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

Sorry can you explain your post a little more what di you say about brai barrier?

Drugs have to be able to penetrate the blood brain barrier to have effects on the brain, if Finasteride penetrated the blood brain barrier it has free reign on thousands of mechanisms. God knows what damage it produced…

I explained our situation by mailing to the dermatologist who wrote the post. me also asked him if I could personally access the material released at the symposium. I am waiting for a response.

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Thank you man.

Thanks everyone for the critical feedback. I believe the theory I advocate for can account for most of the points raised above. I am not claiming that what I am going to say is the only possible explanation but it is certainly a logical one.

The gist of the criticism above is that normal people without PFS do get an androgen response from systemic DHT, whereas people with PFS do not. The quotes below summarize this criticism.

It is important to know exactly what kind of androgenic effects normal people get from systemic DHT. Are we talking about falling hair, higher libido, larger muscles or deeper voice? It is crucial to specify exactly where the effects are and how strong. More about this later.

Of course we need to exclude from this particular analysis any effect of “other androgenic steroids” that in normal people may work through conversion to DHT in tissues or may require the balancing of DHT they already have present in tissues.

For example, you cannot claim that because Testosterone raises libido in normal people but not in PFS people, therefore PFS people are not sensitive to Testosterone. This is because Testosterone may exert its effect on sexual function largely through its conversion to DHT in key tissues.

Back to the effect of systemic DHT. It is entirely possible and is in fact most likely the case that different tissues in the body require a different concentration of DHT in order to function properly. It is known, for example, that skin at different places in the body has a different concentration of 5a-reductase.

This distribution is not likely to be binary - i.e. either 5a-reductase is present or not, but it is likely that even within tissues with high DHT requirement there is a range of optimal concentrations. There must be a lot of research about this and I encourage anyone to try to verify or disprove the claim above.

It is therefore expected that systemic administration of DHT will be adequate to different degrees for different tissues. One tissue may be getting close to optimal or in fact way above optimal levels of DHT, while another may still be starved.

My only evidence of the systemic effects of DHT administration in people with PFS comes from my own experience. I have observed androgenic effects in a wide range of tissues, which does confirm that systemic DHT indeed reaches tissues and has an effect on them, despite PFS.

What I claim, however, is that the effect is differentiated for different tissues based on their base level requirement for DHT. The tissues responsible for sexual function may require a higher level of DHT, which cannot be supplied through reasonably high systemic administration.

Some of the effects of DHT I have observed are the following:

First, my hair is significantly affected and sheds a lot when I supplement systemic DHT.

Second, my joints react immediately to systemic DHT and stop hurting. This is a profound effect and is the main reason I use DHT.

Third, I also experience stronger body odor when I use systemic DHT.

Forth, I experience a deeper voice, which I admit is quite unexpected and puzzling to me, because I have always assumed that voice masculinisation reaches a peak during puberty and it is not possible to further lower the voice with androgens. I did not observe a significant effect on voice previously with a liquid DHT formulation but I am currently observing it with a liposome formulation, which may indicate a different degree of absorption. I don’t know yet if the effect is permanent or transient but this is an androgenic effect nevertheless.

Fifth, I observe psychological effects of increased aggression and impulsivity and reduced anxiety.

Sixth, I also do observe an effect of systemic DHT administration on sexual function (libido, erection frequency and strength, sensitivity and pleasure) which is dose dependent but it is indeed rather weak for the doses I have used. (I do not use doses that would raise my serum DHT above the normal range). This may easily mean simply that the DHT requirements of the tissues responsible for sexual function are much higher than what’s possible to achieve with systemic administration.

This is confirmed by my experience that sexual function improves significantly more when DHT is applied topically to a broad abdominal and genital area, and the effect is also dose dependent. I get no morning and nocturnal erections when I am at my PFS baseline but I do every night when I apply DHT topically. I can also get spontaneous erections of various strength, which is impossible otherwise.

In no way, however, does this local administration of DHT lead to a complete reversal of PFS, as no doubt numerous unreachable tissues in the body are involved in sexual function, such as the pudendal and vagus nerves, the prostate muscle, and regions in the brain.

The fact that application of topical DHT on the broader genital, perineal and abdomen area (likely reaching the prostate and pudendal nerve to some extent) works better than narrow application to the penis, but worse than systemic application (i.e. application on the hands) indicates the importance of high DHT concentrations in key tissues involved in sexual function.

I cannot explain reports about shrinking penis from local DHT application but I do not find them sufficiently credible. I did read reports about such an effect but one guy claimed to have used the formulation only once and the other only briefly. I find it highly unlikely that any perceived shrinkage as a result of a single or brief DHT application represents in fact tissue loss, as that is simply not physically possible in my opinion.

At the same time, I have also read reports about the opposite with topical DHT administration - penile tissue growth, which I do not necessarily trust either. I have so far not observed any effect one way or another in myself. I believe any effect on the penile tissue is likely to require long-term administration.

As I have said before, such application is likely very risky before proper dosing can be determined and I do not recommend it due to cancer risk. I currently apply the DHT only to the abdomen and not on the penis.

I would like to solicit evidence about the effects of systemic DHT administration in healthy people - not on androgenic functions in general but on sexual function specifically. If systemic DHT in reasonable ranges has only a week effect on sexual function, as I believe is the case, this would completely explain the lack of effectiveness of systemic DHT in PFS people without indicating androgen insensitivity.

Finally, this theory supposes that 5a-reductase type 2 function is absent from key tissues to a greater extent in PFS than during regular fiansteride administration in non-PFS subjects. At least it is my experience that while on finasteride I had reduced but almost normal sexual function, whereas now I have almost complete absence of sexual function.

Any further feedback or criticism would be highly appreciated.


Your theory would explain why many people including a friend of mine report increased libido from proviron. Strange how some poeple respond paradoxically but there are people without pfs who notice no libido increase from mast and proviron too.

Why would my hair thicken back up but hair look prepubescent if there was nothing to the localized dht inhibition?

I don’t understand your comment. I am postulating that systemic DHT would have little effect on libido - PFS or not.

If you are aware of any evidence about the effect of DHT on libido in healthy people, please post. That would be very useful. I am sure there are forums with users who have tried it.

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This theory is parsimonious because it explains all available evidence, in my opinion, in the most simple way possible.

It is also a lot more optimistic theory than a theory arguing that not one gene, 5ar2, but many (androgen-dependent) genes are epigenetically silenced, as that would be much harder to fix presumably.

The theory is easy to test. It requires a single test: DHT concentration in prepuce of people with PFS and controls. An additional confirmatory test would be 5ar2 expression from prepuce.

Almost thirty years since finasteride was unleashed on the public, no such test has ever been done, to my knowledge.

Likewise, this community has waited for Baylor for 7 years and has not mobilized resources to do such a simple and cheap study.


I used Proviron before in the past. 20 days of it. Pharma grade. Increased libido, drier muscles and so many hard ons I felt like I took Cialis.

I had a bit of a sex addiction before fin so anytime I felt slightly horny I wacked it so never really got the full experience. I just felt the need to masturbate more. Like less recovery time.

I only ran it at 25mg a day too. TRT dose of test

NOTE: PFS users mileage may vary idk how we respond to hormones anymore

Idk dude Provirion was never really used by docs to make your dick go up and libido rage. That was the bodybuilders who figured that out. Either our bodies hate androgens or we just need something unlike nattys to get us working ok, I’m hoping the latter. I really hope proviron effects me similar. It would make life living again.

Worthwhile experiment.

Also proviron is already 5-ar. It wouldn’t care if you have no 5-ar? I thought you were saying we couldn’t convert 5-ar right? So no DHT made in tissues by TRT.

But Proviron and Masteron are already 5-ar so couldn’t they just act on the tissues since they dont need to be 5-ar?

I’m not saying its a cure. It wont be. It just might help ease my symptoms hopefully not make me worse.

Hopefully androgen genes aren’t suppressed. Hope to god. Some memebers have had success with DHT derivs

Also no offense but are baylor capable of giving people mast and proviron for a potentially unknown condition? Probably not. Its like how many doctors refuse patients cannabis medicine my friend when there are thousands of studies it helps cancer.

@Sibelio are you aware that exogenous androgens fully restore sexual function in castrated rats? Also I believe TRT works great for people with testosterone deficiency. So why doesn’t it work for us.

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According to my theory, T supplementation doesn’t work well in PFS because in order for it to work, it needs to be converted to DHT in the tissues. If our 5ar2 is damaged, as my theory postulates, then no DHT can be produced in key tissues responsible for sexual function.

How does 5ar2 work, is it produced and utilized locally? So when we talk about it not working are we talking about different areas of the body having a common problem of not being able to make DHT for themselves?

How does this account for people who deteriorate with exposure to androgenic substances?


Sibelio, have you ever looked at the phenomenon of “Deca Dick”? Apparently Nandrolone is notorious for causing persistent PFS type symptoms. It looks like there might be some research on it.

I think so. There are three different 5a-reductase enzymes and each of them is prevalent in different types of tissues. The enzyme is encoded for by a gene. The enzyme produces DHT locally.

If PFS is due to a methylated gene for 5ar2 in different tissues, this poses an interesting question. How is it possible for millions of cells throughout the body to simultaneously methylate the same gene?

If someone understands this better, please explain.

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If what you say is true. Wouldn’t 5-alpha reduced DHT derivatives like Anavar, Trenbolone, Masteron and Proviron work?

I think your theory holds some weight… My body hair has never been so white but god damn my hair looks like before I ever took steroids… Its insane how much regrowth theres been, could indicate lack of 5-ar in scalp. Especially since its been proven some PFS patients have methylated 5-ar?

Also my TRT gives me nipple pain depenending on the dose. Could be lack of DHT conversion in that area, never happened before. DHT stops estrogen from binding to the tissue too much.

Injecting Test wouldn’t work because it just wouldn’t convert to DHT in the right tissues. Explains why my TRT gives me temporary issues that fade away as doses lower.

Don’t get me wrong, I believe theres something to do with androgen receptor sensitivity and neurosteroids too but I think lack of 5-ar tissue throughout our body is part of our multi faceted issue. Hopefully the receptor sensitivity isn’t gonna make me reject all steroids or I’ll be pretty damn suicidal.

Few people have reported good results with DHT derivs. I have a friend who fixed deca dick libido with proviron.


Same thing my hair doesn’t even fall out anymore it’s fuller now all over my scalp which is very odd, it should be falling out rapidly like it was before.

I was getting nipple pain on TRT with low dose of 50mg 2 times a week 100mg all together. It’s like DHT is none existent since DHT balances out estrogen so we basically have testosterone and estrogen but nothing in between.

I wrote a very long post about this issue above. The DHT needs to be at high concentrations in certain tissues, which may be impossible to deliver through systemic administration, at least not without frying all other tissues. For example, DHT concentration in prostate is ten times higher than in serum.

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