73; https://doi.org/10.31083/j.jin2102073
 
Submitted: 8 March 2021 | Revised: 25 March 2021 | Accepted: 29 April 2021 | Published: 28 March 2022
 
Abstract

Alzheimer’s disease (AD) is the leading cause of dementia worldwide. Individuals affected by the disease gradually lose their capacity for abstract thinking, understanding, communication and memory. As populations age, declining cognitive abilities will represent an increasing global health concern. While AD was first described over a century ago, its pathogenesis remains to be fully elucidated. It is believed that cognitive decline in AD is caused by a progressive loss of neurons and synapses that lead to reduced neural plasticity. AD is a multifactorial disease affected by genetic and environmental factors. The molecular hallmarks of AD include formation of extracellular amyloid (A) aggregates, neurofibrillary tangles of hyperphosphorylated tau protein, excessive oxidative damage, an imbalance of biothiols, dysregulated methylation, and a disproportionate inflammatory response.

Recent reports have shown that viruses (e.g., Herpes simplex type 1, 2, 6A/B; human cytomegalovirus, Epstein-Barr virus, hepatitis C virus, influenza virus, and severe acute respiratory syndrome coronavirus 2, SARS-CoV-2), bacteria (e.g., Treponema pallidum, Borrelia burgdorferi, Chlamydia pneumoniae, Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, Fusobacterium nucleatum, Aggregatibacter actinomycetemcmitans, Eikenella corrodens, Treponema denticola, and Helicobacter pylori), as well as eukaryotic unicellular parasites (e.g., Toxoplasma gondii) may factor into cognitive decline within the context of AD. Microorganisms may trigger pathological changes in the brain that resemble and/or induce accumulation of Apeptides and promote tau hyperphosphorylation. Further, the mere presence of infectious agents is suspected to induce both local and systemic inflammatory responses promoting cellular damage and neuronal loss.

Here we review the influence of infectious agents on the development of AD to inspire new research in dementia based on these pathogens.

_________________

For more:

Bb Persistence in Lyme and PTLDS

https://journals.asm.org/doi/10.1128/mbio.03440-21

ABSTRACT
The annual incidence of Lyme disease, caused by tick-transmitted Borreliella burgdorferi, is estimated to be at least 476,000 cases in the United States and many more worldwide. Ten to 20% of antimicrobial-treated Lyme disease patients display posttreatment Lyme disease syndrome (PTLDS), a clinical complication whose etiology and pathogenesis remain uncertain. Autoimmunity, cross-reactivity, molecular mimicry, coinfections, and borrelial tolerance to antimicrobials/persistence have been hypothesized and studied as potential causes of PTLDS. Studies of borrelial tolerance/persistence in vitro in response to antimicrobials and experimental studies in mice and nonhuman primates, taken together with clinical reports, have revealed that B. burgdorferi becomes tolerant to antimicrobials and may sometimes persist in animals and humans after the currently recommended antimicrobial treatment. Moreover, B. burgdorferi is pleomorphic and can generate viable-but-nonculturable bacteria, states also involved in antimicrobial tolerance. The multiple regulatory pathways and structural genes involved in mediating this tolerance to antimicrobials and environmental stressors by persistence might include the stringent (rel and dksA) and host adaptation (rpoS) responses, sugar metabolism (glpD), and polypeptide transporters (opp). Application of this recently reported knowledge to clinical studies can be expected to clarify the potential role of bacterial antibacterial tolerance/persistence in Lyme disease and PTLDS.
______________________
**Comment**
What’s truly sad is none of this is new.  This 2017 study talks about the stringent response, and this 2016 presentation by Dr. Zhang discusses the importance of persisters, or the dormant form borrelia takes when it feels threatened.  And this 2017 study also points out that Bb mutates (changes form) as previously described by Barbour and Hays way back in 1986.  I’m sure there are many more older studies presenting all of this.
Why is this simple fact still not believed and accepted?

What is not discussed in this article is the fact most Lyme/MSIDS patients are infected with multiple infections simultaneously, further complicating their cases, and requiring different medications.  This article shows that higher doses of antibiotics are required to eliminate a bacterial infection when other microbes are present, yet corrupt public health ‘authorities’ continue to push a faulty one pathogen, one drug paradigm based on faulty testing that misses 70-86% of cases!

What is also not discussed in this article is the larger subset of patients (30-40%) that are diagnosed and treated late – thereby not even making the PTLDS group, and therefore never studied in research.  This is a huge chunk of people are often seronegative in testing and don’t have the EM rash.  This is me, and everyone I work with.  There is ZERO data on us.  ZERO.

The PTLDS moniker is confusing at best and misleading at worse.  The whole ball of wax is based on faulty premises and faulty researchTime for a do-over.

For more:

Similarly to polarization on COVID treatment, it’s not a scientific debate. It’s a political one.

Non-Funded Study Shows LDN is a Broad-Spectrum Analgesic

https://www.futuremedicine.com/doi/10.2217/pmt-2021-0122

Low-dose naltrexone, an opioid-receptor antagonist, is a broad-spectrum analgesic: a retrospective cohort study

Samuel J Martin, Heath B McAnally, Paul Okediji and Moshe Rogosnitzky

Published Online:https://doi.org/10.2217/pmt-2021-0122

Aim: To evaluate the use of low-dose naltrexone (LDN) as a broad-spectrum analgesic. Methods: Retrospective cohort study from a single pain management practice using data from 2014 to 2020. Thirty-six patients using LDN for ≥2 months were matched to 42 controls. Pain scores were assessed at initial visit and at most recent/final documented visit using a 10-point scale. Results: Cases reported significantly greater pain reduction (-37.8%) than controls (-4.3%; p < 0.001). Whole sample multivariate modeling predicts 33% pain reduction with LDN, with number needed to treat (for 50% pain reduction) of 3.2. Patients with neuropathic pain appeared to benefit even more than those with ‘nociceptive’/inflammatory pain. Conclusion: LDN is effective in a variety of chronic pain states, likely mediated by TLR-4 antagonism.

Plain language summary

Naltrexone has historically been used to treat various substance use disorders, but recent discoveries have sparked interest in using low-dose naltrexone (LDN) to manage chronic pain. This study compared pain levels reported by patients before and after at least 2 months of LDN treatment to those reported by patients with the same painful diseases, who did not take LDN. Overall, patients who took LDN reported significantly more pain relief than patients who did not take LDN. How LDN alleviates pain seems complex, but apparently involves an anti-inflammatory effect on cells in the brain and spinal cord. LDN is extraordinarily safe, with no known risks (unlike most standard pain medications), and should be studied more in the treatment of chronic pain.

_________________

**Comment**

And this has been our personal findings as well.

I wish more offices did this internal research.  The data is all there begging to be collected, organized, and published.  This is a perfect example of how we can get answers without  corrupt, conflict riddled research institutions, government, and government collecting (bought out) researchers.

For more on this:  https://madisonarealymesupportgroup.com/2022/06/29/the-urgent-need-to-break-the-public-health-monopoly/

For more on LDN:

Case Report: Severe Back Pain in Child Caused by Lyme Disease

https://www.sciencedirect.com/science/article/abs/pii/S0735675722002297?via%3Dihub

Radiculoneuritis due to Lyme disease in a North American child

https://doi.org/10.1016/j.ajem.2022.03.063Get rights and content

Highlights

  • Peripheral nerve pain can be a presentation of early disseminated Lyme disease
  • Isolated neuroradiculits from Lyme is rare but important to recognize and treat
  • Patients with painful radiculitis should be tested for Borrelia infection

Abstract

Lyme disease is the most frequently reported vector-borne illness in the United States. It is caused by infection with Borrelia burgdorferi via the bite of an infected blacklegged tick (Ixodes spp.) Lyme disease has three stages: early localized, early disseminated, and late. Early disseminated Lyme disease may include neurologic manifestations such as cranial nerve palsy, meningitis, and radicular pain (also called radiculoneuritis). Isolated radiculoneuritis is a rare presentation of early disseminated Lyme disease and is likely underrecognized. We report a case of isolated Lyme radiculoneuritis in a child in Massachusetts characterized by fever and allodynia of the upper back that was treated in the emergency department. Laboratory investigation demonstrated elevated inflammatory markers and positive Lyme testing. Magnetic resonance imaging with gadolinium contrast revealed nerve root enhancement in C5-C6 and C6-C7. The symptoms resolved with oral doxycycline. Neuropathic pain should raise suspicion for neurologic manifestations of Lyme disease in North America even in the absence of meningitis and cranial nerve palsy. We report how timely recognition of this rare syndrome in North America is important and may prevent progression to late disease.

_________________

**Comment**

Again, this is not a “rare” syndrome, but is just “rarely” reported.  Big diff.  The authors even state that this syndrome is “likely underrecognized.”