If HBOT can knock off that nasty virus, it can surely knock off others...HHV6-A (we acquire as an adult) and EBV reactivated - both linked to MS - and possibly CMV reactivation.
***PGE2 inhibits bacterial killing
and ROI production***
by AM by impairing Fcγ-mediated phagocytosis
through its ability to
stimulate the production of intracellular cyclic adenosine monophosphate (cAMP)
effectors via EP2 and EP4 receptors signaling.
…with HBO therapy (100% O2 @ 1.8-2.0 ATA); whereas levels of prostaglandin E2 and cyclo-oxygenase-2 mRNA are markedly reduced.
PGE2 = up goes cAMP. Berberine and serotonin lower cAMP.
(It is not serotonin that is "protective"...it is the serotonin RECEPTORS that modulate PGE2 when PGE2 is overexpressed. 5HT1A - rhodopsin-based model of 5-HT(1A) serotonin receptor. 5-HT(1A) receptor is a metabotropic G protein-coupled receptor linked to the
G(i/o) signaling pathway.)
***B. burgdorferi-induced expression of mRNA encoding two PGE2 receptors,***
Looks like Bb loves (and needs?) PGE2.
How are macrophages going to polarize to M2 if Bb steals/binds to PGE2?
HBOT upregulates M2a and M2c macrophages (anti-inflammatory) which are down in SLE too.
M2b is up and it is proinflammatory like Th1 cells.
That macrophage (M2b) is linked to SLE.
[ 12-17-2015, 02:43 PM: Message edited by: Marnie ]
Posts: 9432 | From Sunshine State | Registered: Mar 2001
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Jordana
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posted
Marnie, I'm sorry but I have no comprehension of what you said. It seems like what you're saying is that if you can up regulate these macrophages then you can bypass Bb.
But the paper you linked to has to do with the inhibition of prostaglandins, and serotonin as a pro-inflammatory neurotransmitter.
Lost. Prozac will not solve Lyme and I believe HBOT works according to an entirely different mechanism than you describe.
Posts: 2057 | From Florida | Registered: Feb 2015
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
I am hoping researchers may take note and they, in turn, will apply this knowledge (from legit internet sources) to help CLD patients.
I do realize many lyme patients, but not all, are effected neurologically. It is likely his/her genetics play a part, but could, of course, depend on the STRAIN of Bb.
Jordana...
"But the paper you linked to has to do with the inhibition of prostaglandins, and serotonin as a pro-inflammatory neurotransmitter"
Not accurate - HBOT and PGE2 as linked in my post says:
Glycogen synthase kinase (GSK) 3β is an indispensable
***regulator of the oxidative stress response.***
Know what else is a GSK-3B inhibitor?
These findings show that
5-HT1A *receptor* activation
stimulates mitochondrial movement in hippocampal neurons by inhibiting GSK3beta activity via Akt.
Our findings suggest that 5-HT may
mediate the redistribution of energy sources within responsive neurons,
a possibility that has significant implications for understanding the global biological effects of this important neuromodulator.
Axonal ***transport of mitochondria*** is critical for proper neuronal function.
However, little is known about the extracellular signals that regulate this process.
In the present study, we show that the neuromodulator serotonin (5-HT) greatly enhances mitochondrial movement in the axons of rat hippocampal neurons in vitro.
Administration of a 5-HT1A receptor *antagonist* inhibited mitochondrial movement,
whereas addition of fluoxetine (Prozac), a selective serotonin reuptake inhibitor,
promoted mitochondrial movement.
5-HT *receptors* are known to activate the Akt/Protein kinase B pathway.
Consistent with this, directional mitochondrial movement was almost completely blocked by a specific Akt inhibitor.
Moreover,
***an inhibitor of glycogen synthase kinase-3beta (GSK3beta),
a kinase whose activity is blocked by Akt-mediated phosphorylation,
promoted mitochondrial movement.***
>>> THIS <<<
These findings show that 5-HT1A receptor activation
stimulates
mitochondrial movement
in hippocampal neurons by
***inhibiting GSK3beta*** activity via Akt.
Our findings suggest that
5-HT may
mediate the redistribution of energy sources within responsive neurons,
a possibility that has significant implications for understanding the global biological effects of this important neuromodulator.
Senescence = no longer capable of dividing but still alive and metabolically active.
Bb triggers excessive inflammation - the Th2 M2 macrophages (M2a and M2c) are anti-inflammatory while Th1 M1 macrophages and M2b are inflammatory.
A long time ago, Romanian doctors cured lyme by giving lots of IV Mg (anti-inflammatory, anti-histamine and inhibits HMGCoA reductase (works like statin drugs) AND IV abx. Mg also inhibits Mn absorption in the gut.
So a big part of curing lyme involves getting inflammation down while still hitting Bb...via upregulating M2a and M2c PLUS increasing ROI and ROS via inhibiting GSK3b (the oxidative stress regulator).
BTW...in bipolar disease the persons have a problem with GSK3b (upregulated - too much) and lithium is a selective inhibitor of GSK3β! Lithium is VERY protective.
So if you don't want to/can't go the SSRI route, that would be a potential alternative.
I believe genetic predispositions + inflections trigger a LOT of diseases...BD,AD,MS...
MOA breaks down serotonin, norepinephrine and dopamine.
Genetics:
Allelic variation in the HTR2A gene has been reported to affect response to selective serotonin reuptake inhibitors (SSRI) and
risk for adverse drug reactions.
Patients predicted to respond poorly to SSRIs due to polymorphic variants in the
HTR2A/2C serotonin receptors
may be considered for switching to non-SSRI antidepressants.
Treatment with antipsychotics results in significant weight gain (2-3 kg/m[2]) in some patients. Weight gain has been positively correlated with a polymorphism in the promoter of HTR2C (-759C)."
My son's adverse reaction to Prozac (more depressed) and weight gain on Lamictal!
Our antibodies to OspA = IgG1k and to OspB = IgG1.
While OspC type A is the "virulence factor".
Virulence = The ability of an agent of infection to produce disease.
Bb throws off the tryptophan -> serotonin -> melatonin balance ***in favor of*** IDO (enzyme) which causes tryptophan -> KYN -> Quin -> niacin.
For its own benefit.
It has been shown that IDO permits tumor cells to escape the immune system by depletion of L-Trp in the microenvironment of cells.
A wide range of human cancers such as prostatic, colorectal, pancreatic, cervical, gastric, ovarian, head, lung, etc. overexpress human IDO (hIDO). Wikipedia
[ 12-18-2015, 03:48 PM: Message edited by: Marnie ]
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Jordana
Frequent Contributor (1K+ posts)
Member # 45305
posted
Well...
"However, little is known about the extracellular signals that regulate this process. "
I think that's right. Serotonin is very complex and has a multitude of feedback systems and interdependent processes in the body that we don't understand. I mean *no one* understands it. I think neurotransmitters are fascinating but all those Prozac prescriptions in the 90's were irresponsible medicine -- not even doctors knew all the mechanisms of action.
I believe you are right about estrogen but that's because estrogen is hugely inflammatory and is present in every inflammatory process as it is a hormonal signal accompanying shock. Any disease is made worse by estrogen -- anyone with chronic illness should get hormone testing ( or buy it off the internet) and STILL take measures to reduce/antagonize estrogen.
The rest of this -- your argument about cancer for example -- are not really relevant here.
I think HBOT simply changes the environment for certain pathogens to the point that they are no longer interested in being in the host they are in. Betting on one neurotransmitter to simulate HBOT is kind of a stretch; because what you're saying is that HBOT ameliorates disease through the manipulation of serotonin.
In fact since it effects the exchange of oxygen and CO2 my thinking is that what it signals to pathogens is that the host is dying or is not the same species it used to be.
In a way I hope you're right, because people could just eat this drug you mention and get better. I'm skeptical and don't believe in the Magic of Serotonin.
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I got bit by a tick when I was in my early teens. One of my first symptoms was severe depression and anxiety. Lyme was not really on the radar then so I was put on one SSRI antidepressant after another. They didn't really help my depression and they certainly didn't heal my Lyme or halt the disease progression.
I have seen an occasional tendency on Lyme forums for people to go out on these tenuous theoretical limbs, generally in the realm of genetics and biochemistry. I think the general key to getting better is KISS. Test different treatments and continue the ones that make you herx and need to detox a lot. Lather, rinse, repeat.
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Marnie
Frequent Contributor (5K+ posts)
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posted
It is not serotonin!!!
It IS a very specific serotonin *receptor* that is needed;
5-HT1A receptor
Anyone live in Colorado? :-)
Project...
"Patients predicted to respond poorly to SSRIs due to polymorphic variants in the
HTR2A/2C serotonin receptors
may be considered for switching to non-SSRI antidepressants."
Lyme can progress to other life threatening diseases.
Is herxing necessary? Do persons doing JUST HBOT experience a herx response?
Trying to find a KISS (keep it simple stupid) - SAFE and EFFECTIVE treatment for an extremely complex pathogen that effects everyone differently based on their genetics is an enormous task.
Testing different treatments without being aware of and weighing their potential downsides based on one's own genetic profile is not a good idea.
The more knowledge one has (of self), the better decisions one can make.
Translation...tick saliva protein adds sulfate to E2 (major estrogen) = E2-S and this prevents it from locking onto its receptor -> NFkB not properly regulated and inflammation is up.
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Repeating...
Translation...tick saliva protein adds sulfate to E2 (major estrogen) = E2-S and
this ***prevents it from locking onto its receptor*** -> NFkB not properly regulated and inflammation is up.
Estrogen receptor alpha (ER-α), also known as NR3A1 (nuclear receptor subfamily 3, group A, member 1),
is one of two main types of estrogen receptor, a nuclear receptor that is activated by the sex hormone estrogen.
In humans, ER-α is encoded by the gene ESR1 (EStrogen Receptor 1).
***Estrogen receptor alpha has been shown to interact with BRCA1*** (a tumor suppressor gene IF it is not defective) et al. Wikipedia.
Here we report that ***estrogen can up-regulate the expression of the serotonin-1A receptor*** via a new mechanism involving
synergistic activation by nuclear factor-κB (NF-κB)
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