Isn’t this the purpose of the forum, to find what’s causing it and what to do about it.
I never said any of these are facts, it’s one of many propositions across the board.
I’m sorry if it seems that I’m picking on you @RedStaR .
You said “PFS can be a disease of the liver and immune system”. You didn’t say “PFS might be a disease of the liver and or immune system” there’s a big difference. I don’t have a problem with you musing, hypothesising or theorising. But without proof, we aren’t going to state what this condition is.
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Wow. 4.8 times higher risk if using with NSAID’s like ibuprofen? what the actual f
Is there a way for me to view the full study? or did you list the whole thing…It says age was one of the strongest predicators for persistent side effects…does that mean younger = more susceptible ?
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Crazy. I was on quite a bit of ibuprofen around the time I crashed because I have rotator cuff damage from working out and also from breaking my collarbone. I was doing physical therapy and ibuprofen to get my shoulders mobile. I can’t remember exactly if I took ibuprofen the same days I took the drug that made me crash, but It’s likely.
https://www.pnas.org/content/115/4/E715 This study suggests ibuprofen alters testicular physiology and causes LH to surge in order to “compensate for hypogandism.”
The study @Sibelio posted is the first Im aware of that lists who is at risk for developing PFS. I might be as premature as my current sexual performance, but I think this is big.
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There’s a lot of interactions NSAID have in the body to attribute it to any one possibility.
If I had to guess, I would say it maybe the glucocorticoid agonism that aggravates the issue. Or it might be because people who tend to use NSAID have inflammatory issues and are more susceptible to PFS. It’s impossible to tell without first knowing what causes PFS.
Unlikely a coincidence imo.
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.
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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.
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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.
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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.
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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
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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.
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.
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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).