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Stevia V Lyme Disease

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    Posted: July 11 2017 at 4:20am
It appears that stevia extract treats lyme disease far better than any of the official antibiotics.

For those of you who want to find out more about this, and avoid all the loony anti-allopathy sites, this was the actual study:  http://www.ncbi.nlm.nih.gov/pubmed/26716015.  

I would not drop the doxycycline or amoxicillin (standard treatment) if it were me, but would simply use the stevia as an adjuvant (supporting treatment).  Although, studying the images of treated cultures and the apparent amazing effectiveness of the stevia,  it would appear that the adjuvant should be the antibiotics and the main treatment the stevia.  Either way, the two together seem to be by far the best option.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote FluMom Quote  Post ReplyReply Direct Link To This Post Posted: July 11 2017 at 7:13pm
Read the article but how much Stevia do you need to take per day? I think this is a great piece of information that we need to post somewhere if TSHTF it is an alternative if people are out in the woods and get Lyme.

So all you smart computer kids post this somewhere on this site where people can see it and use it if necessary.

Again any of you medical people can you tell us how much Stevia to take per day?
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Technophobe Quote  Post ReplyReply Direct Link To This Post Posted: July 12 2017 at 3:02am
The study did not approach that question, so all I can give you is an educated guess.   

The amount of stevia which produced an effect was 10 microgrames in a mililitre of water.   That equates to 10 milligrammes per litre.  We have 4 litres of water in our bodies (approximately) so that works out at 40 miligrammes in our blood to be an equivalent dose.  The most important missing bit of information is the length of time stevia stays in the bloodstream.  We just do not know that.  Even then there are a few guesses still remaining, like what ways does the bacterium differ in its behavior between our bodies and the petri dish, and what ways do other substances in our bodies modify stevia's behavior.

Assuming the answer to the last two questions is: "not much!" and the answer to the first is more than 6 hours (not such a big guess as most drugs stay over 6) then getting used to very sweet coffee should be sufficient.  

I do not (to my knowledge) have lyme disease, but I do have arthritis.  3 stevia in my coffee 3+ times a day have made a huge improvement to my pain and mobility levels.  The worst joint was replaced, but ALL THE REST HAVE RETURNED TO NORMAL WITHOUT ANY OTHER DRUGS.  I can neither give you official dosages nor offer any guarantees that my problems were bacterial in origin.  But that is my best guess.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote 1NiceGuy Quote  Post ReplyReply Direct Link To This Post Posted: August 01 2017 at 10:52am
So here's the question, is it's effectiveness based on disrupting the bio-film or is it patheogen specific?
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Technophobe Quote  Post ReplyReply Direct Link To This Post Posted: August 01 2017 at 11:16am
Once again, that question was not even asked, let alone answered.

I do not have anywhere near enough medical/scientific knowledge to speculate on that, you might just as well use a crystal ball.  From the point of view of alliopathy, it would be irrelevant, as the clinical result would be the same.  From a scientific standpoint; WOW what a good question!

So here goes with the unscientific speculation. 

Biofilm or not?  -I am clueless!  Hubby (WillowbyBrat) thinks that it penetrates or disrupts the biofilm which explains its positive effect on osteoarthritis.

Pathogen specific?  -I do not think so, though it may be bacteriocidal to varying degrees on other pathogens.  The loony sites claim it treats everything, even cancer!  Although that is demonstrably untrue, it probably points to other areas of (probably quite limited) effect. 

All this amounts to it being a brilliant adjunctive to almost any antimicrobial treatments.  After all, at its best it probably assists - to varying degrees - any alliopathic antimicrobial treatments.  At its worst it does no harm.  Hypocrates would rest in peace.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Technophobe Quote  Post ReplyReply Direct Link To This Post Posted: January 27 2019 at 4:36am

I found out which antibiotics are used for lyme, FluMom. Doxycycline (21 days @ 100mg BD*) and amoxicillin (21 days @ 1g** 3X PD*) for first line attack.

Azithromycin (17 days @ 500mg PD) and ceftriaxone (21 days @ 2g BD) for a backstop if the first line fails. Ceftriaxone is administered by IV there is no oral route.

The BMJ recommendations are here:   https://www.bmj.com/content/bmj/suppl/2018/04/12/bmj.k1261.DC1/crum090318.wi.pdf

Bearing the information on stevia in mind, a good dose of that would accompany the course, of course.






*BD = twice a day and PD = "per day" or "daily"
**1g = 1000mg
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[But that may still be only half the story..........]

New Scan Technique Reveals Brain Inflammation Associated with Post-Treatment Lyme disease Syndrome
02/04/2019

A radiotracer (that binds to a marker of inflammation) shows elevation of the chemical marker in the brain scans of 12 participants with post-treatment Lyme disease syndrome, compared to 19 healthy control participants. Credit: Coughlin et al, Journal of Neuroinflammation, 2018

More than 1 in 10 people successfully treated with antibiotics for Lyme disease go on to develop chronic, sometimes debilitating, and poorly understood symptoms of fatigue and brain fog that may last for years after their initial infection has cleared up. Now, in a small study, Johns Hopkins Medicine researchers report they have used an advanced form of brain scan to show that 12 people with documented post-treatment Lyme disease syndrome (PTLDS) all show elevation of a chemical marker of widespread brain inflammation, compared with 19 healthy controls.

Results of the study, published in Journal of Neuroinflammation, suggest new avenues for treating the long-term fatigue, pain, sleep disruption and “brain fog” associated with PTLDS, the researchers say.

“There’s been literature suggesting that patients with PTLDS have some chronic inflammation somewhere, but until now we weren’t able to safely probe the brain itself to verify it,” says Jennifer Coughlin, M.D., associate professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine, and one of the first authors of the study report.

A radiotracer (that binds to a marker of inflammation) shows elevation of the chemical marker in the brain scans of 12 participants with post-treatment Lyme disease syndrome, compared to 19 healthy control participants.
Credit: Coughlin et al, Journal of Neuroinflammation, 2018

Lyme disease is a bacterial infection transmitted to humans through tick bites. An estimated 300,000 people in the U.S. are diagnosed with Lyme disease each year, and their infections can be successfully treated with antibiotics. Doctors diagnose PTLDS if treated patients report fatigue and brain fog for at least six months after treatment. Little is known about what causes PTLDS or how to treat it, and while studies have shown that people with PTLDS have elevated markers of inflammation—such as the chemokine CCL19—in their bloodstreams, it has not been clear where that inflammation may be occurring.

Over the last decade, Coughlin and her colleagues optimized a positron emission tomography (PET) imaging technique in which specially labeled molecules—or radiotracers—bind to a protein called translocator protein (TSPO). In the brain, TSPO is released primarily by two types of brain immune cells—microglia and astrocytes—so levels of TSPO are higher when brain inflammation is present.

With this type of PET scan, Coughlin’s team says it can visualize levels of TSPO—and therefore levels of inflammation, or astrocyte and microglia activation—throughout the brain. They’ve used it previously to see inflammation in the brains of former NFL players as well as to study brain inflammation in autoimmune diseases such as lupus.

In the new study, Coughlin’s group teamed up with Johns Hopkins Lyme disease researchers and compared PET scans of 12 patients with a diagnosis of PTLDS and 19 without. The PTLDS patients all had a history of confirmed or probable Lyme disease infection, documented evidence of treatment and no history of diagnosed depression. All had reported the presence of fatigue and at least one cognitive deficit such as problems with memory or concentration.

Controls and cases were all adult men (18) and women (13) over age 18 and did not differ significantly in age or body mass index (BMI).

The scans revealed that across eight different regions of the brain, PTLDS patients had significantly higher levels of TSPO compared with controls. On average, when all brain regions were combined and the data was adjusted for genotype, brain region, age and BMI, there was a mean difference of 0.58 between the TSPO levels of controls and patients with PTLDS.

“We thought there might be certain brain regions that would be more vulnerable to inflammation and would be selectively affected, but it really looks like widespread inflammation all across the brain,” says Coughlin.

The Johns Hopkins team cautioned that their study was small, and whether or not the results apply to all people with post-treatment Lyme disease syndrome—such as those with chronic pain but not cognitive symptoms—must await far larger and broader studies. In addition, the current study did not include people who recovered from Lyme disease and did not develop PTLDS, a key control group. But for now, the researchers hope their results give PTLDS patients some hope that the science of PTLDS is advancing.

“What this study does is provide evidence that the brain fog in patients with post-treatment Lyme disease syndrome has a physiological basis and isn’t just psychosomatic or related to depression or anxiety,” says John Aucott, M.D., a senior author of the new paper, associate professor of medicine at the Johns Hopkins University School of Medicine, and director of the Johns Hopkins Lyme Disease Research Center.

In addition, Aucott says, the results suggest that drugs designed to curb neuroinflammation may be able to treat PTLDS, although clinical trials are needed first to determine the safety and benefit of such therapy. Future variations of the PET scan may be able to narrow down more specifically which subsets of microglia and astrocytes are activated, helping guide drug development further, he added.

Other senior authors on the paper were professor of medicine Mark Soloski, Ph.D., and professor of radiology Martin Pomper, M.D., Ph.D., at the Johns Hopkins University School of Medicine.

Other authors on the paper include Ting Yang, Alison Rebman, Kathleen Bechtold, Yong Du, William Mathews, Wojciech Lesniak, Erica Mihm, Sarah Frey, Erica Marshall, Hailey Rosenthal and Robert Dannals of the Johns Hopkins University School of Medicine, and Tristan Reekie and Michael Kassiou of the University of Sydney.

This work was supported by a Johns Hopkins Discovery Award, the Alexander Wilson Schweizer Fellowship, a Johns Hopkins Doris Duke Foundation Early Clinician Investigator Award, the National Institutes of Health under grant number EB024495 and the Steven and Alexandra Cohen Foundation.

The authors had no competing interests to declare.

Source:   https://www.hopkinsmedicine.org/news/newsroom/news-releases/new-scan-technique-reveals-brain-inflammation-associated-with-post-treatment-lyme-disease-syndrome
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