How do we know the mice with the adenomas had pfs? I ve not seen the paper so perhaps a link if you have one.
I don’t see how a growth would cause a crash? Would it not be a slow onset of symptoms as the adenoma developed and begun interfering with homeostasis?
Seems like for most of us the crash occurs after withdrawing.
If PFS is classified as persistent hormonal changes after cessation then the mice must have had PFS as a testicular adenoma is tissue which autonomously hyper-produces hormones. So their hormone levels must have been altered persistently. Alterations in hormonal levels means changes in behavior.
We do not know the actual mechanisim which fin causes the adenoma. It is proposed that it happens with LH changes but there has been no real proof given for this apart from the fact mice taking higher doses of fin were more likely to get it. Higher doses of fin increased LH.
Some of us crashed after quiting, some before. I do not think that matters too much it could have been that the fluxuations in hormones or lh set it off or made it worse or even that the metabolite created via the adenoma was being blocked by 5ar inhibition, but this may be unlikely.
Here is the abstract.
ncbi.nlm.nih.gov/pubmed/8005373
If you want the full study which goes into a lot of detail and really needs to be read, send me a message.
Thanks.
I see that 24% of the contril group had cell hyperplasia. So these growths occur with or without finasteride and pfs?
THe figure you mention is for diffuse hyperpaysia which is not pictured. Of the controls 1 had an adenoma and one focal hyperplaysia which is basically a small adenoma.
In the high dose group a 10 out of 50 had focal hyperplaysia and 16 had adenoma.
And some people crashed 15 minutes after taking 1 pill
My brother took finasteride a couple times. After only one pill he got ED almost right away but not PFS. I suspect that was directly related to the changes fin makes to his hormones. He stopped using fin and recovered without problems.
Some may crash after 8 years others it may be in the first day. Most of us lasted days/weeks/months or often years with no PFS. Only to see somewhat sudden onest. For me it was about 4 weeks on fin with very few sides then a crash overa 48 hour period in which my libido went up before it crashed totally.
I know of a guy, one pill, 15 minutes, felt sick, testicle pain, zombie like feeling, next day penis curved to left, legs and arms got skinny overnight, ED, etc full blown PFS after one pill
I got pelvic pain (a common PFS symptom) within hours of the first pill. So I don’t think anything like this could be causing pfs.
I know one guy too who only took one pill and has modestly bad sides a couple years later. I also think the testicular pain is very telling, the man I know who took one pill also had testicular pain. While some get testicular pain and do not crash. I think it indicates that some kind of damage is going on in that area. But then again men can develop testicular cancer with out having noticeable pain.
You read stories like this
"I noticed problems from day 2 when I had pain in my left testicle. I should’ve stopped from right there (but the damage might’ve already been done). This continued for a week and I felt it was best to stop taking it. The pain went away but now 6 days after taking SP I’m suffering from ED, no morning/random erections, having problems sleeping, zero libido, and all the other Fin-like symptoms checked above. " While this man took saw palmetto I have heard the EXACT same story from a fin user who had the pain in left testicle after 3 days then lost all libido and quit after one week and has not recovered.
We also here stories of some having increased libido before crashing which I did. This is interesting as libido is controlled partially by T and perhaps a sudden increase in libido could indicate that the leydig cells are indeed central to our issue.
I also think that people with varicoceles may be more susceptible to PFS due to low cellular defensive mechanisms in that testicle. This is well documented and is usually found on the left testicle. Varicocles are well known to decrease the antioxident protection of the testicle.
Of course this does not mean you have to have a varicocele to get PFS. I crashed quite quick, 4 weeks and my left testicle is soft due to a varicocele. I have asked a few others and the data is not that consistent. The many I know who crashed after one pill also says he has a soft left testicle.
This seems like a very plausible theory vincent, especially since studies in the past have shown it happens to mice. Has anyone ever been screened for this? It seems to me like it would be one of the first things checked for in any of the previous studies on this condition.
My pain is not in the testicles. It’s in the pelvis, in the area of the bulbospongiosis muscle. Rarely when it’s severe it will radiate to some other places.
I do not think any local pathology causes the pain. With how it oscillates, it seems neurological in origin. It also seems to correlate with muscle twitching along the sciatic and gluteal nerves, which are part of the same nerve branch. And when the pain is severe the pelvic muscles twitch.
Focal hyperplaysia is very small - the size of 3 seminiferouse tubules. Which is minute so I doubt that it can be seen with anything other than a microscope. Adenoma is bigger than that and it can get much bigger which if big enough would be seen on ultrasound or mri. But considering the regular size of leydig cells by the time it becomes visable it would have to be 100 or 1000 times times bigger than normal I guess?
So it is very hard to detect, in fact I do not know how it possibly can be detected apart from a testicular biopsy. But the biopsy would have to be done right at the area of the hyperplaysia or adenoma which can not be found. So really the only chance would seem to be if someone died from PFS and microscopic analysis of tissue was completed.
I think we can be pretty sure PFS is not something that can be seen with an ultrasound or MRI, if so we would have found it years ago? So we could assume then it is more of a microscopic change.
On top of that PFS can develop in a day so that also indicates PFS is related more to a microscopic change which has systemic consequences. And really as far as I can see only an adenoma of some sort fulfills that criteria. Ie, a small change in the body having system wide effects very quickly.
I had similar issues. It lasted a few months. I think pfs is neurological damage. The lucky ones that felt sides, stopped and recovered would not be so lucky if they got back on the drug for a bit longer. I also believe this is why hormone therapy has limited effects. People that experience slow vision processing (rare) is neurological. The Chronic fatigue, insomnia ,and anxiety is all neurological. I highly doubt that it has anything to do with genetics. The German brothers got destroyed about the same time but I know of other brothers that did not. If it were genetic then why do some crash right away and some take years. Parkinson’s and MS patients have relapsing-remitting symptoms as described frequently here. Those conditions are also neurological.
People recovering some after many years could be indicative of slow neurological healing. Unlike Parkinson’s and MS Propecia is a neurological toxin. Once the toxin is removed, aside from the delayed neurological syndrome it seems to create (aka why people fully recover then get worse after stopping. That is what a delayed neurological syndrome is BTW brain fogged guys)… But for the most part people slowly recover instead of slowly decline like MS and Parkinson’s. (Because the toxin has been removed.)
Studies are nice, I honestly hope they prove this shit causes this damage. I think the Italians are on the right track. At the vary least get this god awful drug off the hair loss market. Maybe the cancer market to… Knowing what I know about this drug, I would rather die from cancer then take this.
Can you please try and keep unrelated comments to another thread. That would be great.
As for comments like this. - “The Chronic fatigue, insomnia ,and anxiety is all neurological.” Perhaps some of these are neurological but all of us here know that hormones affect the brain and cause changes in behavior just like they do in any other tissue, like the skin, fat cells, muscle cells, digestive system, tissue in the penis, hair follicles and the rest. There is 0 doubt hormone changes can cause “Chronic fatigue, insomnia ,and anxiety”.
So you can expect that once your hormones balance is destroyed you should simply assume that you are going to feel changes in your brain as you would in any other tissue. Your brain is not somehow immune from the effects systemic hormonal changes.
Actually mci I completely disagree that there is any damage. Neurological doesn’t imply neurological damage. It means involving the nervous system. And, as vincent said, metabolic disorders can/will affect the nervous system.
This theory is just as unlikely or likely as any other theory out there. Good that new ideas are being shared
In a 2-year carcinogenicity study in Han Wistar rats, at doses up to 53 mg/kg/day for males
and 15 mg/kg/day for females, there was an increase in Leydig cell adenomas in the testes
at doses of 53 mg/kg/day (160-fold the expected clinical exposure). An increased incidence
of Leydig cell hyperplasia was present at doses of 7.5 mg/kg/day (79-fold the expected
clinical exposure) and above in male rats. A positive correlation between proliferative
changes in the Leydig cells and an increase in circulating luteinizing hormone levels has
been demonstrated with 5α-reductase inhibitors and is consistent with an effect on the
hypothalamic-pituitary-testicular axis following 5α-reductase inhibition. At tumorigenic doses
in rats, luteinizing hormone levels in rats were increased by 167%. In this study, there may
have been limited exposure to the major human metabolites.
I can not find the actual study for this? This is taken from the product info for avodart
A positive correlation between proliferative changes in
the Leydig cells and an increase incirculating luteinizing hormone levels has been demonstrated
with 5α-reductase inhibitors and is consistent with an effect on the hypothalamic-pituitarytesticular axis following 5α-reductase inhibition.
what does this mean? LH was high in the blood? we all have low LH.
What they are saying is that taking high levels of fin or dut increases LH because it lowers DHT very low. LH then increases. They are saying the LH causes the adenoma not the dut or fin. But this is WHILE on the drug not after quiting. If it is so simple why does estrogen also cause leydig hyperplaysia when it should lower LH?
your RAT study about adenoma and GoldFish both say the same thing. Therefore I trust them. Here are main points
ncbi.nlm.nih.gov/pubmed/7570607
1-Both your rat and Goldfish say damage to testicular cells.
2-Both say primary damage to testicles cause an increase in LH which agree with medical text books that primary damage cause an increase in LH. This is opposite to our condition. you (and no body in the world) can say how within hours LH can go high and then come back to ground? how withing hours an adenoma is formed.
3- Goldfish points at testicular damage but without creating any adenoma.
The bottom line from the link above are
1-Beta Sitosterol caused an increase in GnRH.Plasma GtH-II levels were elevated in male fish treated with beta-sitosterol on Day 4 and further increased in response to Ovaprim, suggesting that reduced plasma steroid levels were not due to effects on pituitary function
2-The damage to leydig cells was reconfirmed invitro
In other studies, testes pieces from beta-sitosterol-treated goldfish produced reduced levels of T and pregnenolone in vitro both basally and in response to the GtH-II agonist human chorionic gonadotropin (hCG) when compared to the testes from control fish. Basal and hCG-stimulated pregnenolone and hCG-stimulated T were reduced in follicles from beta-sitosterol-treated fish
So unless there are few cases of elevated LH,FSH I am not going to believe that our case is the same as that of rats or Goldfish.
To me looking at these two studies our issue is either brain damage or something else