P.O.I.S Syndrome, Depakene and Bipolar Disorder

[Robson]

After years of self-treatment, I have few symptoms of P.O.I.S. and two of the symptoms that persist the most are: fatigue and mental weakness.

A week ago, I decided to come clean and tell a doctor that I discovered that I had P.O.I.S., because I didn't know what to do anymore.

After I described all my symptoms to the doctor, she didn't rule out the possibility, however, she said that it would be good if I tried using a medicine called Depakene (Valproic Acid).

From what I can understand so far, the medicine is a mood stabilizer and can be used to treat both epilepsy and bipolar disorder.

I accepted the proposal to use the medicine for at least two weeks and it's been about 9 days, during which I've noticed that the medicine is having some positive effects, such as a decrease in dementia and an increase in concentration and social affection.

So, with that, I would like to know from you if anyone has ever taken this medicine, what the sensation was and also if any of your doctors have ever considered that you actually have Bipolar Disorder and what you thought about that.

[demografx]

After years of self-treatment, I have few symptoms of P.O.I.S….

Congratulations!

[Aladin]

I have been diagnosed with bipolar 15 years ago (with hindsight, that might have been a wrong diagnosis because of ignorance about POIS under medical staff); Up to this day, it's not clear for me which diagnosis is the right one.

I was prescribed Lamoctrigine, another mood stabilizer and anti-epileptic, also with good results: it helped for a long time with my mood swings, but there have been moments when the symptoms were to strong to be stopped by it.  For the moment, i have sexual anhedonia (no pleasure at the time of orgasm), which also completely eliminates my POIS symptoms. 

I wonder wether it is the long intake of the mood stabilizer that brought along the anhedonia. It is no fun, but at least it's better then POIS.

[Progecitor]

I have been diagnosed with bipolar 15 years ago (with hindsight, that might have been a wrong diagnosis because of ignorance about POIS under medical staff); Up to this day, it's not clear for me which diagnosis is the right one.

I was prescribed Lamoctrigine, another mood stabilizer and anti-epileptic, also with good results: it helped for a long time with my mood swings, but there have been moments when the symptoms were to strong to be stopped by it.  For the moment, i have sexual anhedonia (no pleasure at the time of orgasm), which also completely eliminates my POIS symptoms. 

I wonder wether it is the long intake of the mood stabilizer that brought along the anhedonia. It is no fun, but at least it's better then POIS.

The most sound explanation for lamotrigine’s effectiveness is that it is a combined ERbeta and sigma-1 receptor agonist. As a comparison saffron and berberine have similar properties. The decreased sexual drive in men may be due to the ERB’s effect on androgen receptors, though saffron and many other ERbeta agonists are regarded as aphrodisiacs.

Anti-epileptic drugs exert their positive effects on prostate cancer (PCa) cells through histone modifications. We recently identified a regained expression of estrogen receptor B, which is lost during prostate carcinogenesis, as the pivotal benefit from HDACi valproic acid for LNCaP prostate cancer cells. To widen the scope of HDACi regimens for PCa we now investigated further drugs (carbamazepine and lamotrigine) on PCa cells.
Carbamazepine and lamotrigine markedly reduced tumor cell viability and proliferation for LNCaP and PC-3 cells. Both drugs evoked a two- to threefold increase of ERB expression in all PCa cells which peaked at 1mM of carbamazepine or lamotrigine, respectively.
Consequently in LNCaP an impact on the androgen receptor and the IGF-receptor-axis occurred, as PSA secretion decreased to <33%, IGF1 receptor expression decreased to <16% and IGFBP-3 expression increased 3-fold - to 6-fold.
For all cancer cells, ERB, a tumour suppressor and regulatory factor of proliferation was restored due to HDACi treatments. In androgen-sensitive cells this had a rectifying impact on androgen receptor and IGF-receptor signalling.
https://www.auajournals.org/doi/pdf/10.1016/S0022-5347%2809%2961360-4

Could it be that Flibanserin has a similar mechanism as Lamotrigine? Just because it seems to be a very strong women’s aphrodisiac.

Lamotrigine does not have enzyme inducing properties and monotherapy lamotrigine treatment was noted to have minimal sexual effects in men but improvement in all spheres in women.
This report presents lamotrigine-induced decreased libido as a probable treatment-emergent adverse drug effect. The mechanism for such is unknown.
https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=Lamotrigine-induced+sexual+dysfunction+and+non-adherence%3A+case+analysis+with+literature+review&btnG=

It is interesting and kind of funny to read how lamotrigine improves sexual drive. I guess most of these are women, however I think there may have been some men among them. Of course some of them report decreased libido, who were most likely male.
https://www.reddit.com/r/lamictal/search/?q=sex&cId=d9010877-4173-4b46-8264-c6fce53416bc&iId=e196c52a-a168-49a7-99f9-8bbc00320fd3&rdt=59719

More on ERbeta receptor:
https://poiscenter.com/forums/index.php?topic=4061.0
More on Sigma-1 receptor:
https://poiscenter.com/forums/index.php?topic=4634.0