Can someone explain if/how neurosteroids are affected and what it means?

I’m barely in range on the dht blood test. I wish these deca guy’s had dht bloods just to compare but I didn’t notice any.

So something is up with your conversion to T to DHT since…DHT comes from T (DHT is a metabolite of T). The conversion is not happening or something.

I have no idea what my DHT levels are; but I am going to supplement heavily with creatine and all other supplements to hopefully ignite and restart the 5AR and then DHT. Starting with creatine… then DHT / 5AR boosting foods. For e.g.


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Great. I will take all from this. Not touching any of the drugs though. I made my mistake.

Get some feedback on creatine before you jump in. Maybe the amount you take or brand makes a difference on how safe it is.

OK creatine has been tried by many…some with even worse later results. This is scary.

Yes thanks. I did a bit more research. Some scary stories on this forum with those that took creatine.

Sobering; Crash with Creatine

Looks like Creatine is a temporary thing at best and something that will interfere with androgen signalling / T to DHT conversion permanently at worst.

It seems that the high that people experience when supplementing creatine is a small temporary boost in DHT which makes them think they are cured. However, this obviously ends when they stop the exogenous supplementation, not to mentioned the increasing creatine dosages they need to feel the same effects as time goes on.

At this point I am going to hold off the creatine. I did take some and feel a bit better but its definitely a slippery slope. I think at this time I am just going to stick with natural methods to increase DHT (food, exercise, cold showers etc.). This should hopefully naturally stimulate whatever is damaged to heal…hopefully.

Having said that, I have no idea what my DHT levels are. If your DHT levels are high, I doubt you would be having any issues and would not be on this forum (thoughts on this assertion @Sibelio?).

The issue at this point is a signalling, receptor and/or 5 Alpha Reductase issue… I think the way forward is only natural means to naturally heal. Supplements would only offer a temporary solution, unless of course they have stimulatory effects that will support long term self sufficiency.

I think at a minimum one should measure his DHT level and 5 Alpha Reductase levels to at least narrow down where the issues are, then go from there.

Hi @Sibelio, i am going through this thread. I was healthy and abused Proviron and had amazing libido on DHT. If you go to steroid and bodybuilding forums you will find the same.

You can have normal serum DHT but still have low DHT in tissues responsible for sexual function. There is not a strong correlation between the two. DHT in prostate for example is 10 times as high as in serum. If 5ar2 is damaged, 5ar1 might still work and produce DHT in other tissues and be the source for serum DHT.

How many are there 5ar enzymes, 3 right? What are they all responsible for?

Yes, there are 3 types. They catalyze at least 10 different hormone conversions - T to DHT, progesterone to 5a-dihydroprogesterone and so on. Here is a list from Wikipedia:

Different tissues have different concentrations of each type. Type 2 is the most prevalent one in tissues responsible for sexual function. Type 1 may be more prevalent in tissues producing neurosteroids.

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Very interesting. So in your case, initially Finesteride works by basically selectively blocking one, several or all 5AR to stop the conversion of T to DHT to prevent hair-loss. This has disrupted/retarded the AR signalling and 5AR activity.

At this point to me it seems there is only one reliable way but to reactivate those two components; the AR in the tissues and thus in turn the 5AR and thus T/DHT conversion… but going through your theory, it seems you think there is a tri-dependent relationship between AR, 5AR and the T to DHT conversion. I wonder if activating one as a tinder can act as a spark to jump start the other two…

I wonder that is probably way people on this site were so drawn to the creatine as it instantly metabolises T to DHT and gives them instant relief. I’m wondering if creatine at low doses (say half a teaspoon every second day for an example) can give a stimulatory effect to activate 5AR and thus the T/DHT conversion which will slowly awaken the down regulated AR in parts of the body over a sustained period of time. Slowly increasing circulating 5AR in the body may stimulate the AR is just my thought. In turn, the AR will be stimulated to produce more DHT, thus stimulating 5AR and thus the tri-dependent relationship starts working again.

This combining with a 5AR supportive diet and resistance exercise which I believe will stress/urge and demand the body to restart this tri-dependent relationship. Exercise is likely to deplete DHT, and thus when depleted will demand the body to produce more through the tri-dependent relationship - this is where the 5AR will need alot of support through 5AR support foods, low dose supplementation (as it has been selectively damaged blocked from Finesteride).

In my case though, I have not selectively blocked 5AR but just damaged the tri-dependent relationship thought exogenous DHT (disrupting the signalling of AR and 5AR). In which case, I believe the same approach as above (for me) is worth a shot.

I have not looked into creatine. I will try to read about it.

In general, whenever you have a self-regulatory system which is propped up by an exogenous supplementation, the challenge is how do you avoid crashing the system when you withdraw the exogenous element. I guess slow withdrawal is better but would it be sufficient - I don’t know.

The AR is upregulated in PFS. The reason for this, I believe, is that AR is negatively regulated by DHT. When DHT is low, AR gets upregulated. Notice that my theory is based on the assumption that it is the opposite with 5ar2 - there is a positive regulatory effect of DHT. There are papers that show this for 5ar2 but not for 5ar1. In any case, things are definitely more complicated than this simple model.

I don’t think it is correct to say that DHT gets depleted from exercise. It is indeed increased by exercise though through upregulation of 5ar. Interestingly, AR is also increased by exercise. So the entire system is forcibly put into overdrive by exercise to increase androgen signal.

NB!

I hope I will write a separate post about this but I have already noticed the effects of resistance exercise on increasing DHT in the muscles/joints. My joints/muscles are DHT insufficient and as a result there is inflammation, which results in extreme joint pain (I have provided a paper about this in the thread above). I control the pain with exogenous DHT.

Since I have started exercising, the pain has gone down significantly and I require a lot less DHT. I have lowered my DHT to less than half what I needed before to remain pain-free. I don’t know yet if this effect will be permanent but I guess I would have to do this for longer.

While I have no doubt this is working in muscles/joints, the question is can it also work in peripheral tissues such as pudendal nerve, penis, prostate, etc? From what I have seen in the literature it can but the effect on 5ar there might be smaller, so it might require a bigger exercise load/full body effort, plus might take much longer.

Yeah you are right. My guess is not to rely on creatine as a means of reliance but to stimulate 5AR and in turn the AR - as well as stress the body to demand the creation of DHT (and in turn further stimulating AR signalling and 5AR).

Yes not depleted by DHT but stimulate the demand for it through exercise - or any activity that will require the body to produce DHT in general (watching porn?) without masturbation?

Shit, thats complicated. So you got a see-saw, inverse relationship…where you can fix one but not the other and vice versa.

Does Finesteride target all 3 5AR?

It probably targets all 3 but with different affinity. Type 2 is affected the most. They used to think type 1 is not affected but now they know it is, just less. It might be interesting to observe how people with PFS from finasteride vs. dustasteride differ. 5ar1 may have a different regulatory mechanism than 5ar2 so it might be more resistant to crashing. It’s possible.

In your case, even though you did not take a specific 5ar inhibitor and you just had a sudden drop in DHT, your 5ar silencing may still be concentrated in the type 2, since that may be more sensitive to drops in DHT.

There is a paper about the sensitivity of the different types of 5ar to DHT. Will try to remember where I can find it.

@provironabuser Do you have changes in urinary function as well - reduced pressure, slower urinary flow, urinary drip, incomplete emptying of the bladder, etc?

Yes. I attributed this to having an enlarged prostate due to the exogenous DHT (Proviron) but it could also be due to the new veins (varicose) in the penis?

It could also be due to the structural size change of the tissue due to decreased size of the penis (due to low DHT)

If you fix the entire issue, I am pretty sure this issue will go away.

DHT is what makes men, men. So it is more a Testosterone (T) to produce DHT issue than a Testosterone issue. Focus of effort must be in assisting and supporting the Androgen Receptors (AR) and 5 Alpha Reductase Enzymes (5AR) to support the conversion of T to DHT. Although boosting T will also indirectly stimulate AR and 5AR to assist in the conversion. Sorry just a brain dump of what I have learnt being on this forum to address my issue.

Insights;

If you have PFS, urinary problems are likely due to lack of DHT in prostate and other pelvic muscles, not to enlarged prostate. The prostate requires DHT to function. Lack of DHT may also lead to prostate inflammation (similar as in joints), and of course to shrinking of the prostate. Most people with PFS don’t have and have no reason for an enlarged prostate since they never had high levels of DHT.