A new theory about why PFS happens

I have a theory which I think might be a decent explanation for why PFS occurs. As we all know, PFS is strongly correlated with having overly upregulated/dense androgen receptors. This by itself is a vital clue which tells us something about the etiology of PFS. Namely I think that PFS is caused by a “runaway receptor effect”.

Its factually known that when you lower a hormone, its corresponding receptor will upregulate. Therefore when you take propecia its going to drop DHT which in turn will lead to the androgen receptors being upregulated; keeping this in mind, it explains the two different ways in which guys get PFS.

1.Some guys get PFS while they’re taking propecia without having any kind of crash which precipitates the onset of PFS. This can be explained by the fact that maybe guys who experience this had a high density of androgen receptors to begin with; therefore the usage of propecia upregulating their androgen receptors even more was the proverbial straw that broke the camels back and caused the body to freak out and silence the androgen receptors when it sensed that there were too many receptors

-This also explains why the likelihood of PFS happening seems to increase the more times that you quit and restart propecia. Its literally probably because you are “accumulating” androgen receptor density every time you go on propecia
-This also explains why there seems to be a rather large proportion of PFS sufferers (I dont factually know this, this is just my perception. I could be wrong) who claimed to have a large libido/be very masculine prior to taking propecia; its because they had a high density of androgen receptors to begin with and propecia was what tipped them over
-likewise there are many guys who claim that propecia has made them more masculine and increased their libido; this is because they had a low/average amount of androgen receptors to begin with and it was thanks to propecia that their androgen receptors upregulated, thus pushing them into the highly upregulated androgen receptors category without quite pushing them over it (yet)

2.The second way is the one that we’re already familiar with. A guy goes on propecia, while he’s taking it his androgen receptors get upregulated, he goes off of it and a flood of DHT swamps his newly dense and sensitized androgen receptors thus causing his body to freak out and silence the androgen receptors

In both cases, I suspect that an over-proliferation of androgen receptors (hence the “runaway receptor effect”) is what increases the chances that the body will sense that there are too many androgen receptors/overstimulation of androgen receptors and will then silence the androgen receptors. This is particularly the case for #1 since you have to keep in mind that this happens while the person is taking propecia. While a person is taking propecia their body is being forced to deal with artificially low androgen levels and their body has no way around this as long as the person is taking propecia. As a result of this artificial, external pressure, the body is unable to act differently and thus continually upregulates and upregulates the androgen receptors until finally something breaks.

It might be more proper to view the two types of onsets of PFS as being the same type of onset but just happening at different stages. The first type of onset of PFS is what would happen to guys who experienced the second type of onset of PFS if they had stayed on propecia long enough. Obviously though, what “stage” you get PFS at depends on your initial androgen receptor density when you first started taking propecia

With that being said, I think that the way to treat PFS involves two things:

1.you must downregulate the androgen receptors

2.you must resensitize the androgen receptors

Its important to keep in mind that these are two separate things which must be addressed individually. Do not conflate these two. Just because you downregulate the androgen receptors doesn’t automatically mean that the remaining androgen receptors will get resensitized or unsilenced.

In order to do #1, you need to use soy. As I have written on here before, there is something very unique about soy. Its an anti-androgen yes, but it works in a different way than say saw palmetto or zinc. To clarify this, the way that soy primarily works is that it downregulates the androgen receptors, meanwhile saw palmetto blocks the androgen receptors themselves and as for zinc it simply lowers 5ar. Therefore for a PFS victim, working on the assumption that their androgen receptors are overly upregulated, they probably want to do a cycle of soy first in order to help bring the androgen receptors down to a low or at least normal density.

Personally I can vouch for this; I clearly remember being extremely sensitive to small amounts of creatine or tribulus before I discovered soy. However, after discovering and using soy for a long time I became permanently “less sensitive” to small amounts of creatine or tribulus and instead would only respond to normal dosages of these supplements. This strongly implies that my androgen receptor density decreased after taking soy and this is what caused me to react in a more normal fashion towards normal doses of tribulus or creatine.

To give a more concrete example of this; before experimenting with soy I would experiencing good effects by just taking 200 mg of creatine, if I took a larger dose than this then it would trigger my PFS and I would get shrinkage, ED etc. However after experimenting a long time with soy, I could take a heaping tablespoon of creatine (approximately 25 grams) and be completely fine without experiencing shrinkage, ED, headaches or any other negative effect. This is really a monumental difference, I went from only being able to handle 200 mg of creatine to being able to handle 25 grams of creatine; and this effect was permanent as well.

As for #2, this can be done by using saw palmetto, zinc or any other anti-androgen which either lowers 5ar or blocks the androgen receptor itself. The primary idea here is that in theory you should be able to safely use anti-androgens to resensitize the androgen receptors as long as your androgen receptor density is relatively low. This makes sense because we are dealing with the same dynamic as when you first started using propecia. Depending upon your androgen receptor density, you will have a greater or lesser chance of worsening your PFS by using anti-androgens like saw palmetto or zinc (which upregulate the androgen receptors as a side effect). According to my theory, In order to SAFELY use these, you need to make sure that your androgen receptors have been sufficiently downregulated by doing a cycle of soy beforehand

I can definitely vouch for step #1 (downregulating androgen receptors), however I am still in the process of experimenting with step #2. Personally I think this theory is probably pretty accurate and it makes sense, but I do remain modest in my expectation that step #2 can be easily achieved. Like I said, it will just require more experimentation to confirm or deny it. At that point I will give an update on it. Anyways I hope you guys find my theory useful

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Are you the user ihatefin88 from solve?

So are you going to try your own method? It seems risky. I would never try to downregulate my receptors even more.

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If we had some rat models with PFS then we could test out these theories.
Let’s get the rats first.

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Most of this theory is not new, or at least the parts that make sense aren’t. Let me ask you something though. Hopefully you will answer me, because no other proponent of this theory has.

Why do some people get PFS from their very first pill of Finasteride?

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Or 1 pill of isotretinoin like me. Or 1 pill of SSRI. This theory doesn’t add up.

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@borax yes I am

@Cooper Yes I have and I continue to carry out experiments. I wrote this in the OP

@Sibelio

I addressed this point in the OP albeit somewhat indirectly which is my fault:

1.Some guys get PFS while they’re taking propecia without having any kind of crash which precipitates the onset of PFS. This can be explained by the fact that maybe guys who experience this had a high density of androgen receptors to begin with; therefore the usage of propecia upregulating their androgen receptors even more was the proverbial straw that broke the camels back and caused the body to freak out and silence the androgen receptors when it sensed that there were too many receptors

Basically some guy already has a high density of androgen receptors; he then takes a single pill of propecia which proceeds to dramatically drop his DHT (keep in mind how potent propecia is), afterwards his androgen receptors dramatically upregulate in response to the shock caused by taking the single dose of propecia and boom, his androgen receptor system goes offline due to the androgen receptors becoming overly upregulated. In other words it totally depends upon your androgen receptor density starting out as well as how strongly your body upregulates androgen receptors in response to suddenly lowering androgens, assuming this theory is correct.

@slick1
isotretinoin and SSRI bring about PFS like symptoms in a different manner. Although I seem to recall that isotretinoin is a 5ar inhibitor but I have problems finding studies showing this (I havent looked particularly hard though). Therefore I dont really think its right to compare what happens with one pill of isotretinoin or some SSRI to one pill of propecia, although a similar receptor dynamic might apply to those cases as well. Anyways to answer your question look at my response to @sibelio

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The people who get PFS from 1 or just a few pills must have something in common?

Are these people all highly creative? I think they might be.

Did they share similar upbringings? What’s their parents occupations or background.

according to my theory, the people that get PFS from a single pill satisfy two conditions:

1.they had high androgen receptor density to begin with

2.their bodies’ response to suddenly dropping DHT is stronger than usual which in turn causes the body to violently upregulate androgen receptors in response to the shock, this in turn exacerbates the condition of them having high androgen receptor density to begin with and ultimately results in shutting down their androgen receptor functioning.

If 1 is correct wouldn’t they have above average body muscle.

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different people express high androgen receptor density differently. There are some really muscular guys that can’t grow facial hair while there are some really skinny dudes with a fullbeard. My point is that due to the complexities of genetics, having a high androgen receptor density doesnt always express itself in the exact same way for every single person

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I remember there was another guy with similar thread and approach. He was willing to use fin again for resensitizing AR’s. Think he was a doctor. Maybe someone can find his thread ?

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yeah I would love to see his thread

in theory, if you are taking soy concurrently with propecia, or at least do a cycle of soy before taking propecia, then this would make propecia safe to take for resensitization purposes since the androgen receptor hyperdensity problem would be resolved. That being said, im not quite willing to experiment with propecia, although I am currently doing major experiments with anti-androgens and I will write an update about that when I finish the experiment

A lot of good theorizing… I agree with Part 1 as it explains how people get PFS without a crash. It also explains why it seems like hypersexual people often get PFS.

However I disagree with your proposed method of curing the condition. I don’t think that it is the receptors themselves that regulate androgen response. The body is constantly regulating receptors in order to induce the right response. There is most likely some gene higher up which is responsible for that. And I believe that in our case this gene has been silenced. Otherwise, our body would simply regulate AR correctly again. So getting cured would involve demethylating this gene. There may also be other genes involved in the androgen response that are silenced, maybe even AR itself. This explains why every PFS case is so different.

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Pre PFS my dick was way above average regarding size (naturally high AR). My dick got hit hardest by PFS cause I was never able to recover my size, while other symptoms got way better.

Pre PFS I wasn’t dominant or alpha (low AR density in brain) . Since PFS I’m extremely dominant, more aggressive etc. also during sex.

This theory makes pretty good sense for me.

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Yeah I actually agree with you. Curing the condition might be the hard part, but at least its helpful to have a theory like this as a general model for understanding what happened to our bodies

that being said, you can still get some partial recovery by using soy, saw palmetto, zinc etc. Additionally I have a theory that by incorporating elements from @Invictus’s tomato juice theory that its possible to “shock” the androgen receptors into becoming sensitive again

Saw palmetto is dangerous

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The dominant theory has two parts: 1) finasteride reduces androgen levels which upregulates ARs. 2) stopping finasteride restores androgens which overwhlems the ARs and an epigentic downregulation happens (downstream from the ARs, while ARs remain upregulated). The second part happens when androgens rise. You manged to sorta explain the first part - that a single pill violently upregulated AR. You have not explained why there is simultaneous epigentic downregulation, as that needs to be in response to too much androgenic signal. What we have here is too little androgenic signal, that’s why the AR upregulation happens in the first place. Unless you argue that AR upregulation overshoots, and then this overshot is corrected by the epigenetic downward shift, which would be very creative indeed.

Anti androgens like saw palmetto are responsible for some posters being here in the first place. Those substances can also make existing cases worse.

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after i have developed pfs, i tried to do something to get better like anyone else, so i went to the gym for about two months, and at that period i bought a random protein, accidentally, i noticed that there was saw palmeto in protien, BUT, i got better while on it, after that i left the gym+protien and the symptoms got worse, so the theory make sense to me.

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