Just want to be clear. If we already have PFS, should we not take aspirin or ibuprofen? @awor and @axolotl can you help clarify for me? Are we able to use it even intermittently? Thanks guys.
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Not all NSAIDs are the same, you cannot extrapolate pharmacodynamics from other drugs.
Why would you bring up a thread I made 5 years ago. I made it clear in the thread later that it was not worth the risk and the side effects are understated in a wide range of systemic effects.
Proposing theories and coming up with solutions is very clearly the primary goal of the forum. If we can nail it down, no one would be here in the first place.
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This is cancerous cell lines from the prostate. Aspirin is widely considered to be protective in a whole host of organs from tumors. In this case, it is a modulator, and in normal prostates, it would not act the same way either as a mRNA repressor, or AR antagonist.
Iām not saying Aspirin is good or bad for PFS, to reiterate, we cannot use control subjects as a representative.
You can infer possible peripheral effects based on drug class and mechanism of action.
Making statements such as āPFS can be a disease of the liver and immune system,ā aspirin is āandrogenic if anything,ā and āThere is no evidence that Aspirin downregulates androgen receptors in epithelial or fibroblast cellsā is pure conjecturing against all of the evidence available in regards to its effect on androgens and the androgen receptor, as well as contemporary research concerning the NSAID class being anti-androgenic.
You havenāt provided an iota of evidence to hold up these statements or the baseless notion of the involvement of glucocorticoid and pregnane X receptors in PFS, but have put the burden of proof on others.
Bottom line is that joining this forum and badgering fellow members, the admins, and the mods within the first 48 hours is a bad start and wonāt be tolerated beyond this point.
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Iām going to go ahead and switch to acetaminophen, which is not an NSAID. At this point, there is data supporting that NSAIDs combined with finasteride posed a 5x greater risk of developing long lasting sides. Iām not sure if NSAIDs hurt you after you develop symptoms, but Iām going to play the safe route and not take them.
Theyāre not without side effects as it is (https://www.mayoclinic.org/drugs-supplements/ibuprofen-oral-route/side-effects/drg-20070602).
Iām sorry, but you seem to have trouble properly reading studies. Go back to my statements, and refer back to the studies.
Classes of drugs can have vastly different actions, that claim is simply appalling. It doesnāt take much to compare Rofecoxib, Acetaminophen, and Ibuprofen. Itās not even close.
Providing cell samples from tumour tissue as evidence for anything beyond effects on tumor tissue is equally inappropriate, for obvious reasons.
I provided no evidence because there isnāt any, we can only hypothesise based on what we understand from the actions of finasteride and the symptoms that follow. That is literally the starting point of every scientific study in history. A hypothesis.
I badgered no one. I correct misleading conclusions. It doesnāt take anything off my skin to stop posting here, instead of continuing to support those with some background on the issue. Feel free to ban me son, hope you donāt choke on it.
COX inhibitors. No, it really doesnāt take much to compare these 3 NSAIDs. In fact, the study of aspirinās effect on GnRH response suggests COX inhibition as a potential explanation for deleterious effects on testicular function and this MOA has been linked with decreased AR function.
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That explains more than anything else you have said up to this point.
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That is good also. We are at least in agreement on one point. No regrets.
Something that I canāt wrap my puny brain around is the fact that there are two articles of research that specific to PFS, which actually provide some insight into the condition. That is:
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There is a profound decrease in key neurosteroids in PFS patients
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PFS patients exhibit overexpression of AR in foreskin
Yet this theory-crafting focused on unrelated or loosely-related systems continues.
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you mean overexpressed as in silenced or upregulated?
i know methyltrienolone upregulates the AR receptor in dick tissue while dht downregulates
i have both mtren/mdht + dmso and willing to try
Some feedback on the article. Check out the line in bold below.
Written by
Robert Haber MD, FAAD, FAAP
This is an important article as it serves to remind dermatologists that sexual health and sexual function need to be considered in our patients. It is safe to say that a negligible number of dermatologists routinely obtain sexual function information from our patients, yet multiple studies from virtually all regions of the world have consistently revealed a disturbingly high prevalence of sexual dysfunction in men of all ages. It makes sense to attempt to find causality and discover if our dermatologic treatments may be to blame. Unfortunately, this high ābackground noiseā of sexual dysfunction makes it more difficult to prove causality and can lead to misleading conclusions.
The authors investigated 10 commonly used dermatologic medications, and reported level 1 evidence for causality only for finasteride. They identified 5 studies not supporting an association between finasteride and sexual dysfunction, but discovered āmore compellingā findings showing the opposite in 10 other studies. Unfortunately, at least 2 of these latter studies are considered extremely biased, having been supported by the Post-Finasteride Syndrome Foundation, and having drawn subjects from sexual dysfunction clinics, where no valid control groups exist. In an upcoming article to be published in the Journal of the European Academy of Dermatology and Venereology , this author found no difference in the reported incidence of sexual dysfunction between finasteride users and age-matched controls.
The topic is uncomfortable, and adds time to our visits, but we are often the only physicians that some of our patients see on a regular basis; so, it behooves us to take a more active role in investigating sexual health and counseling our patients appropriately.
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Oh so studies supported by the PFS foundation are biased but the studies done by Merck arenāt? Okaaaaay buddddy
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Exactly what I was thinking.
Talk about financial motivation if there ever was one
he looks like a jerk
And there goes your honor, Case Western Reserve. Arenāt universities the final stop when it comes to upholding the truth?