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Would like some information about how physical sex drive works

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arkaeik


Hi,

Firstly I'd like to say I really appreciate this forum, there's tons of great information and insight here.

I've had PSSD for 6 months now but it seems to be different from most cases I've read about. My sexual functioning is basically normal: I can get an erection easily and experience exactly the same sexual sensation as before. I also have no mental symptoms.

My problem is my complete lack of physical sex drive. By this I mean that my body does not require ejaculation anymore. I can go weeks without orgasm without experiencing any sexual frustration.

Before PSSD, when I attempted NoFap, I would get an aching sensation in my testicles due to the lack of ejaculation. Now, I never have this sensation, even when I edge close to orgasm and then stop. What I've noticed is that my scrotum is much tighter than it should be (seems prepubescent), permanently. I suspect that this is connected to the lack of sex drive in some way.

I've experienced significant improvement after taking extrogenous testosterone and a dose of HCG, unfortunately it seems very hit or miss. Right now I've decided to take a very high dose testosterone for some weeks. Already after the first dose I've noticed my scrotum is almost back to normal.

Does anyone have information about what causes sex drive, specifically the build-up of sexual energy that I'm lacking? I would greatly appreciate some advice. Thank you in advance!

EDIT: forgot to mention I'm an 18 yr old male



Last edited by arkaeik on Sat Mar 02, 2019 10:30 am; edited 1 time in total (Reason for editing : added age)

kpavel

kpavel
Area-1255 Intelligence Oversight
Area-1255 Intelligence Oversight
Hello,

in fact the exact mechanism how libido works isn't known. Moreover what people report as libido seems to vary. Some can be glad to what you described for your past months situation. But of course real libido is tension and pleasure, not only good erection. Quite a lot people with pssd do not have problems with getting it up. Testosterone definitely influences something, however people with more than enough endogenous levels of T or DHT can have pssd.
Ginkgo does something for passion. That's my experience. Look for pssdlab for substances that helped someone. It is generally much easier to return erections (for this there are numerous things we are aware of, even more than on forums) including morning ones than passion. Conventional ones are T and caber I think. Some people without pssd even used orgesterone with testosterone. However progesterone is more risky thna T and seems to worsen situation. May be someone uses something that is cure right now, but simply the dose isn't enough. But I'm not sure it's dangerous levels ot T. Be careful.

I also think, the more objective changes in your body functions you notice and report, the more chance to find something.

I ordered black maca, to see if the claims on reddit are real. And a pair of special things I can get in my town. By the way cholinergic things like galantamine (nicotinic alpha4beta2 receptor) or betanechol (muscarinic m2r, m3r) could be anti-anhedonic in spite of claims that acetylcholine is prodepressive.

arkaeik


The high doses of T were definitely a bad idea. They've made my testicles shrink a lot and I've also realized that T is not the problem in PSSD. It's how the T is utilized.

I think I've pinpointed the root mechanism of most PSSD cases, maybe not the ones in females though. It's been demonstrated that sertraline (and presumably other SSRI's) can have epigenetic effects on steroidogenesis. This is most likely the case for finasteride too, which is less surprising given that it's known as a 5a reductase inhibitor. The symptoms of PSSD, PFS and PAS are identical to my knowledge so this indicates that the cause is the same.

In my opinion the root cause of these syndromes is altered gene expression regarding steroidogenesis. Only certain individuals are genetically predisposed and are unlucky enough to get this which is why the majority who take these drugs do not have permanent effects. Altered gene expression results in lower DHT and several other steroids. This will have a profound effect on the body.

The way I came to this conclusion was observing that my genitals became physically normal upon taking DHT (in the last post I said it was T, but I took them at the same time and I think it's the DHT). DHT is responsible for external genital development. My genitals are now back to PSSD state a few weeks after the DHT dose.

There is also a study that demonstrates that rats treated neonatally with clomipramine displayed sexual dysfunction. When given estradiol and DHT as adults, their sexual function was restored. The researchers explicitly mentioned that testosterone did not work. Also, the estradiol and DHT had to be taken at the same time or it would not work.

The key seems to be finding a way to reverse these epigenetic changes. Unfortunately I don't know of a reliable way to do that. If epigenetic changes are induced in the same direction as the effects of a drug then perhaps you could reverse the changes by taking the lacking substances (estradiol and DHT it seems).

Sources if interested:

https://academic.oup.com/toxsci/article/163/2/609/4947780
https://www.researchgate.net/publication/326657434_The_Post-finasteride_Syndrome_Clinical_Manifestation_of_Drug-Induced_Epigenetics_Due_to_Endocrine_Disruption
https://www.ncbi.nlm.nih.gov/pubmed/25449595

kpavel

kpavel
Area-1255 Intelligence Oversight
Area-1255 Intelligence Oversight
arkaeik wrote:The high doses of T were definitely a bad idea. They've made my testicles shrink a lot and I've also realized that T is not the problem in PSSD. It's how the T is utilized.

I think I've pinpointed the root mechanism of most PSSD cases, maybe not the ones in females though. It's been demonstrated that sertraline (and presumably other SSRI's) can have epigenetic effects on steroidogenesis. This is most likely the case for finasteride too, which is less surprising given that it's known as a 5a reductase inhibitor. The symptoms of PSSD, PFS and PAS are identical to my knowledge so this indicates that the cause is the same.

In my opinion the root cause of these syndromes is altered gene expression regarding steroidogenesis. Only certain individuals are genetically predisposed and are unlucky enough to get this which is why the majority who take these drugs do not have permanent effects. Altered gene expression results in lower DHT and several other steroids. This will have a profound effect on the body.

The way I came to this conclusion was observing that my genitals became physically normal upon taking DHT (in the last post I said it was T, but I took them at the same time and I think it's the DHT). DHT is responsible for external genital development. My genitals are now back to PSSD state a few weeks after the DHT dose.

There is also a study that demonstrates that rats treated neonatally with clomipramine displayed sexual dysfunction. When given estradiol and DHT as adults, their sexual function was restored. The researchers explicitly mentioned that testosterone did not work. Also, the estradiol and DHT had to be taken at the same time or it would not work.

The key seems to be finding a way to reverse these epigenetic changes. Unfortunately I don't know of a reliable way to do that. If epigenetic changes are induced in the same direction as the effects of a drug then perhaps you could reverse the changes by taking the lacking substances (estradiol and DHT it seems).

Sources if interested:

https://academic.oup.com/toxsci/article/163/2/609/4947780
https://www.researchgate.net/publication/326657434_The_Post-finasteride_Syndrome_Clinical_Manifestation_of_Drug-Induced_Epigenetics_Due_to_Endocrine_Disruption
https://www.ncbi.nlm.nih.gov/pubmed/25449595

Yes, I'm aware of DHT+E2 study, it was posted by Ghost long time ago. Guys on hackstasis forum experimented with hormones a lot (forum is used by a number of pssd sufferers too). Generally I agree that something like cyp17a1 should be affected by ssri.
Sulforaphane is a broad hdac inhibitor. And you may be interested in acetyl-l-carnitine for these and pro-sexual properties.
However I think that approaches that will increase libidogenic dopamine/glutamate/acetylcholine in right places will be based on other paradigms.

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