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» LymeNet Flash » Questions and Discussion » Medical Questions » Dr. Davidson on TUDCA for lyme

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Author Topic: Dr. Davidson on TUDCA for lyme
Marnie
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TUDCA AND LYME DISEASE: THE LYMPHATIC CONNECTION

https://drjaydavidson.com/tudca-lyme-disease/

(TUDCA is a particular bile acid that contains taurine.)

The goal is to suppress a liver enzyme called CYP7A1. The inflammatory cytokines suppress CYP7A1.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC151029/

Backing way up:

The Western Fence lizard has something in its blood capable of destroying all forms of Bb.

It produces a LOT of rhodopsin – the active form is metarhodopsin II -which releases all-trans-retinal which is a potent
***suppressor of CYP7A1***

(a liver enzyme that converts cholesterol to bile acids)

Tauroursodeoxycholic acid binds to the G-protein site on light activated rhodopsin.

Exp Eye Res. 2018 May

Borrelia burgdorferi contains a lactate dehydrogenase gene

This subpathway is part of the pathway pyruvate fermentation to lactate, which is itself part of Fermentation.

https://www.uniprot.org/uniprot/B7J121

***In comparison, only LDH ( = lactate dehydrogenase )
activity was decreased by TUDCA treatment.***

https://www.jci.org/articles/view/18945

Problem...the vitamin D receptor (when it isn't available):

CYP7A1 is also up-regulated in VDR-* knockout* mice.

Berberine and bile acids -

https://bmccomplementalternmed.biomedcentral.com/articles/10.1186/s12906-016-1367-7

MS and TUDAC:

https://www.biorxiv.org/content/biorxiv/early/2019/05/07/627356.full.pdf

TUDAC is in trials for many diseases: Parkinson's, AD, etc.

Posts: 9371 | From Sunshine State | Registered: Mar 2001  |  IP: Logged | Report this post to a Moderator
Marnie
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Bb is dependent on Mn-SOD

https://www.ncbi.nlm.nih.gov/pubmed/22500025


Induction of MnSOD by ER Stress

https://www.researchgate.net/figure/Induction-of-MnSOD-by-ER-Stress-A-Expression-of-MnSOD-mRNA-HeLa-cells-were-treated_fig1_8406178

TUDAC alleviates ER stress

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5931650/

In summary, the data presented here suggest that TUDCA attenuates the

uptake of ox-LDL by macrophage

that is augmented under insulin resistant conditions.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3253999/

IR = insulin resistance

Bb has the p66 protein

https://www.uniprot.org/uniprot/H7C7N8

In conclusion, the protein p66Shc exerts an inhibitory effect on β-cell insulin signaling and can mediate the ability of SFAs and excess body fat to cause β-cell IR, which results in both reduced survival and impaired secretory function.

https://diabetes.diabetesjournals.org/content/68/Supplement_1/195-OR

p66 is physically associated with OspA.

https://books.google.com/books?id=L-cCqW4IVj0C&pg=PA244&lpg=PA244&dq=p66+protein+OspA&source=bl&ots=ZAKJqAXHV3&sig=ACfU3U2mLI3BVzm5C_VkDMu-se79bJjBvQ&hl=en&sa=X&ved=2ahUKEwitgM3G25 HjAhVimeAKHeLSDqk4ChDoATABegQIBhAB#v=onepage&q=p66%20protein%20OspA&f=false

SIRT1 represses the transcription of p66.

Upregulation of p66Shc in human ECs is linked to a significant reduction of the antioxidant enzyme SOD2, suggesting that p66Shc mediates mitochondrial ROS production and promotes downregulation of scavenging enzymes, leading to unopposed ROS accumulation in vascular ECs.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5824538/


TUDCA is available OTC. Brand most effective =? Dosage? I have it on order to hopefully treat diaphragm weakness - TUDCA apparently lowers cPLA2.

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Marnie
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Difference between men and women with regards to UDCA (women produce LESS bile acids):

Furthermore, the mean concentration of total bile acids was 51% higher in men than in women...

https://pdfs.semanticscholar.org/dac8/87c232e6f84869e21d94985ee86ba17c50da.pdf

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Marnie
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Women produce less bile salts from cholesterol due to estrogen and especially progesterone.

https://www.sciencedirect.com/science/article/pii/0039128X9490071X

When pregnant and progesterone levels are high and bile salts are low, a fetus is NOT protected from contracting lyme from his/her mother.

See detoxing here (including Dr. B's suggestion):


https://www.associationlymesansfrontieres.com/wp-content/uploads/TRansmission_sexuelle_placenta_lait.pdf

Cysteine converts to taurine.

Fellow researchers:

CsrABb (carbon storage regulator A protein) is required for the infectivity of B. burgdorferi.

https://iai.asm.org/content/79/3/1270?maxtoshow=&HITS=10&hits=60&RESULTFORMAT=1&andorexacttitle=and&andorexacttitleabs=and&fulltext=BioVision&andorexactfulltext=and&searchid=1&FIRS TINDEX=0&sortspec=match&fdate=12/1/2010&resourcetype=HWCIT

? OspA – Bb’s p66 she - which is inhibited by SIRT1

TUDCA upregulated SIRT1-FXR activity, which inhibited expression and acetylation of NF-κB and p53 and increased FoxM1 expression, leading to decreased inflammatory response and apoptosis and increased proliferative capacity in hepatocytes, and attenuation of liver injury.

https://www.ncbi.nlm.nih.gov/pubmed/30998645

The carbon storage regulator A (CsrA) is a protein responsible for the

repression of a variety of stationary-phase genes in bacteria.

CsrA negatively regulates gluconeogenesis, glycogen biosynthesis and catabolism, and biofilm formation (14, 23, 25).

Additionally, CsrA can activate glycolysis, acetate metabolism, and flagellum biosynthesis (25-27).

CsrA acts posttranscriptionally by repressing gene expression of essential enzymes in carbohydrate metabolism, like ADP-glucose pyrophosphorylase (glgC), glycogen synthase (glgA), glycogen branching enzyme (glgB), and glycogen phosphorylase (glgP).

CsrA destabilizes target mRNAs by binding in a region within the −18 and +31 nucleotides of the coding region, which includes the ribosome-binding site (18).

This prevents translation of the corresponding mRNA and promotes its degradation by endogenous RNases.

As a result, a decrease in the intracellular levels of the glycogen biosynthetic enzymes and decreased synthesis of intracellular glycogen are observed.

https://jb.asm.org/content/187/10/3496

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Marnie
Frequent Contributor (5K+ posts)
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p66Shc, a 66 kDa proto-oncogene Src

homologous-collagen homologue (Shc) adaptor protein,

is classically known in mediating receptor tyrosine kinase signaling and recently identified as

a sensor to oxidative stress-induced apoptosis and as a longevity protein in mammals.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909029/


Our findings indicate that expression and

activation of p66Shc

renders CNS cells more sensitive to Aβ toxicity by promoting mitochondrial OXPHOS and ROS production while

repressing aerobic glycolysis.

Thus, p66Shc may represent a potential therapeutically relevant target for the treatment of AD.

https://www.nature.com/articles/s41598-018-35114-y

Reactive oxygen species are required for driving efficient and sustained aerobic glycolysis

during CD4+ T cell activation.

https://www.ncbi.nlm.nih.gov/pubmed/28426686

Read also my post about autoimmunity triggered by Bb's OspA

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