Archive for the ‘Treatment’ Category

20% off Hyperbaric Treatment Packages – Fox Valley Wellness Center

HBOT – 20% Savings For the Month of March

March is Traumatic Brain Injury (TBI) Awareness month. Fox Valley Wellness Center Midwest Hyperbarics is currently offering 20% off all HBOT treatment packages.
The Brain Injury Association of America (BIAA) conducts an awareness campaign each year in March to educate about the prevalence of brain injury and the needs of people with brain injuries and their families.

Each year an estimated 2.4 million children and adults in the United States sustain a traumatic brain injury (TBI), and another 795,000 individuals sustain an acquired brain injury (ABI) from non-traumatic causes. TBI’s can affect the functionality of the brain and can have a significant impact on individuals and their families.

How does hyperbaric oxygen help with a traumatic brain injury (TBI)?

In TBI patients, some of the injured brain tissues may be “dormant” and non-functioning. HBOT can stimulate these “dormant” tissues and return them to more normal function.

Hyperbaric oxygen therapy, used in conjunction with other therapies, ensures the best recovery possible for traumatic brain injury.
Fox Valley Wellness Center Midwest Hyperbarics is offering a 20% discount for all HBOT treatment packages for the month of March.

Learn More About HBOT Benefits


Peptide Therapy With Dr. Kent Holtorf, MD

 Approx. 1 hour 18 Min.

Peptide Therapy With Dr. Kent Holtorf, MD

In this episode, you will learn about the use of peptide therapy in Lyme disease and related complex, chronic illnesses.

About My Guest: My guest for this episode is Dr. Kent Holtorf. Kent Holtorf, MD is the medical director of the Holtorf Medical Group. He is founder and director of the non-profit National Academy of Hypothyroidism (NAH), which is dedicated to dissemination of new information to doctors and patients on the diagnosis and treatment of hypothyroidism. He has personally trained numerous physicians across the country in the use of bioidentical hormones, hypothyroidism, complex endocrine dysfunction, and innovative treatments of Chronic Fatigue Syndrome, Fibromyalgia, and chronic infectious diseases, including Lyme disease. He is a fellowship lecturer for the American Board of Anti-aging Medicine, the Endocrinology Expert for AOL Health, and is a guest editor and peer-reviewer for a number of medical journals. Dr. Holtorf has published a number of peer-reviewed endocrine reviews, including on the safety and efficacy of bioidentical hormones, inaccuracies of standard thyroid testing, testosterone replacement for men and women, the diagnosis and treatment of growth hormone deficiency, and on the diagnosis and treatment of adrenal dysfunction in Chronic Fatigue Syndrome and Fibromyalgia. He has helped to demonstrate that much of the long-held dogma in endocrinology is inaccurate. He is a contributing author to Denis Wilson’s Evidenced-Based Approach to Restoring Thyroid Health. He has been a featured guest on CNBC, ABC News, CNN, EXTRA TV, Discovery Health, The Learning Channel, The Today Show, Dr. Dean Edell, Glenn Beck, Nancy Grace, Sean Hannity, and more and quoted in numerous print media including the Wall Street Journal, Los Angeles Times, US New and World Report, San Francisco Chronicle, WebMD, Elle, Better Homes and Garden, US Weekly, Forbes, Cosmopolitan, and Self magazine among many others.

Key Takeaways: 

  • What are peptides?
  • How are peptides created? 
  • What conditions might peptides be helpful for? 
  • What are the key contributors to aging? 
  • How are thymosins used to modulate the immune system? 
  • How is Th1/Th2 dominance measured? 
  • What is the role of LL37 in treating chronic infections?
  • What is the connection between hypercoagulation and mast cell activation?
  • How might BPC-157 be helpful in chronic illness?
  • What is the role of Epithalon in anti-aging and regenerative strategies?
  • How might peptides be helpful in conditions such as autism, Parkinson’s, and ALS?
  • How well-tolerated are peptides by sensitive patient populations?

Connect With My Guest:


For more:  (Go here for entire article)

Summary of BPC-157

Primary Information, Benefits, Effects, and Important Facts

BPC-157 is a peptide chain consisting of 15 amino acids. It is considered synthetic because this particular sequence does not exist in nature. It is derived from a protective protein found in the stomach.

Researchers have conducted numerous rodent studies on BPC-157 that show it has protective effects extending beyond the stomach and intestinal tract. BPC-157 has been shown to benefit ulcers in the stomach, intestinal damage such as fistulas and inflammatory disorders, bone and joint healing and growth rates, and organ damage. It also has some influences on the brain. Researchers have observed marked protective effects when BPC-157 is administered to rats alongside a research toxin or damaging surgical procedure.

More research is needed to clarify whether BPC-157 has multiple mechanisms of action, but current research suggests BPC-157 influences several growth factors usually involved in angiogenesis (the production of blood vessels) and other factors involved in regeneration following damage.

BPC-157 shows promise, but human studies are needed to demonstrate that these benefits extend beyond research animals.

The majority of studies on BPC-157 are done on rats given injections of the supplement. While BPC-157 is a stable peptide, peptides are a group of compounds that are normally poorly absorbed after oral supplementation, so researchers use injections in rodent studies instead. Furthermore, there is no human evidence for BPC-157 and the majority of the research has been conducted by a single research group. Due to its synthetic nature, there may be legal issues associated with the sale of this supplement in certain regions and it may be banned by some sport organizations.

4.3. Neuroprotection

BPC-157 appears to have protective effects on brain tissue when administered to rats (either in drinking water or injections) alongside the toxin cuprizone by reducing the amount of damaged cells in numerous brain regions, including the hippocampus.[15] Cuprizone[15] is a toxin used to mimic the damages seen in multiple sclerosis[16] and potentially schizophrenia.[17]

5.1. Collagen and Joints

Researchers have observed benefits when putting BPC-157 on a sponge during surgery, where it appeared to improve the rate of collagen reformation, initially outperforming platelet-growth factor after four days but eventually being equipotent after eight days[4]. Benefits have been seen in rats given intraperitoneal injections after an Achilles heel injury, where the rate of injury healing was visually confirmed with smaller cut size and depth.[22]

6.2. Intestines

Most BPC-157 studies on intestinal damage use rats that undergo surgical-induced damage for experimental purposes. BPC-157 appears to have very potent protective effects in rats by mitigating damage to the tissue and structural abnormalities caused by the damage.

It is possible, based on limited evidence, that BPC-157 may be orally active in the alimentary canal (the pathway between the mouth and anus).

7.1. Parkinson’s

One study in rats using the toxin MPTP (which induces damage similar to what is seen in Parkinson’s Disease in rodents), administration of BPC-157 intraperitoneally appeared to mitigate some of the damage caused by MPTP.[36]

7.2. Multiple Sclerosis

In rodents given cuprizone (to induce damage similar to what is seen in multiple sclerosis[16]) those given BPC-157 alongside the cuprizone (0.16 ng/mL or 0.16 μg/mL in drinking water over four days or 10 ng/kg or 10 μg/kg intragastrically on the final day) seemed to exhibit significantly less brain damage and clinical abnormalities from the cuprizone than did control rats not given BPC-157.[15]


“BPC-157,”, published on 14 April 2017, last updated on 14 June 2018,



Patient Lawsuit Against IDSA & Insurers Moves Forward in Texas

Patient lawsuit against IDSA and insurers moves forward in Texas

By Mary Beth Pfeiffer

A federal lawsuit that may just validate the pain of thousands of Lyme disease patients – and the flaws in prevailing tests and treatments — is moving ahead in a Texas courthouse, despite attempts to kill it.

The lawsuit’s progress is a big development in the decades-old struggle of patients whose post-treatment conditions – involving myriad neurological, cognitive, musculoskeletal, and cardiac symptoms — have long been misdiagnosedand minimized. Patients have hence had to seek out-of-pocket treatment from physicians who risk their licenses providing it.

The suit, Torrey v. Infectious Diseases Society of America et al, aims to change that, and, make no mistake, is a serious challenge to the Lyme status quo (see myarticle from 2017).

In the crosshairs of the case are six major architects and proponents of the guidelinesthat have dogmatically ruled Lyme disease care for two decades: Raymond J. Dattwyler, John J. Halperin, Eugene Shapiro, Leonard Sigal, Allen Steere, and Gary P. Wormser. (A seventh, Robert Nadelman, died in 2018.)

Beyond that A-list of Lyme actors, the lawsuit also accuses eight insurers of conspiring with the IDSA and the Lyme architects to advance treatment protocols that limited care options to the 25 named plaintiffs, two deceased, for whom the protocols did not work.

The companies are Blue Cross And Blue Shield Association, Anthem, Inc., Blue Cross And Blue Shield Of Texas, Aetna Inc., Cigna Corporation, Kaiser Permanente, Inc., United Healthcare Services, Inc., and Unitedhealth Group Incorporated.

Here’s what will happen shortly

A hearing on a second motion to dismiss the case will be held on March 11, at 2 p.m., at the U.S. Federal Courthouse, 500 North State Line Avenue, Texarkana, Texas. [Note: this story was edited on 2/27 to reflect the hearing’s recent date change.]

The suit, whose lead plaintiff is Texas resident Lisa Torrey, already survived one motion to dismiss. (See below.)

I’d encourage people who are invested in the outcome of the case to attend. Lyme patients have been portrayed, wrongly, as deluded, unpleasant and aggressive for a long time. Show them who you really are: Informed, concerned, intensely interested, and respectful of the court’s crucial role. Now’s the time.

Here’s what’s happened so far

The judge in part granted and in part denied a previous motion to dismiss the case.

In favor of the IDSA-insurers side, the judge agreed that the lawsuit did not sufficiently describe the alleged fraud that it maintains was committed by the defendants under theRacketeer Influenced and Corrupt Organizations Act (RICO).

The court, however, ruled the patients’ side could redraft the complaint under RICO. A request for an extension to do that will be among the issues considered at the March 12 hearing.

But the motion to dismiss was largely decided in favor of patients, including on the crucial assertion that the defendants violated anti-trust statutes under the Sherman Act.

As the judge put it, summarizing the case,

“Defendants [as alleged] engaged in a conspiracy to unreasonably restrain trade in the relevant market—the Lyme disease treatment market—by paying large consulting fees to the IDSA Panelists to pass the IDSA guidelines which deny the existence of chronic Lyme disease and establish the standard that all Lyme disease is cured with short-term antibiotics.”

Insurers then were able to deny claims, and doctors who treated outside the guidelines were marginalized in what became a monopolistic marketplace, the suit maintains.

In upholding the suit’s anti-trust assertion, the judge wrote:

“Plaintiffs have sufficiently alleged that, in the absence of the IDSA, there would be competition among doctors for the treatment of chronic Lyme disease and competition among insurance carriers for coverage for such treatments. Similarly, Plaintiffs have alleged that Defendants’ adoption of the IDSA guidelines and standard of care for the testing, diagnosis and treatment of Lyme disease has harmed patients and doctors nationwide. … The Court finds a nationwide geographic market has been properly alleged.”

All of this, of course, must be proven at trial.

There’s more

Beyond this, the judge granted the plaintiffs’ request for discovery, but so far it has been limited only to documents from four years before the lawsuit’s filing. The judge wrote, in reference to whether the court has jurisdiction to order discovery:

“The Court finds that Plaintiffs have pointed to enough evidence preliminarily establishing personal jurisdiction over the IDSA Panelists to warrant jurisdictional discovery. Specifically, Plaintiffs point to the declarations provided by each of the IDSA Panelists in which each doctor attests to having visited Texas for professional purposes during the relevant time periods. …Moreover, Plaintiffs have established that the IDSA Panelists’ research and professional activities focus primarily on Lyme disease.”

In a filing Friday, the Torrey lawyers called the four-year timeframe “arbitrary.”

Here’s what is pending

Among the issues that the hearing will consider is whether, essentially, to put chronic Lyme disease on trial. A motion by Anthem, Inc., the IDSA, and what is termed the “Doctor Defendants” asks the court to have all plaintiffs submit to independent medical examinations, or IMEs, by a Texarkana-based infectious diseases physician.

Their motion, which has been challenged by the plaintiffs’ attorneys, states:

“The Lyme Claimants allege that they have suffered debilitating injuries because they have been denied appropriate medical treatments for so-called ‘chronic Lyme disease,’ allegedly due to an unlawful conspiracy among the Defendants to monopolize the treatment of Lyme disease.Nearly all of the Lyme Claimants allege that they still suffer from the disease today and many claim that they are currently disabled or otherwise unable to work due to their illness. … (W)hether they currently or have ever suffered from Lyme disease, the severity of their symptoms, and whether those symptoms are attributable to Lyme disease or some other cause, are at the heart of this case and were put into controversy by the Lyme Claimants themselves. Well-prepared, peer-reviewed studies have established that as many as 88% of patients who have been told they have ‘chronic Lyme disease’ either do not have – or, in many cases, never have had – Lyme disease in any form.”

To support their assertion, the IDSA defendants cite an articleon chronic Lyme disease by Duke University physician of pediatric medicine, Paul Lantos, which cites much of the Doctor Defendants’ research.

And finally…

The hearing will also take up another request related to whether the patients are truly ill and with what.

The IDSA is seeking emails written by them – including any in which the words Lyme appear coupled with antibiotic, literate, chronic, claim*, cover* and den* (presumably meant to refer to claimed/claimant, coverage, denied or denial). Emails with the initials IDSA are also sought.

In its motion, the IDSA asserts:

“Defendants’ email requests seek information relevant to the claims and defenses in this action. In the Complaint, Plaintiffs assert that they ‘suffer debilitating injuries’ and that such injuries impact them on a daily basis, including cognitive deficits, fatigue, and memory loss, resulting in a multitude of alleged harms, including the loss of careers, homes, and the ability to function. … Plaintiffs’ communications about their condition go to the heart of corroborating or refuting their allegations about their conditions and the harms that they allege they have suffered.”

The calendar for the lawsuit lists June 24, 2019 as the start of a jury trial in Torrey v. IDSA et al. Stay tuned.

For more:  

Anti-viral Therapy in Alzheimer’s- Clinical Trial

Anti-viral Therapy in Alzheimer’s Disease

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Know the risks and potential benefits of clinical studies and talk to your health care provider before participating. Read our disclaimer for details. Identifier: NCT03282916

Recruitment Status : Recruiting

First Posted : September 14, 2017
Last Update Posted : January 25, 2019
National Institutes of Health (NIH)
National Institute on Aging (NIA)
Information provided by (Responsible Party):
Davangere P. Devanand, New York State Psychiatric Institute
Study Description
Brief Summary:
Anti-viral therapy in Alzheimer’s disease will investigate the efficacy of treating patients with mild Alzheimer’s disease with the U.S.A marketed generic anti-viral drug Valtrex (valacyclovir, 500mg oral tablet). Valacyclovir at 2 g to 4 g per day, repurposed to treat Alzheimer’s disease, will be compared to matching placebo in the treatment of 130 mild AD patients (65 valacyclovir, 65 placebo) who test positive for herpes simplex virus-1 (HSV1) or HSV2. The study will be a randomized, double-blind, 18-month Phase II proof of concept trial.
Condition or disease Intervention/treatment Phase
Alzheimer DiseaseHerpes Simplex 1Herpes Simplex 2 Drug: ValacyclovirDrug: Placebo Phase 2
Detailed Description:

Many viruses are latent for decades before being reactivated in the brain by stress, immune compromise, or other factors. After the initial oral infection, herpes simplex virus-1 (HSV1) becomes latent in the trigeminal ganglion and can later enter the brain via retrograde axonal transport, often targeting the temporal lobes.

HSV1 can also enter the brain via olfactory neurons directly. HSV1 (oral herpes) and HSV2 (genital herpes) are known to trigger amyloid aggregation and their DNA is commonly found in amyloid plaques. Anti-HSV drugs reduce Aβ and p-tau accumulation in brains of infected mice. HSV1 reactivation is associated with tau hyperphosphorylation in mice and may play a role in tau propagation across neurons. In humans, recurrent reactivation with newly produced HSV1 particles, ‘drop by drop,’ may produce neuronal damage and eventually lead to neurodegeneration and Alzheimer’s disease (AD) pathology, partly due to effects on amyloid and tau. Clinical studies show cognitive impairment in HSV seropositive patients in different patient groups and in healthy adults, and antiviral treatments show robust efficacy against peripheral HSV infection. The study team will conduct the first-ever clinical trial to directly address the long-standing viral etiology hypothesis of AD which posits that viruses, particularly the very common HSV1 and HSV2, may be etiologic or contribute to the pathology of AD.

In patients with mild AD who test positive for serum antibodies to HSV1 or HSV2, the generic antiviral drug valacyclovir, repurposed as an anti-AD drug, will be compared at oral doses of 2 to 4 grams per day to matching placebo in the treatment of 130 patients (65 valacyclovir, 65 placebo) in a randomized, double-blind, 78-week Phase II proof of concept trial. Patients treated with valacyclovir are hypothesized to show smaller decline in cognition and functioning compared to placebo, and, using 18F-Florbetapir PET imaging, to show less amyloid accumulation than placebo over the 78-week trial. Through the use of tau PET imaging with the tracer 18F-MK-6240 at baseline and 78 weeks, patients treated with valacyclovir are hypothesized to show smaller increases in 18F-MK-6240 binding than patients treated with placebo from baseline to 78 weeks. Apolipoprotein E genotype at baseline, as well as changes in cortical thinning on structural MRI, olfactory identification deficits, and antiviral antibody titers from baseline to 78 weeks, will be evaluated in exploratory analyses. In patients who agree to lumbar puncture, plasma and CSF acyclovir will be assayed to establish the degree of CNS penetration of valacyclovir in mild AD, and the investigators will obtain CSF Aβ42, tau, p-tau for subset exploratory analyses with changes in outcome measures.

If this trial is successful, the investigators will apply for funding to conduct a larger, multicenter, Phase III study using a study design that will be informed by the results of this Phase II trial. This innovative Phase II proof of concept trial clearly has exceptionally high reward potential for the treatment of AD.

Study Design
Study Type : Interventional  (Clinical Trial)
Estimated Enrollment : 130 participants
Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: Triple (Participant, Care Provider, Investigator)
Primary Purpose: Treatment
Official Title: Anti-viral Therapy in Alzheimer’s Disease
Actual Study Start Date : February 12, 2018
Estimated Primary Completion Date : August 2022
Estimated Study Completion Date : August 2022
Remember, Alzheimer’s is a label, nothing more.  They are still trying to figure out what causes it.
Dr. Klinghardt has gone on record stating that he’s not had one MS, ALS, or Parkinson’s patient NOT test positive for Lyme:

Medical Stalemate: What Causes Continuing Symptoms After Lyme Treatment?

Medical stalemate: what causes continuing symptoms after Lyme treatment?

19 February, 2019

by Holly Ahern, MS, MT (ASCP)

In 2018, I served on a Subcommittee of the Department of Health and Human Services (HHS) Tick Borne Disease Working Group. This was a Federal Advisory Committee, comprised of federal and public members with “diverse disciplines and views pertaining to tick-borne diseases.”

The group was tasked with conducting a review of ongoing research and resulting advances, federal epidemiological and research efforts, and identifying research gaps.

The HHS TBDWG report included recommendations that were delivered to Congress in December. It is a comprehensive review of the state of the science and medicine of tick-borne diseases, and Lyme disease was a major focus.

What follows is a brief overview of what we know, and what we don’t know, about chronic symptoms associated with Lyme disease.

Not just a single clinical entity

There is a need to broaden the scope of the medical definition of “Lyme disease” because it is not a single clinical entity. Only one subgroup of patients, those with “early Lyme disease,” has been clinically characterized.

This subgroup consists of people for whom an active infection with the bacterium Borrelia burgdorferi has been confirmed.  This is based on either a known tick-bite with development of a skin rash called an erythema migrans (EM, which looks like a bull’s-eye but has a clearing in the center of the rash), and/or positive blood test within one month of a known tick bite.

Standard treatment for this form of Lyme disease is a few weeks of an oral antibiotic. If symptoms persist, some patients may be treated with an additional one month of an IV antibiotic.

At least two other subgroups of this disease are recognized but have not yet been fully characterized and defined.

PTLDS is only one subgroup

Although used very broadly to characterize Lyme disease patients with chronic disease symptoms, the term “Post Treatment Lyme Disease Syndrome,” or PTLDS, specifies ONLY a subgroup of Lyme disease patients meeting the following criteria:

(1) Diagnosed early in the infection;

(2) Treated with the standard antibiotic treatment for Lyme disease; and

(3) Remained symptomatic or developed new symptoms such as headaches, fatigue, joint pain or other neurological symptoms impacting quality of life, that persist or increase in severity for at least 6 months post-treatment.

At present, there are no diagnostic tests for this clinical subgroup, and there are no recommended treatments beyond the standard antibiotic treatment.

The CDC has reported that approximately 10–20% of Lyme disease patients develop PTLDS. Meaning they end up with a chronic illness as a result of Lyme disease.

PTLDS specifies only those diagnosed and treated early

It is important to note that PTLDS specifies ONLY those Lyme disease patients who were diagnosed and treated in the first few weeks of infection. It should never be used to characterize patients who were not diagnosed or treated for months to years after the original infection. Yet it often is.

Disabling chronic disease symptoms with Lyme disease are also known to occur when people are not diagnosed early and do not receive prompt antibiotic treatment. These chronically ill patients DO NOT MEET the criteria for PTLDS and therefore represent a third subgroup of patients.

Because there has been little research done to investigate the clinical characteristics of this particular subgroup, there is no scientific way (at least at the moment) to determine the size of this group.

Best estimates based on existing research indicates that this group comprises 30-40% of Lyme disease patients.

There are no diagnostic tests or recommended treatments for this subgroup of patients.

Diagnosis is not straightforward

The diagnosis of Lyme disease is not straightforward, because the “accepted” medical definition of Lyme disease (at present) is restrictive and applies only to early stages of infection. Not every infected person experiences symptoms within the first few days or weeks. After several weeks, the clinical picture of Lyme disease changes.

Lyme disease is more likely to be MISSED as a diagnosis the longer the infection has been present. The more established the infection, the less likely that it will respond to the standard antibiotic treatment.

Why so often misdiagnosed?

Here are some reasons why a physician might not be able to promptly diagnose a case of Lyme disease and antibiotic treatment is delayed:

(1) a classic bull’s-eye rash is not observed – this applies to 90% of Lyme disease cases;

(2) there was no bull’s-eye rash to observe – which according to surveys of Lyme disease patients, occurs 50% of the time;

(3) an antibody-based laboratory test came back falsely negative – which applies to 50% of all Lyme disease cases;

(4) in the absence of a rash or positive blood test, non-specific disease symptoms overlapping those of autoimmune or psychiatric conditions exclude Lyme disease from the differential diagnosis;

(5) involvement of more than one microbe clouds the clinical features of the disease;

(6) the patient’s tick bite was treated with a prophylactic single dose of an antibiotic, which does not prevent infection but does increase the likelihood of falsely negative blood tests.

10-20% of Lyme disease patients who are promptly diagnosed and treated with an antibiotic within the first few weeks of infection, still end up with chronic disease. This is PTLDS.

30-40% of Lyme disease patients who have been infected for weeks to months before getting diagnosed, and THEN treated with an antibiotic, still end up with a chronic disease. This subgroup has no specific label but it has been referred to as “chronic Lyme disease,” or CLD.

60% of Lyme patients end up with chronic symptoms

Combining these two subgroups implies that up to 60% of people with Lyme disease will experience chronic illness as a result of this tick-borne disease.

The CDC estimates that there are over 400,000 new cases of Lyme disease that occur each year. 60% of those new cases will develop chronic disease symptoms. You can do the math to figure out how many people have a chronic illness attributable to Lyme disease. Because the disease is chronic, the numbers grow exponentially each year.

Whether PTLDS and CLD patient subgroups even have Lyme disease remains contested. The disputed nature of this illness has very little to do with whether a person is actually sick. It has everything to do with the lack of a clinically accurate diagnostic test for the Lyme disease bacteria.

Problematic Lyme lab tests

Current laboratory tests detect antibodies in blood raised against the Lyme disease bacteria. If antibody levels are too low, the tests are falsely negative. If the levels are borderline and the antibody bands are faint, the lab tech who has to spot them with his or her eyes might subjectively declare the test negative. If the specific antibodies covered by the tests aren’t produced by the patient (called seronegative Lyme disease), the test will be falsely negative. If the test is ordered too early in the infection, the test will be falsely negative. If the test is ordered too late in the infection, the test will be falsely negative. If the strain of the Lyme disease bacterium is not B. burgdorferi, the test will be falsely negative. If the patient’s disease is not Lyme disease, but instead caused by certain viruses, the test may be falsely positive.

The current lab tests have repeatedly been shown to have a clinical accuracy of less than 50%. Meaning a person is equally likely to have Lyme disease, whether their blood test is positive or negative.

Negative tests are used to deny medical care

Regardless, a negative blood test result is used by health care providers and insurance companies to deny patients access to care. Meaning they will argue that Lyme disease patients should not be offered antibiotics as a treatment option, because if the blood test is negative, there’s “no evidence” that they actually have Lyme disease.

Because this lab test has such a high rate of false negatives, the opposing argument is equally true – there’s “no evidence” that they DON’T have Lyme disease, either.

The most comprehensive review of the science to date supports the hypothesis that chronic symptoms are most likely due to the lingering presence of bacteria or pieces of the bacteria in tissues. The immune system is aware of the infection, but is unable to clear it. The result is chronic inflammation…

… implying that antibiotics would be a helpful treatment for a chronic Lyme disease patient.

The twist is that the Lyme disease bacteria are remarkable microbes that can disrupt a normal immune response and establish long-term colonies in tissues. Once established, the bacteria are indifferent to antibiotics and are antibiotic tolerant

… implying that antibiotics would not be a helpful treatment for a chronic Lyme disease patient.

Medical stalemate

In the absence of a blood test that can accurately identify patients in the different Lyme disease subgroups, this argument will not be resolved soon. That Lyme disease patients with chronic symptoms are left entirely out of this argument is a violation of the basic tenets of medical ethics – patient autonomy and the right to informed consent.

Click here to learn more about the Working Group and its reports

Click here for Lorraine Johnson’s comments to the TBDWG on “Why we should abandon the term PTLDS “

In addition to serving on the Testing and Diagnostics Subcommittee of the HHS TBDWG, Holly Ahern serves on the NYS Tick Borne Disease Working Group convened by Governor Cuomo and is a member of the NYS Senate Task Force on TBD Advisory Group. Ahern is also a professor of microbiology, and the co-founder of the 501-c-3 education and advocacy organization Lyme Action Network. She also serves as the Scientific Advisor for Focus on Lyme advising research on diagnostic tests for tick-borne diseases, which includes collaborators from the Translational Genomics Institute, Arizona State University, Johns Hopkins University, Tulane University, Duke University, and North Carolina State University.


For more:





How Lyme Evades the Immune System – Video

How Lyme Evades the Immune System

 Approx. 1 Min 30

Chronic Lyme disease complex is the culmination of Lyme disease and it’s co-infections. Treating chronic Lyme disease can be very difficult because of the many ways Borrelia evades the body’s immune system via constant surface antigen shifting (shifting its own genome), biofilm formation, and its ability to travel everywhere in the body, including particularly difficult places to treat.  All of these factors often lead to antibiotic resistance and failed medical treatments.  Finding the correct treatment protocol is crucial to having lasting relief from this debilitating disease.

Study found here:

Chronic Lyme Disease: Persistent Clinical Symptoms Related to Immune Evasion, Antibiotic Resistance and Various Defense Mechanisms of Borrelia burgdorferi


There are several factors involved in the ability of Borrelia burgdorferi to retain a persistent infection within a mammalian host. These factors of immune evasion include regulation of membrane proteins, variable epitopes of surface proteins, protection against the immune system through tick saliva, the ability to migrate to regions where it is not exposed to the immune system or antibiotics, invagination or invasion within various cells, pleomorphic forms, and the potential to produce biofilms. The window of conventional treatment for Lyme disease is short and has the potential to display different symptoms depending on the strain of Borrelia bugdorferi. These symptoms are dependent on the localization of Borrelia burgdorferi which correlates to the significance of diagnosing Lyme disease early to prevent such a spread throughout the body. Such complications of Borrelia burgdorferi may demand new clinical treatment discoveries for patient fighting the chronic form.

Published on Nov 11, 2015

Envita is a leading cancer, Lyme disease, and chronic disease Unipathic treatment center in Scottsdale, Arizona. Our goal is to use the best of real time cancer and Lyme disease diagnostics to determine the best integrative cancer and Lyme disease treatments from around the world to help our patients receive a viable 2nd opinion.

Why Mainstream Lyme/MSIDS Research Remains in the Dark Ages

Why Mainstream Lyme/MSIDS Research Remains in the Dark Ages

By Alicia Cashman

Recently, a study came out by Wormser et al. on the efficacy of a 14-day course of amoxicillin for patients with erythema migrans (EM).  The study purports to be the first clinical study in the U.S. that validates this regimen but states foreign studies have already done so (1).

The most glaring issue with this study is the continuing fixation on the acute stage while continuing to completely ignore treated patients who remain ill.  I refuse to say the words “late stage” as experience has shown “late stage” can happen within two weeks after tick bite.  Bob Giguere of IGeneX told our support group the story of a little girl who developed facial palsy and lost the ability to walk & talk within 4-6 hours of tick bite (2).  Whether or not you label that escalating case “late stage” or not, the infection was able to cross the blood brain barrier and cause severe symptoms in short order.

There were other numerous problems with the study:

  • The small sample size of only 24 patients.
  • The continued use of the “bull’s-eye” rash when only 27-80% get it depending on who’s counting, leaving out a large subset of patients (3). An inconvenient truth is that only a quarter of the first ever patient sample had a rash: 1976circularletterpdf
  • Regarding EM rashes, the study ignores evidence assessments and guideline recommendations that state clearance of the rash does not mean infection clearance (4).
  • The continued denial of the pleomorphic (shape-shifting) & polymicrobial (multiple pathogens) nature of this illness (5).  Pleomorphism allows the organism to hide and reemerge later.  Coinfection involvement makes cases more severe.  Both issues should be factored into any treatment plan.  MSIDS means multi systemic infectious disease syndrome – a far better moniker as it’s often much more than Lyme (borrelia) at play.
  • The lack of lengthy follow-up required due to the plethora of recorded treatment failures in the literature as well as the complete denial of the recommendation to continually treat patients who have not fully recovered until symptom resolution (2).

Microbiologist Tom Grier has written on the issue of treatment failure for years and states that from the very beginning, treatment failures were seen in nearly every antibiotic study done.  He also states that the longer the patient follow up, the higher the treatment failure (6).  

You would think the totality of these facts would set researchers on a different course yet researchers such as Dr. Gary Wormser seem hell-bent on conducting yet more research with a severely limited patient group, short term treatment and follow up, pushing the EM rash criteria, and ignoring those with persistent symptoms.

MSIDS patient and advocate Carl Tuttle has been working tirelessly to let researchers, the IDSA, the tick-borne disease working group, and politicians know these significant facts by refuting the continuing skewed & faulty research.  He writes these entities personally, and has also started the online petition Calling for a Congressional Investigation of the CDC, IDSA, and ALDF:  If you’ve always wondered what you can do to affect change, add your name to the over 70,000 people who are refusing to accept the current standard of research and care.  Then, if you have the energy, write these folks yourself.  Tuttle includes all the pertinent information for you to cut and paste the material that will let your voice be heard.

Circling back to the practical and important issue of treatment failure faced by many patients, it’s important to rewind time, and learn the sordid and politically motivated history of the treatment of Lyme.

Dr. Burrascano, a prominent and experienced doctor who treated Lyme for decades, recently made a must-see video for patient and doctor alike.  Within this short 40 minute video he outlines chronological events that explain the mishandling of this disease as well as the years of treatment trial and error within his own practice utilizing microscopy, a far better method of Borrelia detection.  He debunks much of what is blindly accepted in main-stream medicine, including the extremely biased and faulty science in Wormser’s study.  

Highlights of the video (7):

  • Dr. Burrascano’s office was 10 minutes from Shelter Island where Willy Burgdorfer collected ticks. Patients with mysterious symptoms graced his practice from inception.


  • Early Lyme was described in Europe even as far back as the 1800s as causing dermatological, neurological, rheumatological, & neuropsychiatric problems.  He claims that early history was lost.


  • In the U.S., as far back as 1965, a condition known as ‘Montauk Knee’ was described as well as a circular rash that would clear up more quickly with penicillin.  In 1970 the first paper was published about a physician who was infected while grouse hunting in our very own state of Wisconsin.  Thankfully, the patient presented with EM rash and Dr. Rudolf J. Scrimenti, a Minnesotan dermatologist who was familiar with the European literature, effectively used penicillin during the acute phase of the illness (8).


  • Polly Murray of Connecticut contacted the CDC about an abnormal amount of sick kids with rashes and joint pain in the early ’70s and the CDC sent epidemiologist and rheumatologist Dr. Allen Steere to determine the cause.  Scrimenti wrote Steere and even went to Yale to warn him of the European studies and that Lyme clusters could exist in the U.S. Despite the warnings, Steere concluded what was occurring in Lyme, Connecticut was nothing more than an unrecognized form of juvenile arthritis (8). Later, Willy Burgdorfer found the cause to be Borrelia burgdorferi (Bb), commonly known as Lyme disease.


  • As early as 1985, Pathologist Dr. Alan McDonald developed a culturing technique that showed spirochetes in the blood.  He proved patients can test negative yet still have active infection as shown in blood culture.  Seronegativity for some reason remains controversial to this day.


  • Some patients under Dr. Steere’s treatment in the 80’s got better but many didn’t, so he arbitrarily divided patients into two groups: Major symptoms: Cardiac, arthritic, Bells palsy and Minor symptoms: everything else.  He claimed that successful treatment was the clearing of major symptoms, but 95% of patients with major symptoms found symptoms to clear on their own without any treatment, demonstrating his treatment theory was completely bogus. All those with “minor” symptoms he labeled post Lyme syndrome – a label which has persisted to this day, but there has never been a description explaining what this syndrome is from an immunological standpoint that applies to patients.

Microbiologist Holly Ahern recently wrote about the arbitrary label “Post Treatment Lyme Disease Syndrome,” or PTLDS, which the CDC estimates to be 10-20% of patients; however, Ahern states this label only truly represents a subgroup of patients who have been diagnosed early, treated with standard short-term antibiotics, and whom remained symptomatic or developed new symptoms. It does not and should not include a third group who were misdiagnosed or undiagnosed beyond the first few weeks of infection. She states estimates based on existing research show this unaccounted for group makes up 30-40% of Lyme disease patients. By combining the PTLDS group with the third group, there are 60% of patients ending up with chronic symptoms, a number that more closely matches my experience as a patient advocate (9).

This is an important point as researchers continue to downplay the aspect of persistent symptoms by using the falsely skewed low percentages.
  • Burrascao worked with dermatologist Dr. Bernard Berger and Pathologist, Dr. Alan McDonald, and they cultured EM biopsies for antibiotic sensitivity studies.  Decades ago they knew amoxicillin worked better than penicillin, doxycycline worked better than tetracycline, and while erythromycin worked in a test tube, it didn’t work well in patients.  Burrascano never ascribed to Steere’s pre and post Lyme categories but rather would treat and then wait a few weeks to culture. All the cultures came back positive.  He learned even way back in the 80’s that these patients had continuing persistent Lyme infection. 


  • He also manipulated drug levels. While some patients in- Burrascano’s in house studies had detectable levels, others required higher doses to achieve the same level.  If you don’t have detectable blood levels of antibiotics, you will not be killing pathogens. The CDC guidelines, be it the 200 mg of daily doxycycline or the 500 mg of amoxicillin given in the Wormser study, are both faulty in that they are a one size approach negating entirely the issue of effective drug blood levels. Burrascano is concerned the CDC is setting patients up for severe chronic Lyme because if pathogens aren’t killed they are left to mutate into something that will become treatment resistant.   


  • While the recent Wormser et al. study used 500 mg of amoxycillin three times a day, Burrascano, decades ago, found patients had more improvement on 1000mg three times a day. When he added 500 mg probenecid three times a day, which increases antibiotic blood levels, they improved even more.  Regarding dosages, he explained about an unpublished study with Stoneybrook where there was a failure rate of 100% of patients taking 300 mg of doxycycline a day for 21 days. Yet, how many people are given this exact treatment today?  He found patients required 400 mg as a starting point with many needing 600 mg.


  • Armed with this intel, he then did clinical studies manipulating treatment time with amoxycillin and probenecid. Due to the varying clinical outcomes he defined treatment success as getting back to pre-illness state for 3 months without relapse.  He found 14 days didn’t do much, with 17% doing well after 1 month, and 66% of males plateauing at 4 months, but hormonally active women not until 6 months. 


  • Regarding cefuroxime, he found that 3 weeks after treatment, patients were still culture positive and complaining of symptoms after 14 days of high doses – a 100% failure rate.  Eventually he discovered that Ceftin did work on patients who failed amoxycillin if the dose was high enough for long enough.


  • Because patients weren’t getting better, he took a week off work, and sat down with his coworkers who created spreadsheets of all his patients.  He found the following variables necessitated longer treatment:
  1. Multiple bites
  2. Active Lyme arthritis with a high sedimentation rate
  3. Heart murmurs
  4. Hormonally active women

He found IV’s give much higher blood levels of drugs than orals, and that the following variables necessitated IV treatment:

  1. Spinal tap shows high inflammation (high protein)
  2. High Sed rate and synovitis (inflammation of synovial membrane)
  3. People sick for more than 1 year
  4. Age over 60
  5. Acute carditis
  6. Immune deficiency
  7. Those who used immunosuppressants
  8. Failed oral treatment

To further demonstrate the polarization of how Lyme is treated, a recent report was published by the U.S. Centers for Disease Control and Prevention with the aim of frightening doctors from using IV therapy at all.  The article published in MMWR, was of five extreme cases with poor outcomes amid thousands who have been treated successfully. Two of the ten authors work for the CDC and are personally involved in updating Lyme guidelines for the IDSA, a group that doesn’t even believe in chronic Lyme.  Furthermore, one of the authors solicited IDSA doctors for evidence of harm while dangling the promise of co-authorship of the report, while not soliciting for any success stories using IV therapy (10).  This sort of partiality is rife in Lyme/MSIDS research.

On the other hand, an IDSA founder from our very own state of Wisconsin wrote a book on 51 cases of chronic Lyme where he often used 6-8 grams of IV antibiotics daily with success.

He first learned of the debilitating nature of Lyme in the late 80’s after a son of a woman dying from ALS suggested his mother’s illness may have started when she developed a severe case of Lyme Disease.  He wrote that many of his colleagues denied chronic Lyme (11).

  • Burrascano found Lyme disease has a 4-week cycle, where every 4 weeks patients experience a symptom flair. Burgdorfer found this in mice studies, and IGeneX found the same thing in urine antigen studies.  Borrelia grow and are active, then become inactive.  Four weeks later they activate.  This has been shown recently in vitro. Think of Bb as a slow relapsing fever.  This nuance is important because antibiotics only kill during the active phase.  You need a minimum of a month to bracket a whole generation cycle.  


  • When patients reach a plateau, he recommends cycling therapy where you discontinue antibiotics until symptoms return.  Then, return to full treatment until symptoms are gone. He states that many patients become symptom free after 4 of these cycles.  He used this on himself with success.


  • Burrascano found 3 other physicians doing the exact same thing with patients. This approached worked for all of them despite the different geographical areas they were in.


  • The government came up with a gold stain for detecting Bb, and found Bb excreted bioproducts and an S layer (slime to create a biofilm) even in the dormant phase. Their work even then showed infected animals had gold stained spirochetes in the following areas: bladder, brain, blood, heart, liver, spleen, urine, tears, and in ticks.


  • The government, in conjunction with Burrascano, conducted studies on 73 chronically ill Lyme patients.  Bb was found in 48 of 50 samples of tears, showing that 53% still had living Borrelia antigens that could be seen on the gold stain. 


  • They also found if you tested patients who still had symptoms, and then took a couple weeks break for treatment, 100% still were positive for Lyme (living organisms) by gold stain.  The NIH abruptly stopped funding of gold stain, made them close the whole thing down, and never asked front-line Lyme docs for specimens again.


  • Burrascano states that in those early days they didn’t know anything about coinfections but patients did well on the Lyme-only treatment at that time; however, the patients that did show involvement were the ones who appeared chronically infected. He found if patients were treated early and hard for Lyme the coinfections weren’t a problem for most.


  • Burrascano then discusses the importance of proper exercise for Lyme patients, and that without exercise, patients don’t recover.  The goal of exercise is to increase T-cells, so exercise cannot be too strenuous or too often.  He recommends light exercise making sure to give enough time in between sessions for the body to recover.  It is also important to get good sleep, and to rest as needed.


  • He gave the story of how Dr. McDonald presented his culture findings (direct testing) at a meeting of the NY State medical society where there were many detractors from Yale & Stoneybrook who didn’t want their patented serological tests to be usurped. They accused him of falsifying his results.  Dr. McDonald then went on to prove conclusively it was Lyme by morphology, silver staining, monoclonal antibodies staining, DNA PCR and finally electron microscopy.  Frustrated, he quit the field and moved to Texas leaving all his old files in Burrascano’s basement until twenty years went by and he became interested again due to Alzheimer’s research & picked up his old files. 

There has been an ongoing record of suppression of microscopy for Lyme.  In an interview with now retired professor of microbiology Morten Laane, the facts come rolling out on how he was fired, his lab was closed down, and his published article disappeared without a trace after presenting his findings at a scientific conference on how microscopy showed spirochetes as well as other organisms like Babesia in a number of patients (12).  Laane is far from alone.  Dr. Sin Hang Lee has even filed a $57.1 million lawsuit against the CDC for suppressing direct detection tests, and for employing ‘Lysenkoism,’ a term used for a Russian political campaign using bogus science to suppress true biological and medical sciences and to punish scientists and doctors who don’t follow Party Line (13).

  • Burrascano connected McDonald with Dr. Eva Sapi to develop a culture technique based on McDonald’s 1985 test.  Advanced Lab contracted with Sapi to develop a commercial test using human specimens instead of lab specimens, and they went on to perform over 8,000 successful cultures of which published studies showed the test was 92% sensitive, and 100% specific.  Advanced labs closed but sold the test to IGeneX & it is currently in the process of getting approval.

Dr. Burrascano’s timely and detailed video reveals clearly why many remain ill.  There are stake holders who are purposely using their power to deny thousands if not millions proper diagnosis and treatment for a disease that is over 40 years old.  There are nuances to treating Lyme that researchers and therefore doctors are still not taking into account, which means doctors are utilizing flawed and biased studies from the Dark Ages in treating patients.  Extremely ill patients are left to suffer.

Most researchers continue to fixate on the acute phase, ignore published animals studies, international studies, the advice and experience of  Lyme doctors trained by ILADS, and purposely suppress much better testing.

It is imperative that we continue to educate ourselves and others, so we do not fall prey to ancient perceptions of a disease that has become a pandemic and shows no signs of slowing down.

Medicine fails when it quits listening. 


 1.  Wormser GP, Brady KC, Cho, MS, Scavarda CA, McKenna D.  (2019) Efficacy of a 14-day course of amoxicillin for patients with erythema migraines.  Diagnostic Microbiology and Infectious Disease.

2.   IGeneX presentation to the Madison Lyme Support Group.

3.  Johnson, Lorraine.  “How Many of Those With Lyme disease Have the Rash?  Estimates range from 27-80%.”, 10 April 2014,  Accessed 12 February, 2019.

4.  Cameron, DJ, Johnson LB, Maloney, EL.  (2014)  Evidence Assessments and Guideline Recommendations in Lyme disease:  the Clinical Management of Known Tick Bites, Erythema Migrans Rashes and Persistent Disease.  Expert Review of Anti-infective Therapy.

5.  Garg K, Merilainen L, Franz O, Pirttinen H, Quevedo-Diaz M, Croucher S, Gilbert L. (2018) Evaluating Polymicrobial Immune Responses in Patients Suffering From Tick-borne Diseases.  Scientific Reports.  doi: 10.1038/s41598-018-34393-9

6.  Grier, Tom.  “Chronic Lyme Post-mortem Study Needed.”, 13 April, 2018, Accessed 12 February, 2019.  

7.  Burrascano, Joseph.  “The History of Lyme Disease.”,  Accessed 21 February, 2019.

8.  Kocurek, J.  “How Lyme Got a Bad Rap – Lyme, Connecticut, That is.”  1 August 2006,—lyme-connecticut-that-is.html.  Accessed 12 February, 2019.

9. Ahern, Holly.  “Medical Stalemate:  What Causes Continuing Symptoms After Lyme Treatment?”  19 February, 2019,  Accessed 25 February, 2019. 

10. Hughes, Claire.  “Report on Dangers of Antibiotic Use For Lyme Disease Sparks Controversy.” June 20, 2017  Accessed 21 February, 2019.

11. Waisbren, Burton.  Treatment of Chronic Lyme Disease:  51 Case Reports and Essays in Their Regard.  (California:  BioMed Publishing Group, 2011).

12. Kraaijeveld, Huib.  “Interview With Professor Laane About the Suprression of Microscopy for Lyme Diagnostics.”, 9 December, 2017,  Accessed 21 February, 2019.

13. Milford Molecular Diagnostics.  “$57.1 Million Lyme Disease Lawsuit Filed Against CDC.”  Milford Molecular Diagnostics Press Release,  15 May, 2018.  Accessed 21 February, 2019.