What does the frequency of Light (432 Hz for Rifers), HBOT, the Western Fence Lizard (which can completely destroy Bb), and Prozac have in common?
PLEASE read my 12/8 post in the HBOT thread.
I fear this very critical information may not be read by everyone and it is so important.
God Bless. Miracles happen.
Posted by Marnie (Member # 773) on :
Antibiotic refractory lyme...need to watch closely the Treg (T regulatory) cell levels.
Our initial reaction (DC cells - OspA = Th17 cells - very proinflammatory) look to trigger the downregulation of Treg cells which might not be a good thing in some instances.
Too low...perhaps EBV is free to reign (reactivate).
Posted by Razzle (Member # 30398) on :
I was under the impression that Lyme creates quinolinic acid in the brain from tryptophan.
Is this true? If so, then would supplementing tryptophan or melatonin be counter-productive for helping a Lyme patient with severe insomnia?
Posted by Marnie (Member # 773) on :
Go here to see a easy "picture" of tryptophan to serotonin to melatonin OR tryptophan ultimately to niacin.
Cytochrome C *from* mitochondria to cytosol may help Bb if it is "camped out" there.
Because:
***Cytochrome c nitrite reductase ***
is a bacterial enzyme that catalyzes the six electron reduction of nitrite to ammonia; an important step in the biological nitrogen cycle.
The enzyme catalyses the second step in the two step conversion of
nitrate to ammonia,
which allows certain bacteria to use nitrite as a terminal electron acceptor, rather than oxygen, during anaerobic conditions.
Wikipedia
Posted by Marnie (Member # 773) on :
Since 2008, I've been under the belief that the Western Fence Lizard's rhodopsin level (high in eye rods to help the WFL see at night)maybe the key protein that was capable of destroying Bb.
Now I see another connection:
"a rhodopsin-based model of 5-HT(1A) serotonin receptor."
While Minocycline and Berberine DO look to impact the KYN pathway...the "flip" side is to instead increase serotonin -> 5HT1 receptors -> dopamine receptors -> inhibition of cAMP raising Melatonin.
Repeating from above...
with ***increased cAMP*** generally
down-regulating
inflammatory mediator generation, phagocytosis, and microbial killing.
Back to the beginning...
"a rhodopsin-based model of 5-HT(1A) serotonin receptor."
DHA prevents altered 5-HT1A, 5-HT2A, CB1 and GABAA receptor binding densities in the brain of male rats fed a high-saturated-fat diet.
An inverse agonist is an agent that binds to the same receptor as an agonist but induces a pharmacological response opposite to that agonist . The above “reminds” me of M2a and M2c macrophages which are upregulated by HBOT and M1 downregulated.
In fact...regarding M2 macrophages:
5HT (serotonin) inhibited the LPS-induced release of proinflammatory cytokines without affecting IL-10 production, upregulated the expression of M2 polarization–associated genes (SERPINB2, THBS1, STAB1, COL23A1),
and reduced the expression of M1-associated genes (INHBA, CCR2, MMP12, SERPINE1, CD1B, ALDH1A2).
Therefore, 5HT modulates macrophage polarization and contributes to the maintenance of an
anti-inflammatory state via 5HT2B and 5HT7,
whose identification as functionally relevant markers for anti-inflammatory/homeostatic human M2 macrophages suggests their potential therapeutic value in inflammatory pathologies.
It is important that you know serotonin is not only produced in the brain.
Approximately 90% of the human body's total serotonin is located in the enterochromaffin cells in the GI tract, where it is used to regulate intestinal movements.
But the 5-HT1A receptor appears to regulate gastric tone in humans.
Thus genetically determined levels/otherwise low levels of 5-HT1A could impact GI tone.
"Migraine, fibromyalgia, IBS and related conditions display common clinical, biochemical and pathophysiological patterns that suggest an underlying clinical endocannabinoid deficiency that may be suitably treated with cannabinoid medicines."