There’s no evidence that Aspirin downregulate androgen receptors in epithelial or fibroblasts cells.
Aspirin is a wonder drug on many levels in normal circumstances, and is androgenic if anything. Not to mention one of the best antidepressants around. Like most of everything, that doesn’t necessarily apply to PFS.
Yes, and it is backed up by statistics. I’ve taken NSAIDs since then, but don’t recall how they effect me… I’ve consciously stopped taking ibuprofen unless absolutely needed after taking a pharmacy class and learning all the undesirable effects of them.
However, with regard to human testis,
these possibilities seem to be unlikely because the
present study indicates that aspirin treatment does not
affect steroidogenesis in conditions of nonexposure to
exogenous hCG.
Hi @RedstaR,
There is clear evidence of this demonstrated using pca cell lines - the predominant area of focus from which the understanding of effects on AR expression is derived due to its known role in the pathology. From the study cited by @awor:
To confirm aspirin’s effects on AR expression, we examined mRNA and protein levels of AR in LNCaP cells after aspirin treatment. Both AR and PSA mRNA, and both AR and PSA protein levels, were decreased by aspirin treatment in a dose-dependent manner (Fig. 1A and B respectively). Aspirin (1 mM) also decreased AR and PSA protein in a time-dependent manner (Fig. 1C).
Furthermore, the study cites previous transcript level AR suppression observed in other NSAID drugs (Lim et al. 1999, Pan et al. 2003) as the basis of the hypothesis. Several meta-analysis of chemopreventative potential of aspirin similarly acknowledge this.
Perhaps so. However, given your track record on the promotion of wonder drugs…
…I would still consider the aforementioned evidence in line with the past ten years of patient experience here, clinical study and theoretical underpinnings that have been put forward in recent literature reviews by professors investigating PFS.
Additionally, I am curious as to why you are here. In addition to knowing you very vocally espoused finasteride use and discredited this issue, I see you are reporting the side effects you described when I last came across you. I recall you were at that time taking the drug.
To clarify, this is a patient support site for users who are experiencing persistent symptoms after cessation of antiandrogenic treatment. What they choose to discuss is up to them as long as it abides by the community guidelines. This is not a site for simply proposing theories.
ibu or aspirine may be a trigger but i highly doubt it could lead alone to a full blown pfs symptom complex. but thats just my opinion. i mean these drugs are so commonly used. i dont know anybody who hasnt taken them once. i know many people who havent taken finasteride, tbh i only know one that has taken it and i only know him since pfs . so finasteride is not so commonly used than many think. i asked a guy with hairloss if he takes finasteride. he answered : „no only minoxidil. i dont want to get impotent“ . another guy told me the same. so the info is there among the general population. Not the knowledge what our horrible condition is about, but the info that finasteride is a dangerous drug
Pharmacist friend of mine said the same. He’s losing hair but won’t touch fin due to side effects he’s heard about.
It’s worth noting that sexual dysfunction was at least acknowledged as a potential side-effect of Accutane/Isotretinion in this study:
Isotretinoin
Our review identified a single case study describing a 29-year-old man who developed a progressive inability to ejaculate within several weeks of initiating 1 mg/kg/day; the ejaculatory dysfunction resolved within 3 days of discontinuation of the medication. Per the authors correspondence with the drug manufacturer, there were 150 reports of sexual side effects in men taking isotretinoin, including ejaculatory dysfunction and ED.60
ED was described in 1 non-randomized, prospective trial of 55 patients with refractory acne, treated with either isotretinoin or minocycline. A significantly higher proportion of patients taking isotretinoin had an inability to maintain an erection (30% vs 5.7%; P < .05). Symptoms improved after discontinuation of isotretinoin, and no difference in serum testosterone or dihydroepiandrosterone sulfate was identified between groups.61 However, 60% of the isotretinoin group reported depressive symptoms,61 which may be confounding the relationship between isotretinoin and ED. Moreover, these side effects may be dose dependent, such that dose reduction should be considered in patients presenting with sexual dysfunction.
Thanks for posting this @Sibelio
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.
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.
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.
I’m 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 “PFS can be a disease of the liver and immune system,” aspirin is “androgenic if anything,” and “There is no evidence that Aspirin downregulates androgen receptors in epithelial or fibroblast cells” 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 haven’t 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 won’t be tolerated beyond this point.
I’m 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. I’m not sure if NSAIDs hurt you after you develop symptoms, but I’m going to play the safe route and not take them.
They’re not without side effects as it is (https://www.mayoclinic.org/drugs-supplements/ibuprofen-oral-route/side-effects/drg-20070602).
I’m 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 doesn’t take much to compare Rofecoxib, Acetaminophen, and Ibuprofen. It’s 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 isn’t 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 doesn’t 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 don’t choke on it.
COX inhibitors. No, it really doesn’t take much to compare these 3 NSAIDs. In fact, the study of aspirin’s 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 can’t 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:
There is a profound decrease in key neurosteroids in PFS patients
PFS patients exhibit overexpression of AR in foreskin
Yet this theory-crafting focused on unrelated or loosely-related systems continues.
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 “background noise” 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 “more compelling” 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.
Oh so studies supported by the PFS foundation are biased but the studies done by Merck aren’t? Okaaaaay buddddy
Exactly what I was thinking.
Talk about financial motivation if there ever was one