If you say that it’s a red herring, do you think then that the current research in Kiel isn’t looking for the right thing? Or did I just didn’t fully understand what you mean.
Not exactly in the mood to write up a lengthy essay on what I may or may not think, especially being that I am confident sporadic posts I made on the subject are sufficient, so I do not want to make any rewrites either. I wager you do not follow my posts, so please read this below post I have made on the subject, then reread the entirety of my post you quoted in this topic. I hope that will satisfy your inquiry.
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I touched base briefly what PFS is on this post.
Not only does PFS components tick every single highly unique box comparing it to the same mechanism as CRPC, but I’m living evidence myself. How castration has led to reversal of the majority of my extreme symptoms and given me more energy than I’ve had since before the crash.
I felt like an old man now I’m turning into the energiser bunny. My energy to do things is just there.
Btw saying “epigenetics” doesn’t really do the huge amounts of literature around CRPC and the many decades spent on it much justice. There are obviously many components to its mechanism.
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Gracias for reaching out. Not sure what you are trying to convey with some of this, but I will still go along and cooperate.
Firstly, before that, I’m pleased that you are faring better. It is quite a liberating feeling to overcome a disease. In my case, I refuse to call the disease “PFS” because I never used finasteride.
Interpretation: Aromatase inhibitor victims (PAIS) must have over-expressed estrogen receptors, possibly under-expressed androgen receptors, and so lowering estrogens to hysterectomy levels should alleviate their symptoms. Men can get PAIS too. Notably, saw palm has anti-estrogen actions in addition to the anti-androgenic actions, possibly anti-progesterone too. My understanding is that it is an estrogen receptor antagonist rather than a direct aromatase inhibitor. Perhaps a blind patient has over-expressed ocular genes. Maybe not so weird after all, considering licorice paradoxically simultaneously both mimics and lowers aldosterone at the same time.
So we both agree that epigenetics is a red herring? Splendid! I’d prefer to not parrot myself, but since you presented the subject to me, I am confident the genetic expression profiles of patients with and without CRPC will be different. I thought I carved my stance in stone when I said above that it is a red herring in some previous posts. Furthermore,
I alluded to that by stating in posts above that epigenetics is not unique or exclusive to PAS, PSSD, post saw or PFS. Instead, such events happen in all states of disease. The subject has become stale for me. Wake me up when the subject is about autoimmunity. Post statin syndrome is autoimmune - fact, not opinion. I have posted proof ad nauseam. That said, if anyone can give me 1 good reason post saw, fin, accutane, etc is not autoimmune, I’m all ears. I’m waiting, lets hear it. Why do people think autoimmunity is a red herring? If Johns Hopkins would have chased the epigenetic ghost, then maybe we never would have known statins induce autoimmunity.
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Thanks for the well thought out response.
In theory if PAIS has the same mechanisms as PFS although affecting ER rather than AR; the symptoms would be similar to PFS.
ER over-expression would lead to overly estrogen sensitive tissues to the point of no response and at the same time AR would be underexpressed which may be similar to overexpression in PFS.
I’d suspect certain estrogen mediated functions would become more dysfunctional than usually seen within PFS such as joint problems.
There is less known about PAIS however assuming the above similarities are true then lowering estrogen for PAIS and / or lowering total hormone content to castration would resolve many of the symptoms. At the same time estrogens would likely not help or worsen the symptoms.
I really can only speak for PFS. It’s uncertain if the other conditions are similar in mechanism or if the other ones just fall under the same category in terms of symptom profile.
Regarding autoimmune it wouldn’t surprise me at all. As far as I know there is not a full understanding of CRPC / PFS mechanisms. However in terms of potential future cures / treatments if one way is related to autoimmune; that is not to say another can’t be gene therapy; and again this is also not to say another way can’t be epigenetic modification. In fact within CRPC there are many ways - it’s only limitations such as toxicities that prevent successful treatment.
How much closer or further away would an autoimmune cure be than gene therapy, assuming both ways would be successful.
How much evidence is there for the autoimmune direction compared to gene therapy.
What do the leading scientists who work in the CRPC field say.
Rhetorical questions that have likely been thought of before by people in the field.