Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Me...yes, for real.
Okay now, but very, very scary. I too have a lot of ongoing inflammation and a chronic infection that triggered left ventricle failure. Thank God our firemen (1st on the scene) knew to give me an immediate CPAP treatment. They literally saved my life.
Like many of you, antibiotics have failed me.
I am meeting with a Duke infectious disease doctor tomorrow and while writing my history tonight regarding my fight with this pathogen the past 10 years ...
for one reason or another I cam across this:
Polydatin AND nicotinamide to combat Cpn’s
mitochondrial dysfunction
and this:
Mitochondrial dysfunction, iron accumulation, lipid peroxidation, and inflammasome activation in cellular models derived from patients with multiple sclerosis.
Polydatin prevents angiotensin II-induced cardiac hypertrophy and myocardial superoxide generation
So while our infections (Cpn and Bb) share SOD2, they both cause mitochondrial dysfunction so I wanted to let you know about these supplements available on Amazon. Polydatin comes from reservatrol the second from B3.
Whatever you do, PLEASE discuss this with your doctor first and make sure it will not interact negatively with anything else you are taking - Rxs and supplements.
I now have enough supplements to open my own vitamin store. Amazon loves me. Those of you who know me, know I research a LOT before trying anything.
God Bless. Keep the faith. We will, with His help, find a CURE.
[ 08-19-2025, 09:24 AM: Message edited by: hiker53 ]
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Bartenderbonnie
Frequent Contributor (1K+ posts)
Member # 49177
posted
Sorry to hear Marnie, sounds so scary.
I learn so much from your research so I appreciate your posts, thank you.
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
While Bb does not use iron to replicate, it is an essential nutrient in Bb’s Lux S biofilm for protection and quorum sensing. Sorta like talking in a tight group.
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Bartenderbonnie
Frequent Contributor (1K+ posts)
Member # 49177
posted
Marnie You mentioned mitochondria dysfunction and Dr Richard Horowitz just posted about this on his substack.
(Dr Richard Horowitz’s practice is closed now so I hope I can finally post his name).
“ Mitochondrial dysfunction in the heart can lead to various cardiac conditions, including conduction defects, cardiovascular disease, cardiomyopathy (an enlargement of the heart that leads to poor cardiac output and congestive heart failure), and atherosclerosis.”
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
I have more...a lot more and it is a blockbuster! Copy this and give it to your LLMDs!
Polydatin (from reservatrol) AND nicotinamide (from B3) to combat Cpn’s mitochondrial dysfunction induction
and combat respiratory distress. They are available on Amazon and are not costly.
Hum…
“In vivo blockade of the pentose phosphate pathway using the G6PD inhibitor polydatin
reversed this metabolic state, shifting towards
glycolysis (= 2 ATP) ,
***oxidative phosphorylation (=36 ATP), ***
and fatty acid synthesis.
This change resulted in a functional shift characterized by
decreased IL-17 (from infected mast cells releasing histamine - triggering adrenaline release and histamine triggering Th17 cells to release IL-17) and
increased IFN-γ production.” (= Th1 pathway “on”, not Th2 or causing a Treg/IL17 imbalance)
ATP5A1 and SOD2 are reportedly involved in mitochondrial dysfunction.
ATP5A1 is a gene that encodes the alpha subunit of the mitochondrial ATP synthase, also known as Complex V. This protein is a crucial component of the enzyme that generates ATP, the primary energy currency of cells, through a process called oxidative phosphorylation
Both Chlamydia pneumoniae and borrelia burgdorferi have SOD2 = MnSOD to protect themselves from free radical damage. It is manganese superoxide dismutase.
MnSOD/SOD2 is present in our own mitochondria.
We also have SOD1 and SOD3. They are all located in different areas of the cells. SOD1 is in the cytosol. SOD3 is in the extracellular space, particularly in blood vessels and other tissues.
Mitochondrial dysfunction, iron accumulation, lipid peroxidation, and inflammasome activation in cellular models derived from patients with multiple sclerosis.
(Chlamydia pneumoniae believed to be the MS trigger in susceptible persons.)
Ferroptosis triggers airway inflammation in asthma. Ferroptosis is a regulatory cell death characterized by
intracellular iron accumulation and lipid peroxidation (proteins damaged by free oxygen radicals) that leads to oxidative stress.
The pentose phosphate pathway takes place in the cytosol of the cell (which is where many intracellular pathogens reside.)
The purpose of the pentose phosphate pathway is mainly to produce NADPH and ribose-5-phosphate.
The pathway also helps detoxify oxidative stress within the cell (by producing NADPH), and generates ATP.
The pentose phosphate pathway (PPP) is a metabolic pathway that exists in Borrelia burgdorferi, the bacterium responsible for Lyme disease,
although it's not a central pathway for ATP production in this organism.
B. burgdorferi primarily relies on glycolysis for ATP generation and utilizes the PPP to produce NADPH
and ribose 5-phosphate.
the bacterium that causes Lyme disease,is not known to produce its own ATP5A1 protein or to be directly related to the human ATP5A1 gene. However, research suggests that B. burgdorferi may affect mitochondrial function, potentially impacting ATP production in infected cells, The pentose phosphate pathway (PPP) is a metabolic pathway that plays a crucial role in both host cells and the bacterial pathogen Chlamydia
pneumoniae
It is possible that C. pneumoniae employs different strategies to manipulate host cell ATP production depending on the stage of the infection cycle
it may rely more on host mitochondrial ATP at the early stages of infection,
and later utilize its own energy production mechanisms, possibly through a sodium gradient-based system...such as Na out, K in!!!
Chlamydia pneumoniae, like other Chlamydiaceae, possesses genes for a respiratory chain that appears to utilize a sodium gradient for ATP synthesis.
Bottom line…both Cpn and Bb use the PPP which is inhibited by polydatin.
BUT by adding nicotinamide = supplying the precursor to NAD+, which can be converted to NADP+ and subsequently NADPH which detoxifies oxidative stress.
Thus NAD is available
but ribose 5-phosphate is *not* available
as the building block for RNA and DNA. It is a pentose sugar.
Normally Thiamine increases ribose-5-phosphate and NADPH. Thiamine is so important that...
C. pneumoniae must acquire thiamine from its host cell, likely through transporter systems designed to scavenge needed molecules from the host environment.
RpiA in C. pneumoniae, catalyzes the reversible conversion between ribose-5-phosphate and ribulose-5-phosphate. This reaction is critical for the non-oxidative phase of the PPP, which is involved in generating R5P
B. burgdorferi does not use thiamine, a cofactor used by many other organisms, but instead
relies on lactate dehydrogenase
to convert pyruvate to lactate and maintain a proper NADH/NAD+ ratio.
But…
Borrelia burgdorferi, the bacterium that causes Lyme disease, relies on ribose-5-phosphate (R5P) for its survival and metabolism,
particularly within the pentose phosphate pathway (PPP).
So both need the 5 carbon sugar R5P and both cause mitochondrial dysfunction and both use MnSOD.
But we might be able to knock them out via 2 eadily available supplements.
BTW...this ties into cancer also.
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
If you genetically are deficient in IgA, it is very important you take additional zinc and vitamin A. It is a fairly common genetic problem. R5P (the sugar!) has a supporting role in B cells -> IgA. Be very careful if you need a blood transfusion. Warn the staff. You can be tested for low IgA which, if low , may hinder your recovery.
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
SIRT3 is playing a part in both C pneumoniae and Bb infections- that cell signal/response apparently is low. Nicotinamide and polydatin look to raise SIRT3. Ialso read adding vitamin E along with nicotinamide and polydatin makes for an even better response (need less). I’ve taken my first dose today at 4pm eastern time. I will let you know how it impacts me.
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