I’d say that 95% is way, way off the mark especially younger men you’re almost agreeing with mercks orginal stats on those that suffered sides which everyone knows was fabricated in order to pass FDA approval. There’s a difference between enzymes and receptor sites and we’re not talking about those who don’t suffer. I’m not a scientist and don’t pretend to know all the pieces to the puzzle but what I am saying shouldn’t be thrown down the toilet either until everyone here gets a chance to review it and has their say. This matter should be open for debate and if not I think you and the moderators would be doing a disservice. I know I’m right that is why I refuse to back down until it’s proven otherwise either by you or someone else I’m not bothered who it is.
What the mods have proposed here linking these substances is that any reduction of androgens can cause the syndrome…Even some that don’t effect the 5ar enzyme…Any substance that lowers androgen levels through various mechanisms can cause pfs…Some even ed n argued the fact that dht returns after cessation of finastride is what causes the syndrome…So it is possible the receptors no longer function correctly but claims here indicate it is due to an up regulation of them…Many think lowering androgen levels causes this but I have wonderd if it is the change gene in the brain that actually happens first and that is what causes the upregulated reaction instead of the lowering of dht…
Being totally confident about a theory without any evidence to prove it to be the case drastically diminishes your credibility.
I know from my own personal experience that before I took finasteride I could get a paper towel rub it on my face and you’d see the oil (disgusting) I know but that has completely disappeared which would be a strong indication that DHT levels have yet to turn back to baseline and my face is severely dry now with zero oil. The epignetic gene change is finasteride bonding to receptor sites inactivating them holyhead you seem like someone with an open mind please look into what I’m saying.
Plenty of evidence do you need reminding that my phone is broke?
I think this is all wrong. Here is what it’s really doing:
In biochemistry enzyme substrate is the material upon which an enzymeacts
“In the presence of nicotinamide adenine dinucleotide phosphate (NADPH), steroid 5 alpha-reductase converts testosterone to dihydrotestosterone (DHT)”
“Knowing that finasteride is a mechanism-based inactivator of 5α-reductase type 2 and that the mechanism of inactivation has an obligatory requirement for NADPH”
“Finasteride was originally thought to act as a competitive inhibitor with nanomolar affinity for 5α-reductase type 2 (12). More recently, it was found that finasteride acts as a mechanism-based inactivator of this enzyme (13). Subsequent to inhibitor binding, there is hydride transfer from the NADPH cofactor to the Δ1-2-ene double bond of finasteride.”
“The intermediate enolate tautomerizes at the enzyme active site to form a bisubstrate analogue in which dihydrofinasteride is covalently bound to NADP+”
Here is my understanding of what this means.
NADPH is the substrate required for 5AR to convert T-DHT (material upon which enzyme acts) Fin is fucking with the substrate. More specifically “forms an analogue of itself called dihydrofinasteride which is covalently bound to NADP+”
It’s forming dihydrofinasteride and than “covalently bonding” with the substrate that the enzyme needs to convert T-DHT. In other words it’s creating a permanent alteration of the substrate so that it can’t interact with the enzyme like it normally would.
Source:
If you look up what the strongest bond in bio chemistry is you get this definition:
The strongest bondsthat are present in biochemicals are covalent bonds, such as the bondsthat hold the atoms together within the individual bases shown in Figure 1.3. A covalent bondis formed by the sharing of a pair of electrons between adjacent atoms.
In my opinion what this means is dihydrofinasteride has been covalently bonded to 5AR’s substrate. But we still produce enough DHT and I don’t think our symptoms are due to lack of DHT. I’m sure it does not help but probable is not the cause.
I think we need to look harder at 3B-HSD. I have evidence that 3B-HSD is not working right in me. I also think when you fuck with that substrate you are making 3B-HSD not work as good.
I think that T-DHT conversation occurs in such a large systematic level in our bodies that just because some substrate gets “dihydrofinasterided” haha we are still ok because enough DHT is still getting made.
If you look at the functions of 3B-HSD it’s more specific in scope. For example the 3B-HSD enzyme makes 3b-adiol a very specific steroid metabolite that you are less likely to see getting made up in different places. I’m low in 3b-a diol. At least according to some old labs from 2014. I wonder if messing with the substrate NADPH is responsible for possible issues with the 3B-HSD enzyme
Thank you for digging into the subject I really appreciate it but if you do more searching you’ll find out that finasteride once binded to the receptor changes the structure thus even if the key and lock fit it won’t activate the receptor sites it permanently “denatures” them which would absolutely explain why there is epignetic changes being registered. What about other key neurosteroids being inhibted by the same mechanisms is this plausible?
I genuinely believe this is what’s going on there are only a handful of these drugs that make covolant bonds to the receptors and it would explain why our bodies can’t find a state of equilibrium because it hasn’t got a f’n clue what’s happening and trust me our bodies want to get better, it’s probably caught in the middle of wanting to be a man or women lol but that’s the truth it doesn’t know how to balance itself. Why Merck and Co would use this method is completely insane!
I’m going to bed now hopefully I die in my sleep or wake up in paradise somewhere from this God awful nightmare.
An irreversible antagonist is a type of antagonist that binds permanently to a receptor, either by forming a covalent bond to the active site, or alternatively just by binding so tightly that the rate of dissociation is effectively zero at relevant time scales.
This concept is real thing.
Please post your source that Fin is an irreversible antagonist to which ever receptor you are suggesting that it is
Are my onto something or not?
Go to the library and get on a PC. Since you’ve done all the research and have screenshots to prove it, none of us are going to waste our time recreating your amazing work.
Finasteride is an irreversible inhibitor. However this doesn’t explain the permanent side effects because the enzymes are constantly being regenerated.
We could be. If you find any good sources on what you are proposing post them here. Don’t stress over it though it’s not a big deal.
troll detected
It’s forming dihydrofinasteride and than “covalently bonding” with the substrate that the enzyme needs to convert T-DHT. In other words it’s creating a permanent alteration of the substrate so that it can’t interact with the enzyme like it normally would.
The enzymes can regenerate but if they try to react with their substrate that’s bonded with
“dihydrofinasteride” this could still be a problem seeing that according to the source I posted above in order for the 5AR enzyme to convert T-DHT it needs its substrate.
I think the question you want to ask is does the substrate regenerate it self resulting in new substrate not covalently bonded with this dihydrofinasteride? Or does the dihydrofinasteride “stick around” and continue to bond to the new regenerated substrate? When you see people talking about Fin preventing it’s own metabolism I think this is what they are talking about. We would need a bio chemist to chime in haha …
Either way I don’t think Lack of 5ar, t or DHT is the problem so I don’t think we need to worry about it. It’s about making the T and DHT we still have work again.
Not sure if above link is working just copy and paste into search engine duckduckgo. Having to write these word for word as phone won’t connect to site
The above gives detailed info as to what’s going on inside the receptor sites and the studies that say finasteride is a competitive inhibitor are only feeding off what Merck has published it’s all just recycled misinformation. It would explain why we can’t get better because the chemical bonds are nailed into the receptor sites stopping them from activating even if people go on HRT they won’t see any significant difference as the hormones are just circulating in the body doing nothing or abeit attaching to a small number of sites that haven’t been nuked yet depending how long you took it. There’s another 5alpha inhibitor but less potent in terms of reducing DHT it’s only legalised in China (someone look up the name please) it is heavily documented as a non competitive compound even though finasteride holds almost indentical properties and it’s interesting that it’s use is banned in America and elsewhere this would hold weight as to why they would lie to bypass the FDA as there’s no way this would have got the go ahead or maybe it would just to get the money rolling. American corporations work in unison which is why you’ll not find too much info on Google. If people on this forum want to put it down to a conspiracy that’s fine but there’s countless evidence if you look hard enough you’re doing youselves an injustice otherwise. Merck and Co knew of the sides a long time ago and the truth is they probably had a small team working on a fix as it would save them millions in lawsuits but this is irreversible coming from a chemistry point of view some might see improvements years down the line if the body produces new receptors which I’m not sure it does. This would also go hand in hand as to why epignetic changes are being picked up using genetic diagnostics.
Have a look at my latest post please, I was only able to post a few links as I’m having to type everything manually but the evidence is out there especially on duckduckgo. If people want to know what’s happening to them then I beg them to read into what I’m saying.
I just wanted to add this info that I found online about Fin.
Is it possible that the drug is still in our system and our body has hard time getting read of it? because it is insoluble in water.
what do you guys think any comments?
could alcohol consumption help body get read of this drug.
In fact anaerobic exercise have helped some people recover from this condition.
Just an idea.
The empirical formula of finasteride is C23H36N2O!
But wouldn´t everyone be damaged, not just a small group experiencing a crash and getting PFS. Also how do crashes come into play here?