The androgen insensitivity theory is fairly precise though.
None of the crash triggers should affect that. I don’t see a possible link between low allopregnanolone (which is clearly significant) and resulting AR insensitivity. I’m all ears though if someone can come up with a theory.
Moonman,
The study you mentioned (but no link?) is very very interesting. I was going to say bingo this is exactly what some of us have but the again BENS mentions a reasonable challenge to this idea, which is why our symptoms fluctuate.
If indeed we have androgen insensitivity The answer to this is difficult obviously but any theory can be equally challenged, let me try:
We do not have complete androgen insensitivity, that is for sure. But insensitive enough that even a normal level of hormones in the blood no longer causes baldness nor sexual sensation, hmmm.
But, since clearly some receptors are still working OR all receptors are working just they are less sensitive then increases in DHT binding to the receptors that is not counteracted by increases in other feminizing hormones or by a further desensitization of receptors does some good. For example, if i take 3 pills of androhard twice a day, i feel better, sexually and mentally, but this only happens when i use androhard very very rarely, like once every 3-4 weeks. If i take it 2-3 days in a row this effect goes away. Similarly stress is known to reduce T and thus DHT and alcohol reduces T but the next day increases T as the body tries to compensate for the drop (there are studies on this).
So my bottom line is that i think we have enough evidence of some degree of androgen insensitivity, but because it is not complete there are days when the conditions are good enough for us to feel almost normal. What are these conditions? Hard to say but clearly changes in T/E and DHT play a role, however had we absent androgen insensitivity it is hard to explain how a doubling of dht will not make us more sexual, in a persistent way that is.
So it is very possible that we have both, a disequilibrium in hormones and androgen insensitivity, but i think the latter is the problem, cause i think we would have managed to get back to equilibrium over a short period of time or through medications if the AR are not reacting oddly to stimulants…
my own experience: before propecia i was using RU, a flutamide like agent. One day i overdosed on this pretty badly, i had immediate exhaustion and over the following 2 weeks i had weird genital numbness that drove me crazy. Stupidly, i was not sure whether to associate this with RU or with biking induced pelvic pain. I stopped both but i continued to feel like shit. Nit wanting to neglect my hair i went back on small dose of RU thinking it is impossible for this to be the cause, and i remember that within few days everything normalized and i was again horny like hell… Had i linked the numbness at that time correctly to that RU super dose i would probably have never tried propecia…
I really really think that what moonman says supports my theory and we need to see how we can experiment with that without hurting ourselves (not with antiandrogans but maybe food). Think about it this way: more T makes most of us worse, so it is not crazy to think that less will make us probably better (it is clearly not given but one possibility, …). When i do resistance training (which increases T) my penis get numb like hell. When i go for a long long walk or long slow run(reduces T) i feel better.
Hmm…
One thing we need to understand is that serum DHT is useless. It does not function in an endocrine fashion. DHT is an autocrine hormone. ie it is produced on the spot right next to a receptor to be used right away. That is why tissues have their own (and different types) of 5ar.
So for guys who supplement DHT… that isn’t how DHT is used by the body. Although I can understand it having some effect. By supplementing DHT you could be down-regulating DHT production in the manner it is supposed to be (and is effectively) used. Then after a few days you are left with a bunch of (relatively useless) serum DHT.
Grueling exercise will stimulate the sympathetic nervous system, whereas light exercise will have the opposite effect.
I am not saying AR insensitivity isn’t the answer. But if we want to figure this out, we have to look at what we know. And the information we have does not point in that direction IMO. It should be tested for however and honestly they should be able to figure that out.
Thanks Bens, i like your scientific approach. I do not deny the fact that serum hormones are not providing the full picture but i cannot see what is the basis of rejecting this hypothesis (of receptors being desensitized). I think you are rejecting them in the basis that one some days some pfs sufferers feel almost normal, but these days could involve an abnormally high dht production or any level of hormone level or ratio that somehow compensate for the partially densensitized ARs.
I have two additional reasons:
1- we are not the only one to mess with hormone levels, body builders do it all the time, but they manage to recover, and do not experience pfs symptoms (insensitivity, hair stabilization,…). People here are here either because of 5alpha inhibitor or because of an antiandrogen (few cases). Fin is also known to have a secondary direct effect on the receptor as far as i understand.
2- the studies conducted so far on PFS have not shown a consistent difference in hormone levels between PFS and healthy, and the only one that has found something is the italian study: showing overexpression of AR!!! So if AR is over expressed and we are not managing to find a difference in hormone levels that seems to suggest that ARs are acting weird. Of course you might argue that the hormone problem is LOCAL … I am not sure if studies have tested that.
So while i agree we do not have any solid theory, i would not rule out the AR at all. And i am waiting for moon to send me a link of that paper.
I am basing it on everything I know, not just fluctuating symptoms.
In addition… people crash at different times. I crashed after 7 weeks. From what I understand DHT should’ve been long stabilized by then. There are people who crashed after 3 months. I don’t see why ARs would start to wig out after that amount of time.
The AR overexpression was in the foreskin iirc. That sounds like it could be due to something as simple as poor blood flow and low circulating androgens. Who knows. Poor blood flow seems like a fact. Obitoo from hard flaccid claims that he had hypogonadal T levels just from hard flaccid and poor blood flow.
I’m glad I’ve found a current discussion on here --which is hard to do.
Because I’ve not been studying the potential sources of our problems, the best I can muster at the moment is: are you discussing whether AR gene over-expression might be the source as opposed to inadequate DHT or inadequate 5 alpha reductase?
Also, I can see “bens” discussing insensitivity above. bens, if you think that insensitivity is a good theory, then how would you account for an increase in symptoms after many months or 6 years of symptoms when a guy suddenly takes either an A) an estrogen block (product: “Inhibit E”), or he has taken broccoli extract and experienced a further permanent de-sensitization of his penile tissue, along with further shrinkage of genitalia?
I am beginning study in molecular biology and some genetics this year, so I plan on spending some time getting up-to-speed on our problems.
This site has been long-overdue for some re-organization. I found this discussion via a search on resveratrol on google; not by looking through the index.
T-bone, I find that using the 'view new posts" button in the top right corner of the website the best way to find current threads.
From what I understand, the Italian study is looking at PFS from the 5ar enzyme perspective and the others are looking at it from the androgen receptor perspective. There is also a good mixture of genetic profiling, epigenetic profiling, neurosteroid and hormonal profiling, looking at nerves, etc.
The progressive symptoms related to PFS seem to be physical. ie erection quality, numbness, shrinkage, etc. I think that a lot of these things can be attributed to the often progressive nature of pelvic floor dysfunction. I’ve never read about someone’s libido, brain fog, or sleep getting worse post crash.
However, I don’t think AR insensitivity is likely. Not everyone crashes after ceasing the medication. Many people develop PFS while on the drug and it just never goes away. So the proposed mechanism for AR insensitivity developing doesn’t make sense.
t-bone, glad you joined the conversation. If i was not too old and too sick i would have enrolled in medical school because of this crap.
Bens was skeptic about insensitivity, it is me who was pushing it a bit. I think these conversations are useful.
you mention something VERY important at least for me. Indeed when i took small quantities of an aromatase inhibitor i felt like shit for days after. However my experience with it has been mixed. There are times when i took it and felt much better. It seems very much dose dependent.
I am not sure how that squares with receptor insensitivity, if at all!! I am not pushing this story of receptor problem, it is just that there is not enough evidence in my mind to rule it out. Indeed both studies plan to look into the receptor…
I have heard good stories about broccoli. There are bad ones too? Shoot everytime i go and buy something i hear a scary story about it. I got tribulus and before intake it i read a couple of scary stories.
well, just to let you guys know I am the guy who tried Inhibit E and broccoli extract and saw his symptoms worsen.
I tried broccoli extract just this month for about 5 days only and saw my gentalia shrink even more and pretty the remainder of my glans went completely numb (but for a little bit near the urethral opening (meatus?). It would SEEM that based on my experience with both Inhibit E (2010) and with broccoli extract much more recently, the simplest explanation might be conversion of more protein into female hormones. But I really have no clue and I have to wonder why a female hormone would cause the penis to become numb. What ideas do ANY of YOU have on this? My post-fin crash happened exactly 6 years ago.
Just to make this all crystal-clear: six years ago, during my post-FIN crash, my penis and testicles shrank to their first post-FIN size accompanied by a lot of permanent desensitization all along the penis but somewhat less desensitization in the head (glans) of my penis (exhibit B). When I took Inhibit E in autumn of 2010, my penis was shrunken permanently slightly more and further densensitized (permanently)… that’s penis “C.” Now, over 4.5 years after the Inhibit E, I’ve tried the first product since then, which is broccoli extract (2000 mcg Sulfuraphane) and now found a permanent shrinkage and even further permanent desensitization of my penis (exhibit D). At this point, my junk is “colder” than it ever was, having the sensation of being run over a cheese grater and exposed to frost in the area of the penis under the prostate (the “taint”).
The numbness coincided with the shrinkage. Shrinkage is due to poor blood flow (or rather, dominance of the sympathetic over parasympathetic functions), which is related to hypertonicity of the pelvic floor. I don’t think that any hormone problem could simply shut off the sensory capabilities of a nerve. It seems that the numbness/sensitivity issues are related to blood flow and possible nerve impingement.
I understand that libido, etc. can increase pleasurable sensations, so there’s that. But a lot of guys can’t even feel hot/cold or pain. Or can barely feel it.
My overall body temperature dropped after FIN, but the feeling of “coldness” in my penis or pelvic floor may only the best description of what sensation is there. In other words, it’s hard to know what I’m feeling, but it feels ‘cold’ while I do know that just by palpitating my glans (penis head) that has been colder since 6 years ago.
I am not sure it is a circulation issue, maybe only to an extent. When my penis would get cold and shrunken i use to use a heat pad above my pyjama in this area, and yes i felt more circulation less cold, same if i go for a long walk, but the numbness was still there.
I read somewhere that dht is responsible for this electric feeling in the genital skin. When dht is not binding correctly your genitals feel dead…
Here is an additional data point: me and several others on this forum saw substantial short term improvement in sensation after taking pro dht or dht supplementation… How can we explain that?
The only problem is that they do not last, and it feels as if the body builds immunity to this…
tBone: since you have been suffering for 6 years with apparently very little improvement did you try some of the more aggressive experimental treatments such as progesterone? Or at least tribulus?
I can understand people who are one year in hoping for a natural recovery and afraid to rock the boat but past few years i would try anything…
And finally: are you participating in any pf the studies? We reallly need people, particularly those with genital numbness since they are going to study the epigenetics of this condition…
I’ve participated in the Boston study. I went there last summer.
The thing about our problem is that A) no one has had answers except that B) some who are able to complete a regimen which involves some exercise on one’s feet along with some supplements and special diet (see some recoveries on this forum). In my case, I have not been to an endocrinologist in over 5 years because no one has offered any evidence that they have a real solution in endocrinology. I am just now scheduling to see some endos ASAP and maybe one or two urologists.
If I were able to complete lower body workouts like I would have years ago while using diet, sauna, massage, fasting etc., I know I would have a better chance. Alas, I cannot do all of those things and I am NOT able to exercise like I used to due to a lower body injury 7 years ago (and subsequent 4-5 surgeries).
I am not the only one on this forum who has had this condition for more than 5 years and I’m not the only one who refuses to try injections, Rx drugs, and many supplements. I’ve tried TWO and they’ve made things WORSE for me.
In another world, I would have just gone to a tropical environment, abstained from sex, done moderate workouts, used sauna, got plenty of sunlight, etc. etc.
But I haven’t given up. I want to know what 5 alpha reductase injections might do --if such a thing is possible, or HOW we might increase endogenous production of DHT slowly, over time (not suddenly). Maybe some endo can help me with this.
All I know is the guys at hard flaccid get the same numbness. They even complain about not being able to feel hot/cold, etc. My sensitivity fluctuates.
I know I found it very curious that people who have not taken propecia had some hard flaccid thing + numbness …
BUT most of them do NOT have persistent numbness… most have hard flaccid and most of them recover after a while
I had HF for about a month and it was gone …
I also suspect that those few members who have persistent numbness have messed up hormones. I spoke with few of them, one admitted having taken propecia and the other admitted having abnormally low T…
T-Bone:
what is this exercise with one leg? I would be interested to know.
what is this couple of things that you tried and did feel worse?
I was alluding to the fact that I cannot do enough exercise with only one fully-functional leg/foot/hip joint
I tried only 2 things in six years: 1) “Inhibit-E” and 2) broccoli extract. So, presumably, BOTH of those things would have INCREASED my androgen hormones and perhaps that’ what made things worse for me (more permanent shrinkage and de-sensitization).
If i were you i would try progesterone, or tribulus, or other supplements that cdnuts tried,… If you have not seen a gradual improvement yet are you optimistic about this happening evver again?
This is scary sht. When i read you story i got very depressed. I am two years in and i probably thought about 50 times to kill myself,…
I have read people on here say that their, for example, arm falls asleep more quickly post-fin. We have to keep in mind that we may be more susceptible to nerve compression related numbness than neurologically healthy men.
It is very possible that lack of allopregnanolone/THDOC could cause nerves to go numb/reduce transmission with the slightest interference; ie the pelvic floor contracting on it.
I’m curious if anyone who used alpha-1 blockers noticed an increase in sensitivity.