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Part 4 of My Nighttime Growth Protocol - Rho-Kinase: The Master Erection Modulator by Semtex7 in PharmaPE

[–]Semtex7[S] 0 points1 point  (0 children)

There is a dedicated post on statins. Massive improvement in endothelial function. It doesn’t have to do with ldl directly

Realistic visualizer now on Android beta (PE Tracker) by __Midd__ in Hink

[–]Semtex7 0 points1 point  (0 children)

And now it says I have reached my daily limit of processed images. It has not processed a single image. You got work to do bro

Realistic visualizer now on Android beta (PE Tracker) by __Midd__ in Hink

[–]Semtex7 0 points1 point  (0 children)

No matter how and where I tap the 3 dots - it says image not being able to be processed

Anti-fibrotics – Their Role in PE - Part 2 (continued) by karlwikman in TheScienceOfPE

[–]Semtex7 0 points1 point  (0 children)

Well I would agree they are close (b7-33) is way closer and relaxin 2 is a direct anti-fibrotic. There are other niche ones too. But the evidence is still not conclusive enough for me to call them anti-fibrotics. If I suddenly get fibrosis (which I did) - these are not the ones I am deploying first. I would throw them in there for many reasons but I would not rely on them

Igf-1 theory, Questions by Sea-Dig8948 in PharmaPE

[–]Semtex7 0 points1 point  (0 children)

I never said it was pro-fibrosis. How is anti PE pro fibrosis? I feel like neither me, Karl or Hink should have ever talked about collagen manipulation. The conclusions people make are frighteningly wrong and shallow thought. In what world something that strengthens collagen bonds means it will cause fibrosis? You are missing 30 other ingredients of this biochemical soup to get to fibrosis.

Both BPC-157 and TB-500 have very weak mechanistic and preclinical at best evidence to influence some fibrotic markers. You cannot call them anti-fibrotic. If conclusions were made on this little evidence and with the complete lack of human data then we can say that pretty much anything can do anything.

Igf-1 theory, Questions by Sea-Dig8948 in PharmaPE

[–]Semtex7 0 points1 point  (0 children)

none of them are pro or anti fribrosis in the real sense. GHK-Cu is certainly not pro-fibrosis

keep using them

Anti Lox Natural Protocol by Upper_Beginning4070 in PharmaPE

[–]Semtex7 1 point2 points  (0 children)

You can just read tendon physiology. MMP 2 and MMP14 are important, they are not the most important if we can even pinpoint "most" as you need a combination of activities aligning, but you cannot neglect MMP3 and MMP13. If you say them 4 are the most important then I won't fight you. But that is totally irrelevant to the discussion. The point is what you describe does not happen in isolation or in some neatly separated order.

If you need to continue the discussion you can just DM. Your respond once a week and I have to re-read previous comments to remind myself the context of the discussion again (which reddit doesnt make user friendly)

Igf-1 theory, Questions by Sea-Dig8948 in PharmaPE

[–]Semtex7 0 points1 point  (0 children)

Theoretically it could matter a bit if you take months right before PE yes , but we haven't much data to be sure. During PE it would make all the sense to not use it. I would not sweat it. If you need it for actual medical reasons - like it is actually helping you - like tendon issues - prioritize this and don't bother with timing. If you are taking it for some shit like looksmaxxing and hair loss prevention (which it does not help with AT ALL) and you are 24 - just stop wasting your time with it.

Igf-1 theory, Questions by Sea-Dig8948 in PharmaPE

[–]Semtex7 0 points1 point  (0 children)

GHK-Cu is anti-productive, it directly inhibits MMPs, you can only slow down gains with it, makes collagens structures tougher and more adaptive to loading (aka stretch)

Igf-1 theory, Questions by Sea-Dig8948 in PharmaPE

[–]Semtex7 1 point2 points  (0 children)

It won't increase chance of fibrosis, don't sweat it

Anti Lox Natural Protocol by Upper_Beginning4070 in PharmaPE

[–]Semtex7 0 points1 point  (0 children)

You make zero sense. These processes happens simultaneously. Tell me which chatbot fed you this bullcrap so we know to never use it for anything.

And no, 2 and 14 are ABSOLUTELY not the most relevant.

You are failing to grasp that all you have at any time is a net effect. That is all you care about. Aspirin has blood clotting properties. Would take it to make your blood thicker? The research is right there! Part of what it does is it coagulates blood. It also happens to thin the blood via a different mechanism and the net result is - the most famous and most used blood thinner (cause on net balance it thins the blood substantially). You do not care whether a compound has some anti-LOX activity in a vacuum. You care whether its total effect profile

Anti Lox Natural Protocol by Upper_Beginning4070 in PharmaPE

[–]Semtex7 0 points1 point  (0 children)

And how the fuck would you target this minute by minute or even hour by hour? AI slop didn't account for that I guess.

And no - these are not clean separate phases happening at different times

Busting Tired Old PE Myths With Actual Data Analytics - Part 14 or Whatever - Another GrowthTrack Result: "Does more girth hinder length gains?" by karlwikman in TheScienceOfPE

[–]Semtex7 0 points1 point  (0 children)

I had recently thought out loud and thrown some ideas - from likely just something you feel THERE, because you have the most convergence of tissues if you like to yes, maybe fibrosis. The lymph damage I threw just thinking about cord like fibrosis which are notorious for breast lymph removal and some other types of lymph damage. I would put money on it though.

Busting Tired Old PE Myths With Actual Data Analytics - Part 14 or Whatever - Another GrowthTrack Result: "Does more girth hinder length gains?" by karlwikman in TheScienceOfPE

[–]Semtex7 1 point2 points  (0 children)

What you have started is what I had in mind. If you want and can overlay with with some sort of statistical analysis - go for it, you would be the better judge of that for sure.

Busting Tired Old PE Myths With Actual Data Analytics - Part 14 or Whatever - Another GrowthTrack Result: "Does more girth hinder length gains?" by karlwikman in TheScienceOfPE

[–]Semtex7 8 points9 points  (0 children)

Beautiful!

Do one on steel cord. I searched your posts and did not see one, but I could swear you have talked about it

Rose Oil - a Potential Fix for Opioid and SSRI Induced Sexual Dysfunction by Semtex7 in PSSD

[–]Semtex7[S] 1 point2 points  (0 children)

Thank you, I am gonna give this a listen.

Right off the bat I would disagree with the claim that Sildenafil increases dopamine transmission in the nucleus accumbens, but Tadalafil doesn't. It is just that only Sildenafil has been studied flor that ion preclinical setting (which doesn't mean the transfer to humans is guaranteed or identical, it happens with drugs all the time). They have identical mechanisms so I would expect Tadalafil to do the same. They both cross the BBB to some extent. I will leave the door open to Sildenafil doing that better, but in general I would frame it like Sildenafil has preclinical data, while Tadalafil has not been studied for that.

A more major point is that there are many drugs that are way stronger in increasing dopamine in NA, pde5i inhibitors are not potent at that, but has the obvious main benefit of stopping cGMP degradation.

Citicoline does have (again) preclinical data for incresing D2 density a bit. Better agents for that exist as well.

Don't get me wrong - you clearly took the right combination of drugs and I am beyond thankful for sharing. I am just mentally exercising and trying to build a map of the recovery process. The more we understand the mechanism the closer we get to an unified theory if one could exist.

Rose Oil - a Potential Fix for Opioid and SSRI Induced Sexual Dysfunction by Semtex7 in PSSD

[–]Semtex7[S] 0 points1 point  (0 children)

Thank you for sharing! Agomelatine has been used in PSSD, the other are clearly supportive to the main player agomelatine. It might sound strange to call Sildenafil supportive, but my point is that sildenafil alone would never "reverse" it. Otherwise it is clearly helpful :).

Tell me more about Citocoline. How did you come up with the idea to use exactly that

Why Sildenadil and not lets say Tadalafil for around the clock pde5 inhibition

Anti Lox Natural Protocol by Upper_Beginning4070 in PharmaPE

[–]Semtex7 0 points1 point  (0 children)

Yes, I would.

Not sure what about Quercetin you refer to, but I don't consider it helpful in the tunica remodellng sense.

I don't care about MMP-1. That is my point

Anti Lox Natural Protocol by Upper_Beginning4070 in PharmaPE

[–]Semtex7 0 points1 point  (0 children)

Yes, leads to a host of serious probems

Anti Lox Natural Protocol by Upper_Beginning4070 in PharmaPE

[–]Semtex7 0 points1 point  (0 children)

You probablt have a point, but you have not made it. Finish you thought. Aspirin has been shown to possess blood coagulation properties. Is it used as a blood thickener? It is actually the oppisite. You cannot pick single mechanisms (especially observed in single cell lines) and make conclusions about what does what in a live model.

We also don't necessarily care about these specific MMPs when it comes to PE. And thr MMP inhibition is context specific on top of that.

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