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Increasing MAO-A gene expression, and reducing Serotonin

mao-a mao maoi serotonin dopamine

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#1 BioInfinite

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Posted 11 November 2014 - 12:51 PM


This is very unusual I'm sure, but I really need some help. 

 

Does anyone know any way to increase expression of the MAO-A gene?

I basically need to deaminate more serotonin for this reason:

 

In 2012 I was taking 600mg daily of Moclobemide, and when I tried to quit it I was out of my mind in mental pain, so I was also using Tryptophan, which ended up resulting in Serotonin Syndrome. Very stupid I know.

 

Since then it's been a long hard road to recovery and I've had multiple set backs, the last one was yesterday when I had about 1/8th of a teaspoon of propolis/honey mixture. It feels like serotonin toxicity all over again (like an MDMA comedown but with panic attacks). Is it possible that past MAO inhibition is resulting in reduced ability to produce it? Also I read that stress reduces its production, and I'm very stressed.

 

I've been managing to a degree with Seroquel, but I'm already at max dose and its not enough. The only other one I can have is risperidone, and it's not as sedating. I've talked to my psych and she says thats all there is on offer. I can't have olanzapine or aripiprazole.

 

I would be open to any other ways you know of to reduce serotonin brain levels. 

 

Thank you



#2 Muad'Dib

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Posted 13 November 2014 - 10:19 AM

Check out this links.

 

Ovarian steroid regulation of monoamine oxidase-A and B mRNAs in the macaque dorsal raphe and hypothalamic nuclei

http://link.springer...0213-001-0959-0

 

Tissue-specific effects of estrogen on monoamine oxidase A and B in the rat

http://www.ncbi.nlm....4?dopt=Citation



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#3 Galaxyshock

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Posted 13 November 2014 - 07:46 PM

Tianeptine is a serotonin reuptake enhancer.

 

Shilajit decreases serotonin levels.

"The biochemical studies indicated that acute treatment with Shilajit had insignificant effects on rat brain monoamine and monoamine metabolite levels. However, following subacute (5days) treatment, there was decrease in 5-hydroxytryptamine and 5-hydroxyindole acetic acid concentrations and an increase in the levels of dopamine, homovanillic acid and 3.4-dihydroxyphenyl-acetic acid concentrations, with insignificant effects on noradrenaline and 3-methoxy-4- hydroxyphenylethylene glycol levels. The observed neurochemical effects induced by Shilajit, indicating a decrease in rat brain 5-hydroxytryptamine turnover, associated with an increase in dopaminergic activity, helps to explain the observed nootropic and anxiolytic effects of the drug. "

http://www.ijp-onlin...=Jaiswal;type=0

 

Apigenin and luteolin act as monoamine transporter activators leading to decrease in monoamine contents including serotonin.

"Thus, luteolin and apigenin function as monoamine transporter activators, which would improve several hypermonoaminergic neuropsychological disorders, especially cocaine dependence, through up-regulating monoamine transporter activity."

http://www.ncbi.nlm....pubmed/19815045

Drinking strong chamomile tea will provide you these flavonoids.



#4 Flex

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Posted 15 November 2014 - 12:29 AM

Wouldnt too much mao-a lead to an increase of oxidative damage to the Cells/Synapses ?

 

Propolis has several effects in the brain e.g.

 

Novel Antidepressant-Like Activity of Propolis Extract Mediated by Enhanced Glucocorticoid Receptor Function in the Hippocampus

http://www.hindawi.c...am/2013/217853/

 

So maybe a de-regulation of the HPA axis could be responsible for that.

I would try Passionflower extract or small doses of 5-htp to be certain that 5-htp is the problem.

 

Anyway, You could perhaps also try this besides Apigenin/Luteolin:

 

Feverfew (Tanacetum parthenium L.): A systematic review

http://www.ncbi.nlm....les/PMC3210009/

 

Extracts of feverfew inhibit platelet 5-HT secretion via neutralization of sulfhydryl groups inside or outside the cell. The sesquiterpenes in feverfew contain the alpha-methylenebutyrolactone unit capable of reacting with sulfhydryl groups.

Feverfew extracts are not only potent inhibitors of serotonin release from platelets but also of polymorphonuclear leukocyte granules, providing a possible connection between the claimed benefit of feverfew in migraines and arthritis

 

But, since You´re using Seroquel, You "should" have allready inhibited the more problematic 5-ht receptors ( 5-ht2a/c)

unless its related to other receptors.


Edited by Flex, 15 November 2014 - 12:52 AM.


#5 StevesPetRat

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Posted 15 November 2014 - 09:39 AM

You could try sleep deprivation to lower your sensitivity to serotonin.

Doesn't sound pleasant to me, having spent so much of the past year in that state, but desperate times and all that...

 



#6 Galaxyshock

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Posted 15 November 2014 - 12:44 PM

Valproic Acid Induces Monoamine Oxidase A via Akt/Forkhead Box O1 Activation

http://www.ncbi.nlm....les/PMC3187529/


Edited by Galaxyshock, 15 November 2014 - 12:44 PM.


#7 Flex

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Posted 08 April 2015 - 09:18 PM

@ Bioinfinite

 

You could try to increase autoinhibition via (presynaptic) 5-ht1a activation and/or to increase 5-htt ( Serotonin transporter) expression.

or (very experimentally) to decrease miR-16. Dont ask me how to inhibits this and the consequences (!),

maybe theres an abstract out there which states that a medicament/herb/compound or HDAC inhibitor is capable to do so..

 

miR-16 targets the serotonin transporter: a new facet for adaptive responses to antidepressants.

http://www.ncbi.nlm....pubmed/20847275

 

See my post #22:

Natural 5-HT1A Agonists/Antagonists (PSSD,and Cognitive Function)

http://www.longecity...on/#entry722358

 

and for perhaps some further suggestion, look into PSSD forums and search for ways how some were able to decrease their perresistent increase in Serotonine like one case with Liquorice(!?):

pssdforum

http://www.pssdforum...ewforum.php?f=5

 


Edited by Flex, 08 April 2015 - 09:19 PM.


#8 BioInfinite

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Posted 24 April 2015 - 10:05 AM

@Flex Thank you very much for the updates, I am trawling through those leads.

 

I have a possible idea, I am wondering what you think:

 

Cannabidiol (CBD) isolated from Cannabis or hemp is a non-psychoactive anxiolytic/anti-psychotic 5-HT1A agonist (among other targets) but I am a bit confused as to whether the anxiolytic action is related to it's pre-synaptic agonism - decreasing levels of excitatory serotonin, or to it's possible post-synaptic actions.

 

I must admit, acute serotonin increases have in the past felt very pleasant, calming and reassuring, whereas now I know it can be the opposite - excitatory and anxiogenic. I wonder what the mechanism is here.

 

I can't really afford to try it if there is a strong possibility there will be increased serotonergic activity because my brain is recovering from serotonin toxicity, but it is very tempting due to it's potent anti-stress effects that would be very therapeutic. 

 

Any help is most appreciated :)

 

Thank you



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#9 Flex

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Posted 24 April 2015 - 06:28 PM

Disclammer: Its a pain to provide references for long texts, so either:

dont believe it( no offence, its actually good to be sceptic), do a recherche on Your own and/or ask me for interresting/certain ones.

 

First, You can try to ask for Mirtazapine,
Mianserine -->which is problematic because of agranulocytosis(blood tests are needed every few weeks) but it affects way more 5-ht receptors  which are implicated in 5-ht release from the Raphe Nucleus like : 5-ht2b and 5-ht6
5-ht2b seems,nevertheless, to be actually good because it releases dopamine(in the VTA) and serotonine .
 
The anxiogenic receptors could be 5-ht2c and 5-ht1a (postsynaptic) but 5-ht1a decreases also vasoconstriction and releases Dopamine in the PFC, so I would rather avoid to touch it.
As said 5-ht6 could be interresting but the test results in rats are incoclusive in terms of anxiety.

(afaik)Same thing for 5-ht7
 
A suggestion; I have some enduring problems due to cannabis abuse in the adolescence.
When I began investigating, I had actually the problem that there werent many studies about the consequences and mechanisms, so I looked for a similair disease that is more researched: Negative symptoms in schizophrenia.
Its not the same because THC is able to reverse NMDA inhibition induced cognitive and affective deficits but there were nevetheless some valuable informations.
 
Ergo: I´ve found recently this correlation: autism hyperserotonemia
Google it but rather only for the cases where too much serotonine is the cause or the topic of the study.
You might also find other diseases where too much 5-htp is the cause and look what helped.
 
Now You can find what they tried e.g.:
CURRENT AND EMERGING THERAPEUTICS OF AUTISTIC DISORDER AND RELATED PERVASIVE DEVELOPMENTAL DISORDERS
http://www.google.de...5533,bs.1,d.ZWU
 
As said in a prevorious post, You could look for PSSD (post SSRI sexual disorder) treatments:

Serotonin 5-HT(1)A Receptor and Male Sexual Function / Motivation
http://www.longecity...tivation/page-2

-----------------------------------------------

 

In regards of Your issues:

The funny thing about the brain is, that no one can say anyting definitive on the first look.

From my laymans opinion, only something like a PET, special(?) MRI or  perhaps epigenetic markers could say something to 100 % about You disease/issue.

This is how I think about this:

--> It could be freely just a deregulation (increase/decrease) of:

Serotonine

and/or serotonine receptors

and/or other receptors

and/or a damage.

and perhaps something epigenetic ( but I personally doubt this one)

 

So You have to see whether there is something to narrow it down or reveal like:

too much serotonine (i.e. SSRI side-effects) causes insomnia, mania and so on.

 

Just an laymans Idea:

By taking passionflower You would indeed increase serotonine but also dopamine and (nor)adrenaline.

On the ther hand, 50 mg 5-htp on it self, like endogneous serotonine, can increase and decrease dopamine, noradrenaline and glutamate.

But this would, more or less definitive, point out the issue, if Youre still unsure about having too much serotonine.

 

NOTE: 5-htp is a direct precursor of Serotonine ! 

there is no break, so Your body convert it as 1:1

and You would die or end up in a serotonine syndrome if You´re taking too much !!!  

50mg are for me personally tolerable, I dont give any guarantees that its safe for You

Speak with Your Doctor first about this or any idea.

 

 

 

 


Edited by Flex, 24 April 2015 - 06:43 PM.

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