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» LymeNet Flash » Questions and Discussion » Medical Questions » Serotonin

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Author Topic: Serotonin
Marnie
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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.

Posts: 9402 | From Sunshine State | Registered: Mar 2001  |  IP: Logged | Report this post to a Moderator
Marnie
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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).

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Razzle
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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?

--------------------
-Razzle
Lyme IgM IGeneX Pos. 18+++, 23-25+, 30++, 31+, 34++, 39 IND, 83-93 IND; IgG IGeneX Neg. 30+, 39 IND; Mayo/CDC Pos. IgM 23+, 39+; IgG Mayo/CDC Neg. band 41+; Bart. (clinical dx; Fry Labs neg. for all coinfections), sx >30 yrs.

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Marnie
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Go here to see a easy "picture" of tryptophan to serotonin to melatonin OR tryptophan ultimately to niacin.

https://en.wikipedia.org/wiki/Tryptophan

You will see KYN and Quin along the tryptophan to niacin pathway.

IDO (enzyme) promotes tryptophan to niacin imbalance.

Can't sleep:

http://webcache.googleusercontent.com/search?q=cache:diYmTXthCNoJ:https://umm.edu/health/medical/altmed/condition/insomnia

Lists supplements that may help. L-theanine...

Sirt1…modulates the activity of circadian clock in metabolic tissues.

http://abbs.oxfordjournals.org/content/45/1/51.full

It looks to be active.


http://www.ncbi.nlm.nih.gov/pubmed/25401748 2015

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

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Marnie
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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."

http://tinyurl.com/z634ma6


"the primordial *serotonin receptor
of the rhodopsin-GPCR family* may have first appeared more than 700-750 million years ago,"

http://link.springer.com/article/10.2165%2F00023210-199500041-00005

The 5-HT1A receptor is a subtype of 5-HT receptor that binds the endogenous neurotransmitter serotonin. Wikipedia

Thus, preliminary evidence from two different types of genetic animal models suggests that

anxiety-like behavior can arise if the 5-HT1A receptor function is

eliminated

or

overexpressed.

http://www.ncbi.nlm.nih.gov/pubmed/12775329

IF increased serotonin or its receptor (5-HT(1A)) is the key to all of this, how does it effect our body cells?

cAMP = Cyclic adenosine monophosphate = second messenger and Master Regulator of Innate Immune Cell Function.

Alterations in cAMP levels can profoundly influence the innate immune functions of phagocytes,

with increased cAMP generally

down-regulating

inflammatory mediator generation, phagocytosis, and microbial killing.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720142/


Melatonin increases cAMP.

http://www.ncbi.nlm.nih.gov/pubmed/16449637

Whereas:

Serotonin (5-HT) decreased cAMP levels,

PKA activity and ABCB mRNA expression

but

***increased the mRNA levels for a putative 5-HT1 receptor.***

Interestingly, 5-HT1 was also over-expressed after in vivo exposures to FX (fluoxetine = Prozac)

FX (Prozac)significantly decreased cAMP levels and PKA activity,

and induced ABCB mRNA down-regulation.

FX effects were abolished in the presence of PROP (propranolol).

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0061634

ABCB mRNA...

ABCB 1 encodes Pgp a glycoprotein that functions as a biological barrier by extruding toxins and xenobiotics out of cells.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0061634 and http://www.ncbi.nlm.nih.gov/pubmed/12489979

The 5HT1 receptor (increased by serotonin)increases dopamine release.

Dopamine activates D2-like/D4-subtype receptors in the photoreceptor layer,

leading to the inhibition of cAMP production, which results in the inhibition of melatonin synthesis.

http://www.ncbi.nlm.nih.gov/pubmed/16449637

Bb impacts the tryptophan -> serotonin -> melatonin route in favor of tryptophan -> KYN -> Quin -> niacin via an enzyme called IDO.

The normal balance is off.

"The tryptophan (TRP) to kynurenine (KYN) metabolic pathway is now firmly established as a key regulator of innate and adaptive immunity.

A plethora of preclinical models suggests that this

immune tolerance pathway – driven by the key and rate-limiting enzymes indoleamine-2,3-dioxygenase and TRP-2,3-dioxygenase –

is active in cancer immunity,
autoimmunity,
infection,
transplant rejection,
and allergy."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4290671/

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.

http://www.ncbi.nlm.nih.gov/pubmed/23337348

Uhm...cannabinoid...

serotonin 5-HT(2A) and 5-HT(2C) receptors and cannabinoid CB1 receptor demonstrate
inverse agonism


http://www.ncbi.nlm.nih.gov/pubmed/20691957

Cannabidiol (CBD) is a major, biologically active, but psycho-inactive component of

cannabis.

CBD acts as an agonist at the human 5-HT1a receptor as demonstrated in two related approaches.

http://tinyurl.com/hjyr7ff


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.

http://www.jimmunol.org/content/190/5/2301.abstract

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."

http://www.ncbi.nlm.nih.gov/pubmed/18404144

[ 12-13-2015, 11:26 AM: Message edited by: Marnie ]

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