Cured

[Spartak]

Had a visit to the psychiatrist, diagnosed me bi polar and gave me a medicine, would post a name of it later, not at home atm, and these weeks had dozens of O, no any symptoms, and mentally more stable beside POIS.
Recaver all, for me sky is blue, not grey as before

[berlin1984]

Congrats! 

[gzbking]

please post name of the medicines

[Spartak]

Congrats! 

thank you, whish the same progress to anyone. I noticed that 2 nd day I have some ?slower brain? symptoms, but after a regular dose of medication which I take twice per day around 10 am and 6 pm it goes away.

[Spartak]

please post name of the medicines

I got prescription of 2 medicaments, one is some modern bi polar medication, here it is called Bipodis, but originally it is Aripiprazol, it helps me a lot, especially with anxiety, but makes me very agressive, and low tempered. So I guit, got me into a trouble with a boss recently, and he was right, just it was impossible to control myself.
2nd is also a mood stabilizer so called here Karbapin, which is, Carbamazepine.
That one changed my life.
I take 50mg in the 10 am and 50mg in the 6 am. Made a miracle.
Again, pls, this is my experience, I advocate that no one take it to it?s own, check a professional for any medication.
And sorry for a bad English, I hope it is understandable.

[Spartak]

And again, these are serious drugs, with a lot of possibilitie side effects, do not take anything without visiting professionals, I know how I was hyped to try everything that helped others, which was completely wrong, cause it made my POIS much worse.
This is just my story

[Spartak]

In a month I will post an update, I have a control, so psychiatrist said if that bipodis does not help, he will prescribe some other drug. But that is all bi polar related, not really Pois wise.

[Spartak]

I also wish now that I could be a member of a that new study, maybe it could be useful, but I live in Europe, and by no mean I have no money to go to LA and live there while study is going on. Sadly

[demografx]

I also wish now that I could be a member of a that new study, maybe it could be useful, but I live in Europe, and by no mean I have no money to go to LA and live there while study is going on. Sadly

Thanks for your interest! I forwarded  your post to the POIS Research Team.

[Muon]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852797/

I can’t find any overviews of binding receptor affinity studies for Carbamazepine. It’s a voltage gated sodium ion channel blocker.

[Spartak]

I also wish now that I could be a member of a that new study, maybe it could be useful, but I live in Europe, and by no mean I have no money to go to LA and live there while study is going on. Sadly

Thanks for your interest! I forwarded  your post to the POIS Research Team.

Thank you Demo! hope it will help somehow

[Spartak]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852797/

I can’t find any overviews of binding receptor affinity studies for Carbamazepine. It’s a voltage gated sodium ion channel blocker.

thank you, interesting.
So any explanation why it works?

I have bad news though, had a sex with a gf last night, had 5 times O.
Up to 3rd I haven?t felt any symptoms, after 4th and 5th I got some onset, it is not horrible, compared to before, maybe 20%. Still it is good, no brain fog, no anxiety, no weaknes as before, just feel impatient and find it hard to concentrate, which was one of my regular Pois symptoms.
Anyway update is that I am about to visit psychiatrist again next week, because he needs to prescribe me new medication instead that Bipodis that I reacted bad on, will keep you guys updated.
And wish again everyone to heal feom this nightmare

[Spartak]

I also have one question for everyone, how is situation with a health care in your countries guys?
Here health care is free, but if I said that I have Pois I wouldn?t get the medication, because Pois is unknown, luckily (irony) they diagnosed me with mild case if bi polar disorder so I got it prescribed like that. So I can have it for free forever

[Hopeoneday]

Woow, 5 times in row with girl..wooow

A lot of poisers did tryed OCD medications
in the past( i read), and not so much successful.

I think Quantum mentioned that ocd medications target
to inhibit arhadonic acid in brain, meaning,
inhibit inflamation i think.

Do you feel is this sussces for you come from
gabapentin or ocd meds?

[demografx]

Woow, 5 times in row with girl..wooow

The essential elements of POIS Science!

[demografx]

And wish again everyone to heal from this nightmare.

Beautifully said, Spartak.

Thank you!

[demografx]

I also wish now that I could be a member of a that new study, maybe it could be useful, but I live in Europe, and by no mean I have no money to go to LA and live there while study is going on. Sadly

Thanks for your interest! I forwarded  your post to the POIS Research Team.

Thank you Demo! hope it will help somehow

I will also ask them if you can contribute a semen sample.

[Hopeoneday]

Wait, this is antiepileptic , antyconvulsant drug.
I remeber my seizures, pre eptileptics atacs in pois.

I remeber here and on naked science forum, peoples
discused, antiepileptics for pois.

Spartak, do you hawe amalgams, or mercury exposure?

[Progecitor]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852797/

I can’t find any overviews of binding receptor affinity studies for Carbamazepine. It’s a voltage gated sodium ion channel blocker.

thank you, interesting.
So any explanation why it works?

I have bad news though, had a sex with a gf last night, had 5 times O.
Up to 3rd I haven?t felt any symptoms, after 4th and 5th I got some onset, it is not horrible, compared to before, maybe 20%. Still it is good, no brain fog, no anxiety, no weaknes as before, just feel impatient and find it hard to concentrate, which was one of my regular Pois symptoms.
Anyway update is that I am about to visit psychiatrist again next week, because he needs to prescribe me new medication instead that Bipodis that I reacted bad on, will keep you guys updated.
And wish again everyone to heal feom this nightmare

Additional information that may help in ascertaining the effective mechanism of Carbamazepine (CBZ):

An action on androgen or estrogen receptors could be considered:

Carbamazepine AR; ERa; ERB -8.8(an); -9.6; -9.8(an)

For example, mania and bipolar drugs like lithium, carbamazepine and valproate all inhibit Phospholipase A2 (and AA release).

Carbamazepine and B. monnieri treatments reversed the alterations in 5-HT2C receptor binding, gene expression, and inositol triphosphate content in treated epileptic rats as compared to untreated epileptic rats.
https://www.sciencedirect.com/science/article/abs/pii/S152550500900420X

Table 3. Medications that may delay ejaculation
Line 13: Antiepileptics (Carbamazepine, Gabapentin, Pregabalin):
- Inhibition of calcium currents appears to lead to reduced neurotransmitter release and attenuation of postsynaptic excitability
- Increases the level of sex hormone-binding globulin (SHBG), leading to reduction of free or bioavailable testosterone
https://synapse.koreamed.org/articles/1088855

Taken together, the results suggest that CBZ inhibits L-type Ca2+ channels and Na+ channels, but does not inhibit activation of glutamate ionotropic receptors.
https://www.sciencedirect.com/science/article/abs/pii/S0028390899000581

Findings suggest that adenosine A2A receptor agonistic effects of CBZ contribute to chronic prevention of pathomechanisms developments of several neuropsychiatric disorders associated with proinflammatory cytokines.
https://www.mdpi.com/1422-0067/20/15/3727

CBZ produces local peripheral anti-hyperalgesia via peripheral adenosine A1 receptors.
https://www.jstage.jst.go.jp/article/jphs/100/4/100_4_310/_article/-char/ja/

The initial activation of the adenosine A1 receptors by CBZ may be a triggering factor for the subsequent long-lasting activation of the opioid system, which results in the antinociception effects.
https://europepmc.org/article/med/9533173

CBZ is known to act as a specific antagonist at adenosine A1-receptors. After a 3-week application of CBZ, A1-receptors are upregulated in the rat brain.
https://www.sciencedirect.com/science/article/abs/pii/S0893133X98000591

Caffeine, a non-selective adenosine receptor antagonist, significantly depressed the antinociceptive effects of CBZ and oxcarbazepine, in a dose- and time-dependent manner. These findings indicate that, in a paw inflammatory hyperalgesia in rats, the antinociceptive effects of both drugs are, at least partially, mediated by adenosine A1 receptors. Caffeine consumption could possibly depress the analgesic effects of both anticonvulsive drugs.
https://www.sciencedirect.com/science/article/abs/pii/S0304395904003306

CBZ also affects a variety of other neurotransmitter and peptide systems (vasopressin, somatostatin, ACTH, cortisol and opiate) which could be implicated in its mechanism of action or side-effects in the treatment of pain, seizure and affective disorders. Since CBZ is a good inhibitor of adenosine mediated cAMP increases in brain cortical slices, we tested its effect on adenosine receptor ligand binding and show here that CBZ interacts in a rather potent and specific manner with adenosine receptors in brain. CBZ also had significant, although less potent, effects on "Peripheral type" benzodiazepine receptors. 
https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=Specific+and+potent+interactions+of+carbamazepine+with+brain+adenosine+receptors&btnG=

Valproate and CBZ increase prefrontal dopamine release by 5-HT1A receptor activation.
https://www.sciencedirect.com/science/article/abs/pii/S0014299999005178

Observations that dopaminergic antagonists are beneficial in bipolar disorder and that dopaminergic agonists can produce mania suggest that bipolar disorder involves excessive dopaminergic transmission. Chronic CBZ pretreatment prevented the quinpirole-induced increments in regional brain incorporation coefficients of AA (k*) and in PGE2. These findings are consistent with the hypothesis that effective mood stabilizers generally downregulate brain arachidonic acid (AA) signaling via Dopamine D2-like receptors, and that this signaling is upregulated in bipolar disorder.
https://link.springer.com/article/10.1007/s11064-008-9595-y

Chronic CBZ administration to rats blocks increments in the AA signal k*, and in PGE2 and TXB2 concentrations that are produced by NMDA in vehicle-treated rats. The clinical action of antimanic drugs might involve inhibition of brain NMDAR-mediated signaling involving AA and its metabolites.
https://www.sciencedirect.com/science/article/abs/pii/S0006322307003629
 
The antiepileptic drug CBZ is known to be an inducer of cytochrome P450 (CYP) 3A4 after binding to the nuclear pregnane X receptor. Aside from induction of CYP3A4, CBZ acts as an inducer of intestinal MDR1 mRNA (multidrug resistance), MRP2 mRNA, and MRP2 protein content.
https://ascpt.onlinelibrary.wiley.com/doi/abs/10.1016/j.clpt.2004.04.011

Previous studies have confirmed that the metabolism and efficacy of CBZ can be influenced by xenobiotic receptors, especially pregnane X receptor (PXR), constitutive androstane receptor (CAR), and aryl hydrocarbon receptor (AHR). P-glycoprotein (P-gp) is a drug transporter that has been shown to be upregulated by PXR activation at the human blood brain barrier (BBB). CBZ has been found to serve as a substrate of P-gp because it can extrude antiepileptic drugs to the capillary lumen against the concentration gradient.
https://www.sciencedirect.com/science/article/abs/pii/S0378111920310283

CBZ may be an allosteric regulator on the GABAA receptor.
https://molpharm.aspetjournals.org/content/47/6/1189.short

Chronic but not acute administration of CBZs are associated with up regulation of GABAB receptors in the hippocampus, yielding this action as a potential convergent mechanism for mood stabilization. Antimanic and moodstabilizing properties of CBZ could be related decrease dopamine turnover. CBZ does decrease levels of the dopamine metabolite homovanillic acid (HVA) in the CSF. It modalities increase brain-derived neurotrophic factor (BDNF). Studies demonstrated that CBZ decreases the release of norepinephrine. CBZ stabilizes the inactivated state of voltage-gated sodium channels, making fewer of these channels available to subsequently open. This leaves the affected cells less excitable until the drug dissociates.
https://www.researchgate.net/profile/Getinet-Ayano/publication/309686057_Bipolar_Disorders_and_Carbamazepine_Pharmacokinetics_Pharmacodynamics_Therapeutic_Effects_and_Indications_of_Carbamazepine_Review_of_Articles/links/586b873908ae329d6211f317/Bipolar-Disorders-and-Carbamazepine-Pharmacokinetics-Pharmacodynamics-Therapeutic-Effects-and-Indications-of-Carbamazepine-Review-of-Articles.pdf

Here, we show that CBZ increased the expression levels of PPARG, CCAAT/enhancer-binding protein beta (C/EBPbeta), and fatty acid synthase (FASN) in 3T3-L1 cells. Notably, CBZ inhibited the expression levels of beta-catenin, a negative regulator of adipogenesis, leading to enhanced adipogenesis. These results suggest that CBZ enhances adipogenesis by suppressing Wnt/beta-catenin expression, indicating its potential effects on obesity-related metabolism.
https://www.mdpi.com/2073-4409/8/11/1460

Furthermore, the observed CBZ-mediated Wnt signaling inhibition may help to explain the phenomenon of bone loss and increased adipogenesis in some patients during long-term CBZ treatment.
https://pubs.acs.org/doi/full/10.1021/acs.jmedchem.9b02020

My personal opinion is that we will never figure out POIS based on only one effective drug. Also the benefit that CBZ provides on your bipol and POIS may not be based on the same mechanism.

[taurusthree]

please post name of the medicines

I got prescription of 2 medicaments, one is some modern bi polar medication, here it is called Bipodis, but originally it is Aripiprazol, it helps me a lot, especially with anxiety, but makes me very agressive, and low tempered. So I guit, got me into a trouble with a boss recently, and he was right, just it was impossible to control myself.
2nd is also a mood stabilizer so called here Karbapin, which is, Carbamazepine.
That one changed my life.
I take 50mg in the 10 am and 50mg in the 6 am. Made a miracle.
Again, pls, this is my experience, I advocate that no one take it to it?s own, check a professional for any medication.
And sorry for a bad English, I hope it is understandable.

Spartak, have you got updates?

I was also prescribed low dose Carbamazepine (200mg, extended release, once a day) to potentially help with my “oversaturated emotions” and heavy mood swings throughout a day. Almost a month passed, and I can cautiously tell that it treats the POIS as well. Other symptoms which are seemingly gone: unrefreshing sleep, brain fog after eating and bathing, IBS, MCAS-style stuff…

Anybody who decides to try this drug out, be cautious! Its side-effects include potential bone marrow suppression, hepatitis, life-threating rushes, etc.! You have to do regular blood tests when taking this med.