This is far from a “blatant lie” as anyone here will tell you. This his opinion, incidently an opinion worth more than any of the rest of us due to all the work he’s done on this.
unless the administrators of this board have in fact been lying to us and keeping secrets, perhaps someone with the authority to do so should have a little chat with our friend of the never ending negative OPINIONS, and smack some sense into him … getting really tiresome … oscar, if you have any ACTUAL proof of what you are saying here, lets see it … put up or shut up
For how many yearss do you think its been known that neurosteroids are low? I dont consider it a good thing to not share that information here for such an extended peroid of time.
Disinformation to what end? Those postings surprise you? The twitter feeds are based in fact. A causal link between PFS and Finasteride has been proven scientifically just through the projects that are known publically here, not to mention other things well along in the pipeline.
To what end? - What does it matter, good or bad? Either its true or it isnt.
The twitter feeds are based in fact. - There is a difference between fact, and simply repeating opinion over and over again because you want something to be true
I think you would agree a silenced androgen receptor is a pretty groundbreaking thing if discovered. Im afraid the guy making these tweets also doesnt care to wait for any actual discovery to take place. Or doesnt know if it has. Or care. Or understand either way. This is actually the biggest problem with the ‘androgen receptor theory’.
You mean unlike repeating over and over ad nauseam that there is nothing at all to it because you don’t want it to be true? The research is in the hands of people infinately more qualified to make judgements about what avenues to investigate than any of us here. Why drive yourself mad with the constant second guessing of the scientists and institutions that have chosen to investigate PFS? Maybe focus on things you can control like helping to spread media awareness in the UK?
If you don’t know who is managing the twitter account then why speculate to their motives or knowledge? No part of any of those tweets really surprised me.
I’m not a scientist so I can’t comment on how “groundbreaking” this data collected in these early projects is in the scope of things. I do know that negative autoreguation and epigenetic effects of pharmas and the environment in general is very well documented and is the basis for a huge volume of research currently going on in institutions around the world. As has been said on here… this isn’t the only study underway and further work will confirm 100% causal relationship between Fin and PFS to a degree to make any argument against it preposterous both here in the forum and in front of any federal and/or state court.
Are the twitter statements true or untrue? I have not seen any other reports, official or otherwise, regarding axonal damage. If nothing official has been reported, claimed or published, what is the source/credibility of the precise verbiage used in the twitter posts? If you do not have official inside knowledge, please don’t bother speculating or editorializing here. Patients are trying to get things like MRI testing and treatments in real time and need to know if something has legitimately been discovered or announced. Those with authority to speak: please clarify. Thanks.
The antiandrogen withdrawal syndrome or antiandrogen withdrawal response (AAWR) is a phenomena that can occur in men with progressing prostate cancer after they stop using antiandrogens. It leads to a symptomatic improvement and reduced PSA levels. This is of course the opposite what you might expect considering prostate cancer is fuelled by T/DHT.
There are 2 large differences between AAWR and PFS.
It only occurs in cancer cells.
Not permanent, lasts an average of 5 months.
If you crashed after stopping Finasteride you are suffering from a kind of antiandrogen withdrawal syndrome. So its useful to look at what causes AAWR.
Theories
The molecular mechanism behind AAWR is unknown. There are some published theories I have listed them below. (Sources here [1] and [2] .)
• Androgen receptor mutation. Binding specifity altered to allow other hormones or antiandrogens to effect the AR. (antagonist becomes agonist etc.)
• Non-androgen receptor pathway is activated by the antiandrogen causing ligand-independent cancer growth which stops after use.
• Androgen receptor over-expression. Amplifying the effect of low levels of androgens and the weak agonist effects of antiandrogens. Associated with alterations in the recruitment of coactivators and corepressors to the promoters of the androgen receptor.
• Macrophages/Cytokines. IL-1 can convert androgen antagonists into agonists in cancer cells.
The focus of AAWR theories are on what is present during antiandrogen treatment that could of caused the cancer to grow, NOT on a ‘downregulated’ response to androgens occuring after antiandrogen treatment ends.
none of us here can answer that question … write to the pfs foundation, and perhaps they will have an update … no one here aside from maybe the administrators would have any idea about that kind of stuff
There are only plans for a US study so far. Discoveries in Italy have been made since 2010, others since 2011. The results are known to many, even if nobody here is told!
Prof Melcagni has just sent a paper to be published reporting finasteride sideeffects, so hopefully he will finally review some of these discoveries in a peer reviewed journal.