I don’t have any real arguments other than your sources being trash dude. IDK what else you want me to say; find some better sources to support your argument.
You know how many people developed Covid symptoms in March 2020 during the 2 week lockdown? Check please.
Here is a look at the quality of the studies. Things like sample size, type of study are considered.
Look at the effects of placebo. Some of these studies show the placebo / nocebo very well.
ONLY one high quality study showed persistent sexual side effects, and they were present in both the finasteride and placebo group.
Did you make that meme with paint? Nice attempt.
“your sources are trash” is not an argument friend, didnt you go to school and learn about logical fallacies?
Anyway if you finally have something useful to say, let me know.
Umm, it is literally an argument against credibility so yeah… but you’re dug into your camp and can’t see past the trenches so 
Thanks for posting a study, you actually try.
But let’s read the conclusion of the researchers of your study:
Conclusion
Although the 5αRIs finasteride and dutasteride have been established to be efficacious for the treatment of benign prostatic hyperplasia and androgenetic alopecia by substantially reducing the levels of dihydrotestosterone [2, 3], it has also been documented that they may increase the incidence of sexual dysfunction [10]. Decreased libido, ejaculation disorder, and impotence are among the most commonly reported drug related adverse effects [19]. Erectile dysfunction, or impotence, has been cited as the most common side effect in multiple studies for both finasteride 5 mg/d and dutasteride 0.5mg/d, followed by decreased libido [5, 15, 22, 25, 27, 45]. In the largest meta-analysis to date on 5αRIs, there was found to be a significantly increased risk of sexual dysfunction (156% increase) for men being treated with finasteride or dutasteride for BPH, whereas there was not a significant association for those treated for AGA [10]. Dutasteride 0.5 mg/d has also been shown to have a greater incidence of adverse sexual effects than finasteride 5 mg/d in the treatment of BPH [10]. Unfortunately, there is no consensus regarding the relation between 5αRIs dosage and the likelihood of sexual dysfunction and further study is needed in this area [10, 38, 55]. It is based on these findings that we recommend practitioners both consider and discuss the possible sexual side effects and risk of depression with their patients prior to selecting a drug therapy.
They say the same as what I said, further study is needed. We can’t conclude finasteride is safe at all. (even FDA acknowledges this long term) Also read the meta analysis study I posted since you again seem to ignore that.
Again, the irony. And no, it would be an actual argument if you could properly state and post why all my sourcers are “trash” but you have failed again and again in that regard.
And no friend a meme is also not an argument. Try again.
Our point of contention is on persisting sexual issues after stopping the drug. The conclusion doesn’t mention that.
The point I am at with PFS is there is a lack of evidence to support it. It may or may not exist, but the time to believe it exists is when there is sufficient evidence. We are not there yet.
Did they evaluate these guys before finasteride for penile abnormalities? It seems a bit post hoc to me. Would guys with regular ED have these abnormalities? Could these issues be caused by something like Low T as well?
The selection bias part is a pretty big weakness of the study IMO. I am just not sure how one would get much of value out of that.
Many doctors and endocrinologists strongly disagree with that. Especially since the studies showing finasteride is “safe” are very weak and of low quality.
And PSSD (post ssri syndrome) has only recently been officialy medically recognized in europe: Post-SSRI Sexual Dysfunction Recognized as Medical Condition | Psychology Today And still not in the USA. Because regulation is slow, that doesn’t mean PFS doesn’t exist or that there is no sufficient evidence.
One thing’s for sure, there’s more going on. Like @ readalot posted, more and more studies pointing this out:
Health Risks Associated with Long-Term Finasteride and Dutasteride Use: It’s Time to Sound the Alarm
Also did a quick search here on this forum. It’s quite amazing how many people experience PFS, yet it’s "so rare’.
The truth is many balding men put all their hope in finasteride and cope any way they can, especially with old and low quality studies. I understand though, it’s a classic example of cognitive dissonance. But again do you really believe blocking the most androgenic hormone and disrupting many neurosteroids for a long term will ONLY affect the state of your hair? You haven’t answered that simple question yet…
Another interesting fact:
New Drugs Found to Cause Side Effects Years After Approval
Almost one-third of new drugs approved by the FDA ended up years later with warnings about unexpected, sometimes life-threatening side effects.
And the similarities between PSSD and PFS are also very interesting:
Post-finasteride syndrome and post-SSRI sexual dysfunction: two sides of the same coin?
Abstract
Sexual dysfunction is a clinical condition due to different causes including the iatrogenic origin. For instance, it is well known that sexual dysfunction may occur in patients treated with antidepressants like selective serotonin reuptake inhibitors (SSRI). A similar side effect has been also reported during treatment with finasteride, an inhibitor of the enzyme 5alpha-reductase, for androgenetic alopecia. Interestingly, sexual dysfunction persists in both cases after drug discontinuation. These conditions have been named post-SSRI sexual dysfunction (PSSD) and post-finasteride syndrome (PFS). In particular, feeling of a lack of connection between the brain and penis, loss of libido and sex drive, difficulty in achieving an erection and genital paresthesia have been reported by patients of both conditions. It is interesting to note that the incidence of these diseases is probably so far underestimated and their etiopathogenesis is not sufficiently explored. To this aim, the present review will report the state of art of these two different pathologies and discuss, on the basis of the role exerted by three different neuromodulators such as dopamine, serotonin and neuroactive steroids, whether the persistent sexual dysfunction observed could be determined by common mechanisms.
Only a couple of weeks ago the german national TV did a report about PFS:
How many is many? I don’t think it’s most. Even if so, being a doctor or endocrinologist isn’t a guarantee of the opinion being correct.
This isn’t how 5 AR inhibitors work. They inhibit the 5 AR enzyme from converting testosterone to DHT. Finasteride inhibits about 65-70%. I’ve had past mid range DHT levels while on finasteride and also exogenous testosterone.
Androgen blockers are a bit more dangerous if one wants to remain masculine IMO.
I’d be careful getting your information from a source with a title like this. More serious and less biased studies will generally not have a title with something like “it’s time to sound the alarm”.
Dr. Traish (the author of the “study”) is well known to put out garbage studies against finasteride. IIRC, he is connected (paid by) to the PFS foundation.
Too many to sum up and more and more dermatologists refusing to prescribe finasteride for hairloss too since the risks outweigh the benefits.
Hell, last year Finasteride has been added to the ‘list of drugs to avoid in 2021’ by the French Medical Journal Prescrire
Euh yes that is how they work, 5ari’s block most of the DHT and many neurosteroids. And you’re case is unique since you’re on test. 90%+ of people who take fina is not taking exogenous test. Also this post proves again how you skim over my posts or just blatantly shows your ignorance. Read this:
The following reactions are known to be catalyzed by 5α-reductase and are inhibited if using finasteride:[9]
And here’s a recent study;
Advances in Knowledge of Androgens: How Intentional and Accidental Neurosteroid Changes Inform Us of Their Action and Role
Synthesis of neurosteroids requires 5ɑ-R. As such, finasteride alters neurosteroid levels and can have robust effects clearly related to the adverse effects of finasteride that have been reported in men in the short term and long term following cessation of its use.
And 5ari’s do even much more to the body, if you want I can go into more detail…
Hahaha typical, you don’t like the conclusion of the study and try to undermine it with “but it’s biased”. Come on now I expect better from you.
Hey I can play this game too. If Traish is known to put out “”“garbage studies against finasteride”“” then what do you call Merck studies who have been caught to manipulate their study data?
“Merck Manipulated the Science about the Drug Vioxx”
Scientists from the pharmaceutical giant Merck skewed the results of clinical trials in favor of the arthritis drug, Vioxx, to hide evidence that the drug increased patients’ risk of heart attack.
Tragically, Merck’s manipulation of its data—and the FDA’s resulting approval of Vioxx in 1999—led to thousands of avoidable premature deaths and 100,000 heart attacks.?Dr. David Graham, the Associate Director for Science and Medicine in FDA’s Office of Drug Safety, testified in 2004 before the Senate Finance Committee that the FDA’s failure to recall Vioxx earlier had resulted in as many as 55,000 premature deaths from heart attacks and stroke, calling it the equivalent of allowing “two to four jumbo jetliners” to crash every week for five years. Even years after discontinuing use of the drug, patients who have taken Vioxx continue to experience complications.
And please do give evidence why Traish puts out “garbage studies” or is it just another baseless claim?
I believe most dermatologists will prescribe it… Could be wrong, but it’s a very common Rx.
This isn’t how they work. They inhibit production. An androgen blocker will usually block the androgen from acting at the androgen receptor site. Something like Ru58841 would be considered an androgen blocker. It doesn’t reduce androgens in the body, but does block them from acting.
I read that. No need to attack me.
How do you come to the conclusion that a partial inhibition of those things (things partially inhibited by finasteride) results in PFS? Some have claimed that DHN (DiHydroNandrolone) has caused them sexual dysfunction (Deca dick).
The thing here that is key to understand is these things are “reported”. That is different than “shown to cause”.
Have you looked at his studies? I don’t know all of his work, but he has published work in which he looked at a sample of guys that already claimed PFS. The study is more of a questionnaire of guys that claim PFS. In terms of medical studies, that is pretty low tier. The selection bias alone is enough to kill the study’s legitimacy.
You don’t have to trust merck. I listed a whole table in which large high quality studies not done by merck are listed.
I believe my approach on this is solid. I am trying to use the best information possible (randomized controlled studies with large sample sizes) to come to my conclusion. I think there is a big difference in the quality of the information we are using to come to our own conclusions.
Many people buy it online, HIMS is popular these days. Patients don’t have to see a single derm in the eyes today to get it.
Semantics. Of course it’s an inhibitor hence me abreviating it to 5ari’s.
Because neurosteroids are extremely important for things like libido, focus, etc. Fyi: low libido, brainfog and depression are the most common effects PFS patients have. So is it that surprising that fina causes these things if it inhibits so many imporant neurosteroidal pathways? And again read the study I posted. This is just the tip of the iceberg, fina does much more, I’ll make another detailed post.
And do you believe Deca dick is real?
And? You do know how the scientific process works right? Also fina has shown to impact neuroactive steroids significantly:
Cerebrospinal fluid readings of PFS patients showed significantly lowered levels of several hormones and neuroactive steroids and “abnormal somatosensory evoked potentials of the pudendal nerve were reported”
Still better than Merck studies then who manipulated scientific data huh?
But it’s not high quality, I’ll repost the meta analysis again of all data available:
CONCLUSIONS AND RELEVANCE:
Available toxicity information from clinical trials of finasteride in men with AGA is very limited, is of poor quality, and seems to be systematically biased. In a cohort of men prescribed finasteride for routine treatment of AGA, most would have been excluded from the pivotal studies that supported US Food and Drug Administration approval for AGA. Published reports of clinical trials provide insufficient information to establish the safety profile for finasteride in the treatment of AGA.
See above. But we can agree on one thing, more long term studies are necessary.
Let’s go on to discuss DHT’s effects in the Brain.
DHT has pronounced effects on neurochemistry (it affects neurotransmitters in the brain). DHT has been shown to increase circulating epinephrine levels (adrenaline), this can cause anxiety in predisposed individuals, however, most of the time, this is not the case, since DHT also increases GABA activity in the brain, which is relaxing (10) (11) (12). So in other words, DHT should promote A focused, calm burst of energy, which is what many users of DHT-based steroids, report as the “alpha-male” feeling (13) (14). Dihydrotestosterone increase central and nervous system energy production by increasing not just adrenaline, but cyclic AMP (15). This molecule increase thermogenesis (fat-burning and heat production)(16). Cyclic AMP facilitates the conversion of TSH thyroid hormone, to T4, a more potent thyroid hormone, thus, indirectly, DHT increases thyroid function (by increasing cyclic AMP) (17).
So seeing all this, DHT definitely acts as a nervous system stimulant, and a metabolic “probe”, it also increases GABA. Second to this though, it could indirectly decrease serotonin or serotonin receptors; since DHT antagonizes estrogen activity, and estrogen helps maintain the expression of serotonin receptors in the brain(18) (19). This is also consistent with DHT being shown to stop estrogen induced prolactin release(20).
This is part of the reason behind using DHT Gel to treat gynecomasita. Clearly DHT has anti-depressant effects, since Finasteride causes depression (21) and also based on the above mentioned activity of DHT in the brain. It gives energy, it gives focus, it gives aggression.
DHT also improves spatial working memory(22), according to some studies, by altering NMDA-receptors(23) (namely increasing), and by improving Calcium-induced acetylcholine release & function in the hippocampus(24)(25); a very important area of the brain involved in memory formation and spatial (directional) memory.
DHT also decreases glutamate levels and excitory outputs through other mechanisms (26) (27) (28).
Finally, Dihydrotestosterone, or it’s metabolite 3-alpha-Diol; downregulate alpha-adrenergic receptor distribution, leading to more inhibitory adrenergic (adrenaline influence)(29) (30) (31). For those who don’t know, adrenaline can activate an ‘alpha receptor’ - which stimulates the nervous system, vasoconstricting blood vessels and arteries, raising blood pressure, or it can activate a beta-adrenergic receptor, generally vasodilating artieries, but yet, increasing heart contractile force. This all might just be another result or a reflection of what is mentioned above, that DHT increases epinephrine, GABA, and cyclic AMP. However, in a separate study, Testosterone (without specificity), had upregulated alpha-1-receptors to protect the heart against ischemia(32). Is this an effect of Testosterone or it’s metabolites though. Likely, it doesn’t matter, it was probably case coincidental, but may indicate that if blood pressure falls too low, Testosterone can increase it to maintain homeostasis.
In yet another study however, DHT has been shown to increase alpha-1-adrenergic expression, whereas Estrogen decreased the expression/density(33).
This again reflects the need for DHT and Estrogen to be kept in balance, as both promote vasodilation through different pathways, however, since Alpha-1-receptors are incredibly potent Vasoconstrictors, DHT + an OVERALL deficiency in nitric oxide may actually promote high blood pressure, especially in coordination with estrogen deficiency. Interestingly, Alpha-1-receptor activation may increase serotonin activity at the 5-HT1A receptor(34)(35), this is an auto-receptor that ironically seems to possess anxiolytic (serotonin-typical) effects. 5-HT1A activation has shown to help social anxiety disorder, but worsen anticipation anxieties(36)(37).
In another study, DHT/Androgens also facilitated serotonin 5-HT1A/1B agonist-decreases in aggression, which is controversial, although it appears that estrogen allows for intermale aggression by downregulating serotonin 5-HT1A/1B activity(38)(39). Thus DHT’s only pro-aggressive propertly lies in it’s adrenaline promoting effect, and not with serotonin.
OTHER CENTRAL AND MOLECULAR CHANGES INDUCED BY DIHYDROTESTOSTERONE
So DHT via multiple pathways increases nervous system strength, DHT increases epinephrine levels, decreases prolactin (assuming you have enough dopamine production as well), increases GABA, may decrease serotonin and serotonin receptors. All-round this means DHT has positive effects on your chemistry and nerve cells. By reducing prolactin, and estrogen, and subsequently serotonin, and also regulating catecholamines, by this, DHT can definitely increase libido, and alleviate sexual anxiety in most individuals by increasing GABA. DHT is key to many of Testosterone’s brain benefits. Keep in mind though, despite positive effects on brain chemistry, this still doesn’t give an excuse to OD on aromatase inhibitors, likely, because you need a little bit of estrogen (not much at all), to promote nNOS (neuronal nitric oxide synthase) production. So DHT serves as a great compliment to a little bit of brain estradiol, and a great ratio of DHT to estrogen means optimal sex drive, stamina, charisma and general masculinity.
Let’s summarize in Bullets Here.
I am okay leaving it where we are. I don’t think we will be convincing each other at this point.
Sure, agree to disagree. I’m sure it’s only a matter of time before this gets recognized officialy, more studies are underway too.
Here’s a recent study:
And this is a very complex issue, epigenetics are also at play.
But I’m more interested in finding a solution to PFS and people with chronic androgenic disruption due to various causes and medication.
You should read into L-Carnitine then… rumour has it that it increases androgen receptor density (or sensitivity) in long-term use, which could counteract the effects of androgen receptor blocking mechanisms.
Given this is a meathead forum, the above conversation would be far more interesting IMO.
