Archive for the ‘Activism’ Category

Tuttle’s Letter to the NH Lyme Disease Study Commission on the Limitations of Blood Testing

https://www.change.org/p/the-us-senate-calling-for-a-congressional-investigation-of-the-cdc-idsa-and-aldf/

Limitations of Serological Diagnostic Tests

FEB 17, 2021 — 

I was appointed by Governor Chris Sununu to the NH Lyme Disease Study Commission as a result of HB490. 

Next Zoom meeting: Mar 26, 2021 09:00 AM Eastern Time

Our charter is to “study the use and limitations of serological diagnostic tests to determine the presence or absence of Lyme and other tick-borne diseases and the development of appropriate methods to educate physicians and the public with respect to the inconclusive nature of prevailing test methods.”

Website:

COMMISSION TO STUDY TESTING FOR LYME AND OTHER TICK-BORNE DISEASES
http://www.gencourt.state.nh.us/statstudcomm/details.aspx?id=1515&rbl=1&txtbillnumber=hb490

Here is a statement I read at the end of last Friday’s monthly Lyme Disease Study Group via the Zoom meeting.

Since the last meeting I have sent nine emails with topics to discuss in our meetings. The emails have contained many supporting references to my claim that serology is no better than a coin toss, harm caused by false negative Elisa tests reported to the NH Dept of Health ten years ago, comments from 340 NH residents with many reporting delayed diagnosis due to false negative serology and a list of references identifying seronegative disease.  A recent Johns Hopkins study reveals that if you’re not treated within the very narrow widow of 30 days, you run the risk of ending up with chronic Lyme disease [1] and yet humans won’t produce antibodies to the infection for 4-6 weeks after a tick bite. So, by the time serology is positive, if ever, it’s already too late as the spirochete responsible for Lyme disease were just recently identified in the brains of mice one week after infection. [2]

The possibility of missing a timely diagnosis is extremely high in a state with one of the highest rates of Lyme in the country especially in the absence of a bulls-eye rash. This was the case with all Tuttle family members. None of us developed the bulls eye rash, none of us met the strict CDC criteria for positive test results and as I mentioned previously, if we had not met Dr. Sam Donta, none of us would have been treated.

The sobering fact about this travesty is that it has been going on for over three decades and no matter how many complaints are submitted, nothing changes and lives continue to be ruined by an infection misclassified as a simple nuisance disease; “hard to catch and easily treated.” Everyone here is a single tick bite away from experiencing this health disaster as tick-borne disease infection rates in the ticks found in Litchfield for example are as high as 77% as indicated in the 2009 UMass tick study I sent to all of you yesterday. Of course, all these details are well hidden from the public. So I hope that we can make a difference here, get the truth out to the public and save lives that otherwise would have been upended by this life-altering/life threatening infection.

Ben Franklin once said, “Justice won’t be served until those unaffected are as outraged as those who are.”

Carl Tuttle
Hudson, NH
 
References
 
1. Treatment Delays Increase Risk of Persistent Illness in Lyme Disease
https://www.hopkinslyme.org/news/treatment-delays-increase-risk-of-persistent-illness-in-lyme-disease/

2. A murine model of lyme disease demonstrates that Borrelia burgdorferi colonizes the dura mater and induces inflammation in the central nervous system
https://journals.plos.org/plospathogens/article/authors?id=10.1371/journal.ppat.1009256

______________________________________________

Summary of emails “Topics for discussion at our next meeting”

———- Original Message ———-
From: CARL TUTTLE <runagain@comcast.net>
To: wmarshmd@gmail.com (CHAIR)
Cc: All members of the Study Commission
Date: 02/08/2021 3:20 PM
Subject: Summary of emails “Topics for discussion at our next meeting”

To members of the Lyme Study Commission,

I have organized the emails I have sent since our last meeting so that these topics won’t be missed in the upcoming meeting(s)

Next Zoom Meeting: Friday Feb 12, 2021 9:00AM

Summary of emails “Topics for discussion at our next meeting”

#1 Dec 30, 2020

Presentation request

 -Amanda Elam, President and CEO of Galaxy Diagnostics has a 20min presentation for the Lyme Study Commission

–Galaxy Diagnostics Launches the Most Sensitive Test Available for Direct Detection of Lyme Disease ($295)
https://www.prnewswire.com/news-releases/galaxy-diagnostics-launches-the-most-sensitive-test-available-for-direct-detection-of-lyme-disease-301169364.html

“Galaxy validation data (unpublished) shows that the Nanotrap® Urine Test will often confirm active infection in patients with negative TTT (Two-Tiered Testing) results.”
 
#2 Jan 14, 2021

-2005 Johns Hopkins Study: Serology no better than a coin toss
-2016 Meta-analysis of test accuracy: Serology no better than a coin toss
-2020 Johns Hopkins study: Treatment Delays of 30 Days associated with chronic Lyme disease
-1998 Dennis Parenti’s vaccine presentation: Seronegative Lyme. At 36% is a common presentation

#3 Jan 15, 2021

-1995 Seronegative Chronic Relapsing Neuroborreliosis: The patient never had detectable free antibodies to B. burgdorferi in serum or spinal fluid
-2010 Registered Complaint to the NH Dept of Health: Identifying five NH cases where a FALSE negative Elisa led to patient harm (Willful neglect?)

#4 Jan 17, 2021

-Comments from 344 individuals living in New Hampshire: Individuals in bold lettering have been adversely affected by faulty/misleading Lyme disease testing
 
#5 Jan 20, 2021

-Not Using Ivermectin, One Year In, Is Unethical And Immoral: Used as an example of mismanagement of an epidemic as we have experienced with Lyme disease

#6 Jan 25, 2021

-Dr. Kenneth Liegner’s communication with public health officials at the CDC regarding patient harm to Jennifer Lilly from the faulty two-tiered serology test for Lyme disease.
-Includes many references to poor performance of serologic testing

#7 Jan 30, 2021

-Letter addressed to Rochelle Walensky, MD Director of the CDC: includes references to seronegative Lyme disease and evidence of persistent infection through culture performed by the Centers for Disease Control at Fort Collins, Colorado

#8 Feb 3, 2021

-PDF file identifying Seronegativity in Lyme borreliosis and Other Spirochetal Infections 16 September 2003: “If false results are to be feared, it is the false negative result which holds the greatest peril for the patient.”

#9 Feb 5, 2021

-Study published this month identifying the spirochete responsible for Lyme disease in the brains of mice one week after infection. Lyme tests won’t be positive for 4-6 weeks after a tick bite (if you actually do produce antibodies) and you’ll miss the narrow window of opportunity for successful short-term treatment. Now you’ve gone past that thirty day mark that Johns Hopkins has recently identified as problematic as these patients end up with chronic Lyme disease. Serology is an inappropriate diagnostic tool for this life-altering/life-threatening infection.

Respectfully submitted,

Carl Tuttle
Hudson, NH

____________________

For more:

Category:

Activism, Lyme, Testing

How to Ease Lyme Symptoms With Endorphins, Naturally (No Exercise Needed)

http://rawlsmd.com/health-articles/how-to-ease-lyme-symptoms-with-endorphins-naturally-no-exercise-needed?

How to Ease Lyme Symptoms with Endorphins, Naturally (No Exercise Needed)

How to Ease Lyme Symptoms with Endorphins, Naturally (No Exercise Needed)

by Jenny Lelwica Buttaccio
Posted 2/15/21

You’re probably most familiar with endorphins as they relate to the so-called “runner’s high,” the calm, euphoric feeling that people report after a long run. And it’s true that vigorous aerobic activity is a proven way to spark the release of these feel-good peptides. But if you’re dealing with the daily ups and downs of chronic Lyme disease, lacing up your sneakers to pound the pavement is likely on the bottom of your to-do list.

While exercise gets most of the credit when it comes to endorphins, it’s certainly not the only way your body generates these little wonder molecules that improve your sense of wellbeing. Here, we’ll take a look at endorphins and why they might hold the key to easing such Lyme symptoms as pain, immune dysfunction, and chronic stress, plus offer ways to reap the benefits even when you’re not feeling up to moving, no exercise needed.

An Overview of Endorphins

When your body experiences pain or stress, the hypothalamus and pituitary gland — your body’s largest producers of endorphins —generate these chemicals as a way of coping with physical and emotional pressures. Endorphins may arise from other parts of the body as well: Research suggests immune cells make endorphins in response to inflammatory processes in the body and help to quell certain pain-producing substances.

Endorphins have garnered the reputation of being “feel good” chemicals because they play a pivotal role in the body’s natural pain management process and possess opioid-like qualities. The term endorphin comes from two words: “endogenous,” meaning originating from within the body, and “morphine,” the opioid pain reliever. Indeed, endorphin is a fitting name for the morphine-like chemical produced in the body.

In the mid-70s, scientists were researching the mechanisms by which opioids alleviated pain. At that point, morphine had been around for nearly 200 years, but how and why it worked was still relatively unknown. The research led to the discovery of opioid receptors: When opioid medications like morphine bound to receptors in the peripheral and central nervous system, the drugs blocked pain signals.

Furthermore, researchers also noticed that other, natural chemicals in the body could bind to the same receptors and act in a manner comparable to opioid medications. They called these similar chemicals endorphins.

The Link Between Endorphins, Lyme Disease + Other Chronic Illnesses

There are many different types of endorphins, but the ones most often discussed in the research are beta-endorphins. Although we still have a lot to learn when it comes to endorphins, we know they’re responsible for mitigating pain, modulating the immune system, and enhancing pleasure. Besides stress, endorphins are released during activities you typically enjoy doing — sex, eating, and drinking, to name a few.

scientific image, X-ray of human skull, showing brain. surrounded by neurons, natural killer cells, and borrelia

Although research has yet to look specifically at Lyme disease and endorphins, evidence indicates that when beta-endorphins are secreted in the brain, they trigger the release of natural killer (NK) cells. These immune cells are our first line of defense against infectious agents like Borrelia burgdorferi and abnormal cell growth.

One therapeutic intervention yielding positive results for some Lyme patients, particularly those with neurological Lyme, is the endorphin-enhancing medication low-dose naltrexone (LDN). LDN partially blocks opioid receptors, leading to a slow increase of endorphins while supporting a healthier immune response, dampening inflammatory cytokines, and curbing neuroinflammation.

Endorphin levels can vary from one person to another, and low levels of endorphins have also been associated with several chronic conditions. On the list: fibromyalgia, ME/CFS (myalgic encephalomyelitis/chronic fatigue syndrome), depression, and headaches — and that’s probably just scratching the surface.

But can you begin to reap the benefits of endorphins without a prescription medication or running an all-out marathon? The answer is yes. The following are natural ways to boost endorphins so that you can experience lower pain levels, increased immune function, and a greater sense of wellbeing.

5 Natural Ways to Boost Endorphins + Ease Lyme Symptoms

1. Laugh Out Loud.

bright picture of laughing woman on the beach. backlight sunlight in nbackgroiund. beautiful young female model laugh like crazy. happiness and joyful concept for people in wanderlust

You’ve probably typed “LOL” countless times this week, but how many times have you actually done it? A hearty belly laugh has a host of mental and physical benefits, including a satisfying release of endorphins. It gets your heart, lungs, and muscles pumping, which in turn triggers the release of these euphoric molecules, according to a study in the journal Proceedings of the Royal Society B: Biological Sciences.

Additionally, the pain thresholds of the study participants were significantly higher after participating in laughter-inducing activities (like watching a comedy) compared to those who engaged in neutral or factually-based activities (like watching a documentary). The researchers believe it’s the endorphins’ effects on opioid receptors that create these positive changes.

To get your laugh on, watch a comedy, practice your amateur stand-up routine, find a laughter yoga class online, or do whatever you have to do to get the giggles flowing. The deeper the belly laugh, the more likely you are to experience that pleasant endorphin rush.

2. Try Full-Spectrum CBD Oil.

Many Lyme patients have chronic pain — like myofascial pain or neuropathy — as a predominant symptom. Finding ways to manage that pain effectively can be quite a challenge, however, CBD from hemp oil may be up to the task.

dropper dripping hemp oil into glass bottle, background hemp leaves

CBD (short for cannabidiol) shuts off nerve impulses that send uncomfortable pain signals and counteracts inflammation. Plus, it increases the body’s natural endorphin levels without suppressing them the way opioid medications do. Pain medications run the risk of causing dependence or withdrawal symptoms, but CBD doesn’t have those addictive qualities — most likely because it doesn’t contain the psychoactive component THC.

CBD dosing can vary from person to person, but a standard starting dose is 10-50 mg, one to three times per day. The concentrations of CBD differ by brand, so be sure to check the product label to find out how much CBD is in each dropperful or capsule. Some CBD users might notice its benefits immediately, while others may require two or three weeks of steady use to see improvements.

3. Sweat It Out, Exercise-Free.

You may be familiar with the use of far infrared saunas (FIR) as a means of detoxifyingthe body during Lyme treatment and managing uncomfortable Herxheimer reactions. But saunas have a longstanding history of being used around the globe due to their health-promoting properties.

inside of a wooden infrared sauna, towel on seating

The heat from FIR saunas is deeply penetrating, reaching up to a few inches beneath the skin’s surface. Research demonstrates sauna use may stimulate the release of endorphins and other opioid-like chemicals to fight pain, relieve inflammation, and facilitate a healthy immune system.

Not sure of how to use a sauna? Begin slowly (as little as 5 minutes a day) and increase your time to 30 minutes as your body adjusts to the heat. And aim for two to three times a week — consistency of use rather than intensity wins this race!

4. Get a Massage.

Looking for a reason to indulge in some extra self-care? Think about getting a massage because it can be helpful for increasing endorphins as well as other mood-boosting and pain-relieving chemicals like serotonin and dopamine.

Physiotherapist massaging back of man lying on Massage Table in hospital

One small-scale study showed that participants who received a connective tissue massage had a 16% increase in beta-endorphin levels, lasting approximately 1 hour after the massage was finished. Additionally, because some opioid receptors are located in deep tissues of the body, massages incorporating deeper pressure may even generate higher levels of endorphins compared to the mild touch of connective tissue release work.

If getting to a professional massage therapist isn’t in the cards right now, no problem. Similar to exercise and sauna use, any massage-type activity can get you headed in the right direction. Try a foam roller, a handheld massager, or a massage chair to relax tense muscles and let go of stress.

5. Get Moving at an Accessible Pace.

Yes, running has beneficial effects on endorphin production, but you can achieve results with less demanding forms of exercise as well — including activities that might be more appropriate for the needs and fitness levels of many chronic Lyme patients. Although the greatest endorphin high occurs with intense physical activity that lasts about an hour, almost all forms of exercise will have a beneficial impact.

woman in comfy clothes, rolling up yoga mat in living room

In fact, research suggests even 15 minutes of exercise per day can increase endorphins. Although it might not lead to a giant rush of the feel-good chemicals, you’re still likely to experience an uptick in your mood, a decrease in pain levels, and better immune function.

And there’s no need to push yourself to the max. You can mobilize endorphins with low-impact activities like walking, Pilates, power yoga, or qigong to bring on results. As you get further along in your Lyme disease recovery, the more you’ll be able to up the intensity of your workouts.

The Takeaway

No doubt, there’s still a lot to learn about the benefits of endorphins and how they impact Lyme disease and your health. But aiming to get a daily dose of them in your life may enhance immune function, improve pain levels, provide a more optimistic outlook, and more.

Best of all, boosting your endorphin levels is another cost-effective tool to add to your toolbox of healing modalities. Combine it with a comprehensive herbal therapy protocol, a healthy diet, and lifestyle modifications to achieve optimal healing results on your recovery journey.

Dr. Rawls is a physician who overcame Lyme disease through natural herbal therapy. You can learn more about Lyme disease in Dr. Rawls’ new best selling book, Unlocking Lyme.

You can also learn about Dr. Rawls’ personal journey in overcoming Lyme disease and fibromyalgia in his popular blog post, My Chronic Lyme Journey.

Learn About Dr. Rawls’ Herbal Protocol »
REFERENCES
1. Cabanas H, Muraki K, Staines D, Marshall-Gradisnik S. Naltrexone Restores Impaired Transient Receptor Potential Melastatin 3 Ion Channel Function in Natural Killer Cells From Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Patients. Front Immunol. 2019;10:2545. Published 2019 Oct 31. doi: 10.3389/fimmu.2019.02545
2. Chaudhry SR, Gossman W. Biochemistry, Endorphin. [Updated 2020 Aug 11]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470306/
3. Dunbar RIM, Baron R, Frangou A, et al. Social laughter is correlated with an elevated pain threshold. Proc. R. Soc.2012 September; 279(1731):1161-7. doi: 10.1098/rspb.2011.1373
4. Hsueh CM, Chen SF, Ghanta VK, Hiramoto RN. Expression of the conditioned NK cell activity is beta-endorphin dependent. Brain Res. 1995 Apr 24;678(1-2):76-82. doi: 10.1016/0006-8993(95)00172-m
5. Hussain J, Cohen M. Clinical Effects of Regular Dry Sauna Bathing: A Systematic Review. Evid Based Complement Alternat Med. 2018;2018:1857413. Published 2018 Apr 24. doi: 10.1155/2018/1857413
6. Kaada B, Torsteinbø O. Increase of plasma beta-endorphins in connective tissue massage. Gen Pharmacol. 1989;20(4):487-9. doi: 10.1016/0306-3623(89)90200-0
7. Klockgether-Radke AP. F. W. Sertürner und die Entdeckung des Morphins – 200 Jahre Schmerztherapie mit Opioiden – [F. W. Sertürner and the discovery of morphine. 200 years of pain therapy with opioids]. Anasthesiol Intensivmed Notfallmed Schmerzther. 2002 May;37(5):244-9. German. doi: 10.1055/s-2002-30132
8. Ramanathan S, Panksepp J, Johnson B. Is fibromyalgia an endocrine/endorphin deficit disorder? Is low dose naltrexone a new treatment option? Psychosomatics. 2012 Nov-Dec;53(6):591-4. doi: 10.1016/j.psym.2011.11.006
9. Sprouse-Blum AS, Smith G, Sugai D, Parsa FD. Understanding endorphins and their importance in pain management. Hawaii Med J. 2010;69(3):70-71.

Category:

Activism, Detoxing, Hemp Oil, Herbs, Lyme

VCO as an Adjunct Supplement for COVID-19

https://www.fnri.dost.gov.ph/index.php/programs-and-projects/news-and-announcement/800-virgin-coconut-oil-vco-study-results-on-covid-19-suspect-and-probable-cases-released-by-dost-fnri

VCO-Study

Results of the study on virgin coconut oil (VCO) as dietary supplement among COVID-19 probable and suspect cases showed that 5 of the 29 patients who were served meals with VCO manifested diminishing signs and symptoms as early as the second day, while only one patient served with the same meals but without VCO showed similar improvement.

This is according to the Department of Science and Technology’s Food and Nutrition Research Institute (DOST-FNRI) in a virtual presser dubbed as “Seeing Beyond COVID-19: The VCO Study – Effects of Virgin Coconut Oil among Suspect and Probable Cases” on December 3, 2020.

The VCO Group of patients who were served meals with VCO showed no COVID-19 related symptoms at Day 18, while symptoms persisted in some patients of the Control Group of patients who were served the same meals without VCO until Day 23, DOST Secretary Fortunato T. dela Peña further stated in the presser.

Secretary dela Peña added that VCO could be used as an adjunct supplement to probable and suspect COVID-19 cases to help prevent symptoms from becoming severe.

However, more studies are needed to determine the effectiveness of VCO as adjunct therapy for COVID-19 patients with other co-morbidities, Secretary dela Peña clarified.

In a follow-up interview, Dr. Imelda Angeles-Agdeppa, VCO study leader, Scientist II and Chief Science Research Specialist of DOST-FNRI, said that the study involved 57 suspect or probable COVID-19 cases randomly assigned to the Intervention or VCO Group and the Control Group at the Santa Rosa Community Hospital and Santa Rosa Community Isolation Units in Laguna.

Dr. Agdeppa added that aside from monitoring the signs and symptoms of COVID-19 among the study volunteers, the research team also noted that the mean C-Reactive Protein of CRP levels in the VCO Group normalized to 5 milligrams per liter or less as early as Day 14.

The C-Reactive Protein or CRP is a quantitative marker used to monitor inflammation or infection, and that a CRP equal or less than 5 milligrams per liter signifies recovery from inflammation or infection, Dr. Agdeppa explained.

Dr. Agdeppa further stated that while reduction to normal CRP levels in the Control Group was also evident from Day 1 to 14, it remained at the borderline of 5 milligrams per liter from Day 14 until end of intervention.

The VCO used in the study were strictly analyzed by the Laboratory Services Division of the Philippine Coconut Authority (PCA) to ensure product quality and compliance to Philippine National Standard (PNS).

The PCA requests VCO producers to have their VCO samples analyzed by PCA prior to promotion and marketing, PCA Administrator Benjamin R. Madrigal, Jr. said in the presser.

Administrator Madrigal also states that PCA is planning to develop the protocol in establishing the seal of quality for VCO.

Funding and monitoring of the VCO study was provided by the DOST-Philippine Council for Health Research and Development (or PCHRD), through the overall supervision and motoring of the DOST.

The Ateneo de Manila University Faculty of Chemistry, through Dr. Fabian M. Dayrit, provided research inputs and protocols based on previous VCO studies among HIV patients, like the correct VCO dosages to be given and the analysis to be used.

Dr. Dayrit, also an Academician of the DOST-National Academy of Science and Technology and President of the Integrated Chemists of the Philippines, supported the results of the DOST-FNRI VCO study, saying that several studies have proven the promising anti-viral properties of VCO and more studies are warranted to explore its full potential.

The public is hereby advised to carefully read the label of VCO products to check for PCA or FDA approval and make sure that ingredients, nutrient analysis, manufacturing and expiration dates are clearly declared.

Some media partners attending the presser commented that this development on VCO as promising dietary supplement may cause the skyrocketing of the price of VCO products.

The study team agrees with this inevitable consequence, but stated that the health benefits backed by scientific proof far outweigh the impending price increase, adding that DTI will monitor this.

This VCO study does not only have promising contribution to the prevention and management of symptoms among COVID-19 suspect and probable cases, but could also provide a boost to the coconut industry and the millions of coconut farmers who depend on the “tree of life” to uplift their quality of life.

For more information on the VCO study and other food and nutrition concerns, contact: Dr. Milflor S. Gonzales, Officer-in-Charge, Office of the Director, Department of Science and Technology – Food and Nutrition Research Institute, General Santos Avenue, Bicutan, Taguig City; Telephone/Fax Nos: 8-837-2934 or 8-837-3164; Direct Line: 8-839-1839; DOST Trunk Line: 837-2071 local 2296 or 2284; e-mail: dostfnri47@dost.fnri.gov.ph; DOST-FNRI website: http://www.fnri.dost.gov.ph. Like our Facebook Page at facebook.com/DOST.FNRI or follow our Twitter account at twitter.com/DOST_FNRI.

____________________

For more COVID treatments:

All of these treatments are being debunked and ignored by the CDC.  Please see this to find out why.  

COVID-19 has a 99.991% recovery rate by doing nothing – but you’d never know it from mainstream media.

To read about the numerous deaths/adverse reactions due to this COVID injection, which isn’t a vaccine and doesn’t prevent infection: (list is being updated daily): https://madisonarealymesupportgroup.com/2020/12/21/warning-3150-injuries-in-1st-week-of-covid-vaccines-among-american-healthcare-workers-pregnant-women-included/

Category:

Activism, Supplements, Treatment, Viruses

Treatment Delays Increase Risk of Persistent Illness in Lyme Disease

https://www.hopkinslyme.org/news/treatment-delays-increase-risk-of-persistent-illness-in-lyme-disease/

Treatment Delays Increase Risk of Persistent Illness in Lyme Disease

By

Summary

In this retrospective study, one-third of Lyme disease patients report delayed treatment of greater than 30 days, and delayed treatment is associated with post-treatment Lyme disease (PTLD). Delays in treatment are shown to significantly impact patient outcomes and indicate that improved Lyme disease diagnosis and prevention strategies are needed.

Why was this study done?

The goals of the study were to analyze time-to-treatment in a sample of individuals treated for Lyme disease, including identifying risk factors for time to first medical contact and time under care. The study also evaluated associations between time-to-treatment and the development of post-treatment Lyme disease (PTLD). The study was done to determine if delays in treatment are significant to patient outcomes.

How was this study done?

A retrospective study was conducted of time-to-treatment among a general population sample of individuals treated for Lyme disease at Geisinger, a health system in Pennsylvania, the state with the most confirmed Lyme disease cases in the United States. Using electronic medical records and self-administered questionnaire data, respondents’ experiences were characterized by symptoms, care-seeking factors, diagnosis, and treatment. Associations between time-to-treatment and PTLD were examined, and risk factors were measured for delays in time to first medical contact and time under care.

Questionnaires were mailed to 5,314 adult patients who met previously described EHR-based criteria for Lyme disease between 2015 and 2017. Analyses focused on 778 respondents who reported that they were treated for Lyme disease within the past 5 years and reported a rash and/or a positive blood test for Lyme disease. Time-to-treatment was measured in days as the sum of two time windows: time to first medical contact and time under care. Logistic regression was used to evaluate factors associated with delayed time-to-treatment in each time window (>14 days vs. ≤14 days) and the association between total time-to-treatment (>30 days vs. ≤30 days) and PTLD.

What were the major findings?

In the sample of Lyme disease patients studied, delays in medical contact and care were identified in one-third of individuals and delays were associated with a higher risk for post-treatment Lyme disease. In the sample,

  • 25% had time to first medical contact greater than 14 days
  • 21% had time under care of a medical professional greater than 14 days
  • 31% had a total time-to-treatment greater than 30 days

Factors positively associated with delayed time to first medical contact included being uninsured and attributing initial symptoms to something other than Lyme disease. Diagnoses between November and April, and the absence of rash were positively associated with delays in contact and care. First medical contact in an emergency department or “other” setting showed delays in care.

Individuals whose treatment was delayed, defined as time-to treatment >30 days, had 2.26 times the odds of developing PTLD as those who were treated within 30 days of symptom onset.

What is the impact of this work?

Despite post-treatment Lyme disease occurring in an estimated 10-20% of Lyme disease cases, no peer-reviewed studies have evaluated the role of time-to-treatment in PTLD. This retrospective study indicates timely treatment may be important in preventing PTLD and other long-term consequences of Lyme disease.

Strategies to ensure more timely treatment of Lyme disease should include educational campaigns targeting patients and healthcare providers. Education could improve the recognition of the varied clinical presentations of Lyme disease and the erythema migrans rash and underscore the limitations of diagnostic tests. Although urgent care clinics can help patients be seen earlier, there is a clear need to improve disease recognition and diagnosis and reduce time-to-treatment in this setting. Another opportunity to reduce time-to-treatment is to build awareness among patients and medical providers of the risk of Lyme disease throughout the year in endemic regions.

Education, diagnostics, and prevention approaches are needed and should address the risk factors for treatment delays and aim to reduce both the time before and after contacting a medical professional.

This research was supported by:

funded by the Steven & Alexandra Cohen Foundation

Publication Information

Hirsch AG, Poulsen MN, Nordberg C, Moon KA, Rebman AW, Aucott JN, Heaney CD and Schwartz BS (2020) Risk Factors and Outcomes of Treatment Delays in Lyme Disease: A Population-Based Retrospective Cohort Study. Front. Med. 7:560018. doi: 10.3389/fmed.2020.560018

Johns Hopkins Lyme Disease Research Center

The Johns Hopkins Lyme Disease Research Center is focused on patient-based research in all manifestations of Lyme disease. Our goal is to translate our pioneering research into improved patient care, education, and health outcomes.

USE OF THIS SITE

All information contained within the Johns Hopkins Lyme Disease Research Center website is intended for educational purposes only. Physicians and other health care professionals are encouraged to consult other sources and confirm the information contained within this site. Consumers should never disregard medical advice or delay in seeking it because of something they may have read on this website.

_____________________

**Comment**

Although this study is helpful for demonstrating that delays in diagnosis and treatment are bad, there are a number of concerns:

  1. The continued use of outdated and stringent criteria such as the EM rash and blood serology testing. Reality has proven a huge subset of patients meet neither.
  2. Electronic medical records and self-administered questionnaire data are only as effective as the people are filling them out, the questions being asked, and the objectivity of the person compiling the data.
  3. The PTLD label is deceptive and assumes ongoing symptoms are not caused by persistent/chronic infections.

The major findings; however, were helpful in showing that more than half were not obtaining treatment until 14-30 days.  This is important in the light of this mouse study which demonstrated Bb in the brain within a week of infection.

The factors of being uninsured and uneducated on tick-borne illness led to delayed time to 1st medical contact as well as those being seen between Nov-April and the absence of rash (both of which really should be under the banner of being uneducated about tick-borne illness as you can be infected in any month and getting the rash is highly variable).

Category:

Activism, Lyme

The Shaky Science Behind the “Deadly New Strains” of Sars-Cov-2

https://healthimpactnews.com/2021/the-shaky-science-behind-the-deadly-new-strains-of-sars-cov-2/  9-Minute Video Here

The Shaky Science Behind the “Deadly New Strains” of Sars-Cov-2

Feb. 18, 2021

by Rosemary Frei
Off-Guardian

ACCORDING TO WHAT WE HEAR FROM OFFICIALS AND THE MAINSTREAM MEDIA, THE NEW VARIANTS ARE THE MOST DANGEROUS AND UNPREDICTABLE BEINGS SINCE OSAMA BIN LADEN.

Everyone needs to stay safe from these invisible but murderously mighty microbes by shunning contact with the unwashed, unmasked and unvaccinated.

But is that drastic approach — which is accompanied by severe curtailment of civil liberties and constitutional rights — warranted?

It turns out that the case for the variants’ contagiousness and dangerousness centres largely on the theoretical effects of just one change said to stem from a mutation in the virus’s genes.

And, as I’ll show in this article, that case is very shaky.

I also have an accompanying nine-minute ‘explainer’ video (Highly recommend. Please see link at top of page)

That one change is known as N501Y — scientific shorthand for the substitution of one protein building block (amino acid) for another at position 501 in the part of the virus called the spike protein.

Specifically, position 501 lies in the portion of the spike protein that’s responsible for the intimate coupling between the virus and cells that lets the virus slip inside and multiply.

[Note that any such amino-acid switcheroo is correctly called a change, not a mutation. Mutations occur only in genes. For some reason many scientists and scribes who ought to know better are mistakenly calling N501Y and other amino-acid changes ‘mutations.’ ]

A very preliminary study published Dec. 22, 2020, suggested that N501Y also is present in the South African variant named 501Y.V2. And another very preliminary study, published January 12, 2021, asserted it was also present in the new strain emerging from the Brazilian jungle, dubbed P.1.

On top of that, the South African variant is being reported as evading immunity and B.1.1.7 sharing this escape route. And scientists are depicting new variants with N501Y on board as spreading very fast. Some say they make herd immunity impossible, so every single person on earth has to be vaccinated. The models also suggest B.1.1.7 is up to 91% deadlier than the regular novel coronavirus.

(Yet so far it seems the main basis for officials saying it’s more deadly is shown in the minutes of the Jan. 21, 2021 meeting of an influential UK committee called New and Emerging Respiratory Virus Threats Advisory Group [NERVTAG ]. There, they cite modeling papers which haven’t yet been published – which means that until they’re published there’s no way to check their work.)

THREE NON-PEER-REVIEWED THEORETICAL-MODELING PAPERS WHICH CATAPULTED VARIANTS INTO THE SPOTLIGHT

Public-health officials, politicians and the mainstream media around the world turned their collective headlights on the variants right after the publication of three theoretical-modeling papers on B.1.1.7, a variant originating in the U.K. The first was a Technical Briefing by Public Health England published Dec. 21 (it’s the first of an ongoing series of reports on the variant authored by people working at the agency and at other institutions), the second a paper published Dec. 23 by a mathematical-modeling group at the London School of Hygiene and Tropical Medicine, and the third a theoretical-modeling manuscript posted Dec. 31 by a large group of UK scientists.

None of the three papers was checked over for accuracy by objective observers – a process called ‘peer review.’ Nonetheless, all three were portrayed as solid science by many scientists, politicians, public-health officials and the press.

(I reached out for comment to Public Health England, as well as to the first author of the second paper Nicholas Davies, and to the London School of Hygiene and Tropical Medicine. The only reply I received was from a media-relations person at Public Health England; she told me no one was available for an interview.)

(Neil Ferguson was a co-author of the first and third papers. The UK government has relied on Ferguson’s mathematical modeling for many years. This is despite his work turning out to be highly inaccurate time after time. He  also supposedly stepped down from his government-advisory role last May after being caught secretly meeting with his married lover during a time when it was illegal to make contact with anyone outside of one’s household, thanks in large part to his modelling. But he was quickly restored to positions of influence. In an article and accompanying video coming out next week, I describe the connections and conflicts of interest surrounding Ferguson and the modeling papers’ other authors.)

WHAT EFFECT IS N501Y SAID TO HAVE?

In N501Y, the amino acid that’s swapped out at position 501 in the spike protein is asparagine; by scientific convention it’s represented by the letter ‘N.’ The amino acid that’s swapped in in its place is tyrosine, and it’s represented by the letter ‘Y.’ Hence ‘N501Y.’

Position 501 in the amino-acid sequence sits in the part of the spike protein that protrudes from the surface of the virus. Specifically, it’s said to lie in the region of the spike protein that latches or ‘binds’ to the mechanism that is the gatekeeper for whether the virus can enter the cell. That gate-keeping mechanism is known as the ‘ACE2 receptor.’

This region of the spike protein – known as the ‘receptor binding domain’ (RBD) — binds to the gate keeping mechanism, the ACE2 receptor. When the RBD and the ACE2 receptor bind, the cell membrane, which is the circular barrier between the area outside the cell and the cell contents, opens up and allows the virus to enter.

N501Y is posited to make the spike protein bind tighter to the ACE2 receptor. Influential theoreticians have performed mathematical modeling based on this hypothesis. This modeling suggests that this tighter binding allows the virus to enter more easily, and that therefore this makes the virus more transmissible.

Yet as far as I’ve been able to find, there is still no concrete, direct proof of this. And note that epidemiological data cannot be used to definitively detect the effect of an amino-acid in a virus. Only experiments involving direct observation of the virus’s interaction with the body can determine that.

The main evidence that the top three theoretical-models cite as proof of stronger bonding between the N501Y form of the novel coronavirus and the RBD is from just three scientific manuscripts, and these describe experiments with the virus in mice or petri dishes, not observation of whether in fact the variants are truly more contagious or more deadly.

DETAILS OF THE THREE PAPERS THAT UNDERPIN THE ASSERTION THAT N501Y BOLSTERS CONTAGIOUSNESS

One of those three papers was published Sept. 25, 2020, in Science. It describe experiments involving involving six rounds of division of the virus in mice.

The researchers found a large amount of the virus in the mice lungs right from the first round of division. Based on this, they pronounced the virus to have “enhanced infectivity.” However, they didn’t actually test whether the virus is  more transmissible/contagious – that is, whether it moves from mouse to mouse more easily.

They performed ‘deep sequencing’ and reported that they found the N501Y change in the ‘mouse-adapted’ virus. Next they did ‘structural remodeling’ on it and wrote that this analysis…

suggested that the N501Y substitution in the RBD of SARS-CoV[-2] S protein increased the binding affinity of the protein to mouse ACE2.

All of this is very different than direct observations of the variant virus’s behaviour in mice or humans.

The second paper was posted on bioRχiv on Dec. 21, 2020. It describes an “engineered decoy receptor for SARS-CoV-2.” The complicated series of molecular-biological manoeuvers in vitro were performed that is hard to follow and understand – there is no ‘Methods’ section laying out the details and sequence of what they did; rather, the researchers’ approach to their experiments is scattered across all sections of the paper including in the accompanying Supplementary Material. This is many steps removed from real-life situations. The authors conclude from their manoeuvers that laboratory-mutated novel coronavirus with the N501Y mutation seems to bind more tightly to their ‘engineered decoy’ form of the RBD receptor than the RBD receptor that normally occurs in nature.  (The idea, it seems, is that this ‘engineered decoy’ could be injected into people with the goal of getting the new variant to bind to it rather than to cells, thereby stopping it from gaining entry into cells and reproducing.)

bioRχiv is an online-only journal. (It’s pronounced ‘bioarchive’; that’s because the Greek letter χ is pronounced ‘kai.’ I presume the letter χ is used in the journal’s title because the χ2 [‘chi-square’] test is a widely used form of statistical analysis in scientific papers.) The journal has the tagline ‘The Preprint Server for Biology.’ ‘Preprint’ means non-peer-reviewed. bioRχiv focuses entirely on Covid-19-papers and is sponsored by the Chan Zuckerberg Initiative. It has a sister publication medRχiv that also focuses on Covid-19,

The Initiative is the creation of Facebook head Mark Zuckerberg and his wife Priscilla Chan. Facebook has been among the very active censors of information including scientific papers that diverge from the official narrative about Covid.

The third paper  was posted on the website of the online journal bioRχiv on June 17, 2020, and then in Cell on Sept. 3, 2020.

Like the other two papers, it is extremely removed from direct observation of the virus’s behaviour in live animals or humans. In fact, the third paper doesn’t even use human or animal cells. It involves a ‘yeast-surface-display platform’ as a basis for performing ‘deep mutational scanning’ of the novel coronavirus’s RBD. That ‘platform’ is an artificial structure the paper’s authors constructed for measuring binding between antibodies and various RBD regions containing an array of mutations.

According to this paper, the N501Y amino-acid change results in stronger binding of the virus to the RBD.

However, the papers’ authors state in the last section of their paper that:

It is important to remember that our maps define biochemical phenotypes of the RBD, not how these phenotypes relate to viral fitness. There are many complexities in the relationship between biochemical phenotypes of yeast-displayed RBD and viral fitness.

Translation: “Just because our biochemistry experiments showed that the presence of N501Y or other changes in the RBD seems to make the RBD bind tighter to the ACE2 receptor, we don’t know whether any of these changes make the virus more ‘fit’/transmissible.”

And note also that one of the authors of the third paper, Allison Greaney, is quoted as saying in an August 2020 article from the Fred Hutchison Cancer Research Center where she and several of the other authors work, that:

The virus already has a ‘good enough’ ability to bind to ACE2. There’s no reason to believe that going beyond that level will make it more pathogenic or transmissible…[b]ut the RBD may be able to tolerate a number of mutations.

As another note, the third paper was first published in bioRχiv and then published three months later in the peer-reviewed journal Cell. In Cell the paper is labelled ‘Elsevier-Sponsored Documents’ (see image below) (Elsevier is the publishing empire that owns Cell, among hundreds of other journals). I couldn’t find anything online about what ‘Sponsored’ means, nor about what or who sponsored this particular paper; and I couldn’t find any other papers with this designation. So I emailed Cell’s PR manager John Caputo on the evening of Jan. 18 and followed up by leaving him a voicemail message on Jan. 19. I haven’t heard back from him.

‘Deep Mutational Scanning of SARS-CoV-2 Receptor Binding Domain Reveals Constraints on Folding and ACE2 Binding’ (Tyler N. Starr et al.)

A BRIEF WORD ABOUT ANOTHER AMINO-ACID CHANGE IN B.1.1.7

I’ll quickly turn to another of the key changes said to be present in B.1.1.7. This change, the deletion of three amino acids was described in a paper published on the website of medRχiv on November 13, 2020. (Earlier in this article I mention that medRχiv is a creation of the Chan Zuckerberg Initiative.)

The mutation purportedly makes B.1.1.7 invisible to one of the three key functions of the polymerase chain reaction (PCR) test. That function is detection of the gene that has the genetic code for one of the two main spike proteins on the outer surface of the novel coronavirus.

However, that conclusion is based on only sequencing of the virus in a mere six people who tested positive for the novel coronavirus. On top of that, the paper was not subjected to scrutiny by other scientists (a process known as ‘peer review’) before it was published.

In addition, the Covid diagnoses of those six people were themselves determined by PCR. And PCR has been shown to have a very high rate of false positives — that is, to very frequently give a positive result in people who in fact do not harbour the novel coronavirus at all.

The authors of that paper themselves conclude that:

this result should be interpreted with caution. As a limited number of samples with the S-negative profile [i.e., tests that were positive for two of the three portions of the PCR test but not for the third, S-gene, portion] were sequenced, we could not exclude the presence of other S mutations associated with this profile…. Moreover we could not determine whether the deletion affected the primer or other probe-binding region as their coordinates were not available.

It’s a good bet that similar sleights of hand are behind the new wave of papers and headlines focusing on the amino-acid change dubbed E484K.

WHAT’S THE LESSON FROM ALL THIS?

That the pronouncements about the dire danger posed by the new variants aren’t based on solid science.

They appear to be aimed more at scaring the public into submitting to harsher and longer restrictions than helping to create truly evidence-based policies.

So follow the golden rules. Read the primary scientific-paper sources. Analyze them and think for yourself. Don’t let your reasoning be swept away by the 24-7, fear-filled news cycle.

Rosemary Frei has an MSc in molecular biology from the Faculty of Medicine at the University of Calgary, was a freelance medical writer and journalist for 22 years and now is an independent investigative journalist. You can watch her June 15 interview on The Corbett Report, read her other Off-Guardian articles follow her on Twitter and read her website here.

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Activism, research, Testing, Viruses