Real quick question

  1. I am in the process of filling out a new member sheet so bear with me.

  2. I’ve literally exhausted myself trying to find out what caused this and how to fix it. I’ll keep opinions to myself for now. I’ve read through so many forum posts it’s not even funny so I need some help organizing my thoughts: - when we say to new sufferers “most people recover and don’t worry”, I feel like this isn’t necessarily true.

There’s a clear line: ppl who crashed I feel like do not make full recoveries. People who experience that horrific debilitating like a light switch and grenade went off rarely recover.

Then there’s the other group who have these symptoms but not the crash. Many had sides while on fin and not coming off the drug. People who got severe sides coming off the drug fall into a completely different category than ppl who simply noticed some side effects because of low DHT and it took their body some time to revamp once quitting.

My opinion: there’s one group who got crushed coming off fin. And then there’s another group who simply experienced side effects from 5 alpha reductase inhibitors.

Does this make sense?

The second group you mentioned (experienced side effects) does not have PFS. PFS means experiencing any symptoms persistently after stopping finasteride. And yes there is a distinction between those who crashed and those who did not. A crash seems to cause more serious symptoms. But there’s no reason to believe that those who didn’t crash simply have “low DHT”. If that were the case then taking DHT would work as a treatment.

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I agree with 90 % of what you said. What Im trying to distinguish in my head, and what I firmly believe is that those who crashed have a completely different mechanism and/or body response compared to those with side effects that resolve.

Crash group: yes 5 alpha reductase was lowered and coming off of the drug a huge crash happened and mechanism A caused mechanism B (persistent) to happen

Side effect group: got off drugs and noticed side effects because of 5alpha reductase being inhibited (possibly mechanism A) but they never got to mechanism B.

I guess what I’m saying is from my research and browsing through this, a crash signals much more severe and persistent side effects in majority of cases. Those who did not experience a crash (majority) but do report side effects- they tend to recover. This leads me to believe that there’s an entirely distinct mechanism going on here with the persistent cases and the group who did not crash wasn’t afflicted with the persistent mechanism that gradually resolved.

I know that’s wordy but that is the best I can do!

Our condition is like deca dick. Hormone panels are normal or slightly lower.

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Not sure I fit into either category. I took two pills and felt horrible after the first (don’t ask me why I took a second). Either way after the second pill all hell broke loose with extreme vertigo, dizziness and a feeling like I’ve been drugged. This has lasted ever since for 1.5 years. Agree it’s some sort of “switch” for some of us. I remember being myself, going to bed, and waking up like a literal bomb went off next to my bed. I had to pull myself up to my bathroom sink. Literally as if I was drugged or something. My body adjusted a bit after a week (to the point where I could walk), but still generally have all the same symptoms.

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I believe that the fundamental mechanism is the same in both groups, because the symptoms are the same, just that they tend to be more severe in the second group. So the crash is the same mechanism just much more serious.

I’m not sure why you think the group that did not crash usually recovers. There are very few recovery stories at all. As for myself, I did not crash, and yet my symptoms have become worse since the syndrome started 1 year ago.

Dude literally same. I was going through a ridiculously stressful time and just got over mono, took a 5 alpha reductase inhibitor and then absolutely bam. Complete 180 of myself. Thank you all for replying, it confirms to me that there’s a totally distinct mechanism going on with us.

I don’t believe those who didn’t crash and simply experienced side effects had the, we ll call it permanent mechanism switch and gradually recovered from that mechanism.

What we have is a totally different mechanism going on.

I think it’s a totally different mechanism. Maybe u didn’t crash or experience the hyper androgen stuff and then bam, but I bet one day u didn’t feel like yourself and it continually gradually got worse. I know we and I lump this shit into categories and it is so highly variable-it just makes it easier to understand.

Could deca dick be the same syndrome that we have? If I remember correctly nandrolone has very low androgenic activity. So when nandrolone binds to the AR, there will be very little androgenic activity, and testosterone/DHT will not be able to bind to the AR. So nandrolone could ultimately have an antiandrogenic effect similar to the one caused by finasteride and other substances.

This is speculation, I don’t know if what I described is actually possible.

I think it’s interesting that there are also sporadic reports of guys suffering the same thing as us after severe stress, an extreme illness or virus, or doing a crash diet or cutting weight too fast.

Actually I didn’t have a day where the symptoms worsened suddenly. I simply stopped the drug and the symptoms never went away, instead they became significantly worse during the year.

I do believe that there is a difference between crash and non-crash cases, but I don’t believe it’s beneficial for the cause to attempt to divide the community. We have a better chance of receiving resources for research if we can prove that the same condition is affecting hundreds of thousands, if not millions, of people in the world who have taken different antiandrogenic sunstances.

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Yeah I definitely didn’t start this thread to cause divide. I started it for clarity on my own question cause I have my own theory (been stated here before) but I don’t like stating anything cause everything goes crazy. Also I’m into research (completely different discipline than this) and have a couple studies that will be published and I can tell u relying on research studies and getting funding is absolutely useless (MY OPINION AND EXPERIENCE) unless it is some absolutely serious funding.

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I agree with your theory. The nandrolone becomes DHN by interacting with 5AR. As a result, DHN is created instead of DHT and DHT is reduced.

https://www.sciencedirect.com/science/article/pii/S0039128X17302453

We are not the ones who enjoy strenuous exercise, but I think this material will be a good reference.

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I think there is so much variability with this condition that trying to make sense of the wide range of symptomatic manifestation with the limited knowledge we have available now will only lead to more confusion for those trying to make sense of it.

This same type of variability among PAS patients has divided the community instead of leading us to come together toward productive ends. It even prevents some of those with symptoms identical to the archetype case of PFS from joining here.

IMO there are as many forms of this as there are patients and, in short, trying to categorize “types” won’t lead you anywhere.

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Thank u for ur feedback

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Just to follow your thoughts, it could be all due to individual predisposition and nothing to do with differences in the underlying cause itself. Only speculating here.

Probably a combination just like everything else. Just trying to piece together some of my observations

No crash for me. Started getting some symptoms in 2016 but didn’t link to SP and continued to take that poison for 6 months. Things got worse when I stopped but no sudden crash, more of a slow decline for a few months but this decline may have reflected sinking into depression because of months of having low libido, rather than an actual PFS-induced decline. Symptom severity has fluctuated for last 2-3 years.

On a side note, I was sick for a few days recently and had 4 straight days of nocturnals and libido was so high for a moment that I wanted to masturbate while I was driving.

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