“No, not a single trial has ever detected permanent side effects, they always reverse after a couple of months due to finasteride’s short half life.”

Always, huh? Did you know Merck’s original prescribing insert didn’t make that claim? It said the side effects of Propecia will go away, but they never gave a timeline. Technically, some people have been waiting decades for them to go away, but Merck’s prescribing insert is legally correct.

I’ve noticed this self-assuredness in more than one person taking finasteride, with beliefs, claims, and pronouncements about the physical reality of others that they are neither capable nor qualified to make. In particular, this is representative of a honeymoon effect when some people take exogenous steroids or take finasteride or other types of androgen blockers which artificially raise testosterone. It’s a kind of 'roid rage that appears to come out intellectually on internet forums and in public debate due to increased testosterone and estrogen, rather than physically in sports at the gym or in the bedroom due to inhibited DHT production in the body.

I wish you the best in your mental health journey. The human body is incredibly complex and the genetic and physiologic variation among individuals is nothing short of beyond our understanding. I’m here to discuss raypamycin, which has health consequences we will be discovering decades and centuries from now, we are on the cutting edge of medical discovery (or perhaps rediscovery). I’m not interested in furthering this conversation, I’d just appreciate if you could consider not everyone has the same experience with a drug. Pharma is incredibly profitable, and the profit incentives align behind your needs and arguments and not the side you oppose. Medical research is incredibly expensive and is not only an investment for the firms marketing and selling the drugs, but there is an incentive against funding research studies that can lead to liabilities for these firms, and an incentive to have studies retracted if they are later determined to cause potential liability.

Here is a list of studies about the negative effects of finasteride for those curious. I have not read through the list recently and cannot vouch for all it’s contents. However, as I wrote above, anyone considering taking this drug should extensively familiarize themselves with both Merck’s studies, prescribing inserts for both formulations, these studies linked below, and dig into the relationships between the people doing the studies and their organizations funding. Positive studies often have correlations of cross funding for other pharma projects from drug companies. It takes on average $2 billion to bring a drug to market. The people trying to document negative effects of drugs often have to self-fund, and research scientists and doctors know their pile of money and future funding is dwarfed by the opposition.

Also people seem to only focus on the potential side effects of finasteride. Yet losing your hair is guaranteed to affect the way people perceive you and the way you perceive yourself, which might also influence your sexual and mental health.

Sure, some guys may quickly adapt and move on with their lives, and if you’re Joe Rogan or Derek Jeter, you’re gonna be just fine. But for most guys, I don’t think it’s that easy.

At least for me, personal appearance is an important part of the longevity equation. I think that it impacts psychological health, which in turn impacts physical health.

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Here is the source of finasteride not blocking 5ar1 in humans btw, making rat studies inapplicable to them.

Although in humans FIN acts as a selective inhibitor of the peripheral 5AR type 2, in rats it is known to block efficiently both 5AR isozymes, and is in fact generally used to inhibit neurosteroid synthesis in rats (Concas et al, 1998; Finn et al, 2006).

npp200839.pdf (nature.com)

It is primarily an issue of DHT. Scalp tension is not a factor as was proven by the transplant studies where miniaturization of the hair follicles still occured even on other places of your body.

It’s what makes you feel great and is a primary muscle growth factor.

Naturally produced DHT is disabled in the muscle tissue so it is not a primary muscle growth factor, that is testosterone. And even assuming DHT has a role in mood regulation, finasteride is a selective 5ar2 inhibitor so it should not affect the DHT produced in your brain which relies on 5ar1.

@scta123

A twofold increased risk of sexual dysfunction was observed with the use of finasteride for treating androgenic alopecia compared to placebo in this meta analysis from 2019.

I am not denying side effects. What I am denying is the existence of persistent side effects which last even many months after cessation.

It is worth noting that there are several hypothesis about mechanisms that might persist after discontinuation of finasteride

There are strong association studies indicating that DHT is a risk factor for heart disease which is likely the primary driver in ED rates in older men too.

There is data from rat studies that show that finasteride produces long-lasting alterations in neuroactive steroids in rodent brains following discontinuation of finasteride. These findings indicate that finasteride treatment might have extensive implications for brain function.

In mice, finasteride is a strong dual 5ar1/2 inhibitor. In humans, finasteride is a selective 5ar2 inhibitor. The brain primarily contains 5ar1.

A human study compared histological foreskin findings in individuals experiencing permanent sexual symptoms six months after discontinuing finasteride with those who had not been previously exposed to 5α-reductase inhibitors. It revealed a difference in androgen receptor density between the two groups.

Also a rat study.

And probably I could find more data that shows that permanent and persistent changes are possible.

If you could find a study showing that in humans that would be great.

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Just check out the comments under Attia’s youtube videos every time he interviews another bald man. People deride them for talking about longevity while being old. I would not at all be surprised if other men in the longevity scene besides Dr Stanfield were taking finasteride for appearence as youthful-looking hair is a sign of virality.

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I just think it’s interesting that finasteride is the one drug where people who don’t even use it have such strong opinions. Why is this? It’s almost like they have to constantly justify their indecision to use it, but Darwin might have had thought the explanation lie elsewhere.

At any rate, this is a sensitive topic and I don’t want to argue or offend anyone. I can only say that for myself, Finasteride was a great decision. I only wish I had tuned out the fear mongering and started five years earlier, it might’ve saved me a lot of money.

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Overall, the majority of research indicates that 3.4–15.8% of men with BPH who take finasteride 1 mg daily report having some kind of sexual side effect. Therefore, the likelihood that someone using finasteride won’t have any side effects is between 84 and 96%. A nocebo effect may be at play as evidenced by a clinical trial’s finding that patients who were warned about the possibility of sexual adverse effects experienced a significantly higher rate of them (43.6 vs. 15.3%). Side effects are dose related.
Don’t take finasteride if these odds don’t appeal to you.

I am going to start finasteride 1 mg daily for BPH. You get old, your prostate enlarges, period.

“Finasteride is generally considered an effective treatment for benign prostatic hyperplasia (BPH). Clinical trials have shown that finasteride can improve symptoms of BPH, reduce prostate size, and decrease risk of acute urinary retention and need for surgery. In studies, finasteride has been found to reduce prostate volume by 18-28% and decrease PSA levels by about 50% after 6-12 months of treatment. It improves BPH symptoms, as measured by validated symptom scores, by 15-30% compared to placebo over 6-12 months. The beneficial effects are maintained over 5 years in most men. So in summary, multiple studies confirm that finasteride is an effective option for improving urinary symptoms, reducing prostate enlargement, and decreasing complications in a majority of men with BPH. Its efficacy is comparable to other standard BPH medications. However, it may take at least 6-12 months to see the full effects.”

Finasteride adverse effects: myths and realities. An updated review
https://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872016001200010&lng=en&nrm=iso&tlng=en

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“I am not denying side effects. What I am denying is the existence of persistent side effects which last even many months after cessation.”

Which you have zero standing to claim, and if this were the case a timeline would be included in the patient information and prescribing inserts. It isn’t. Call the FDA and ask them. Call Merck. Find where the vendors of the drug claim a date for cessation of side effects from finasteride.

That was their legal out.

The FDA does though.

In a response this week, the FDA said the group’s petition “does not provide reasonable evidence” of a causal link between Propecia and persistent sexual problems, depression or suicide. However, based on patient reports, the FDA said it is “requiring the addition of suicidal ideation and behavior” to the adverse reactions listed on Propecia’s label.

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This is literally from the article you posted:

The U.S. Food and Drug Administration has previously approved revised Propecia labels that mentioned risks of persistent sexual dysfunction and depression but not suicide.

There is no “causal link” stated because the term “causal link” has significant legal implications and the FDA is mostly funded by pharma, not to mention cross pollination of employees and executives.

Finasteride shrinks the prostate but increases risk of high-grade cancer. From the FDA:

Be aware that 5-ARIs may increase the risk of high-grade prostate cancer.

https://www.fda.gov/drugs/drug-safety-and-availability/fda-drug-safety-communication-5-alpha-reductase-inhibitors-5-aris-may-increase-risk-more-serious

It’s patently obvious when a troll outs himself. Do what you want ya’ll, but you should be able to see enough smoke to investigate this for yourselves.

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So it’s a conspiracy you mean.

I’m not sure either why you are citing the FDA if they are bought and paid for according to yourself. That seems inconsistent. I understand it’s an emotional topic.

Have you looked at the randomized controlled trials for finasteride? That will help you find causal links.

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There is no “causal link” stated because the term “causal link” has significant legal implications and the FDA is mostly funded by pharma, not to mention cross pollination of employees and executives.

I wasn’t aware that you were a legal specialist. From my understanding, it simply means that there really is no pathway for finasteride to cause persistent side effects.

Be aware that 5-ARIs may increase the risk of high-grade prostate cancer.

Which is why you should let your urologist know that you are on a 5ar inhibitor.

It’s patently obvious when a troll outs himself.

You are obviously the troll here by simply claiming that the FDA is controlled by BIG PHARMA and that everything they say you don’t like is therefore wrong but everything that you do like is used as a source.

Do what you want ya’ll, but you should be able to see enough smoke to investigate this for yourselves.

I’ve investigated it for myself and came, just like the FDA, to the conclusion that finasteride is safe, effective and does not cause persistent side effects due to its mechanism.

A trend I’ve noticed in regards to people fearmongering finasteride, statins etc. is that they always attack the FDA and every single systematic review and rct as being somehow wrong because they are funded by the Illuminati but every single Chinese rat study that confirms their bias is taken as the gold standard.

@AnUser

I’m not sure either why you are citing the FDA if they are bought and paid for according to yourself. That seems inconsistent. I understand it’s an emotional topic.

If it confirms their bias they would cite the Soros Foundation only to attack it in the same sentence lol

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The debate is much more complex than that.

The fact (I can share the pubmed studies of course… if needed) :

So you can continue the debate the way you want, but still we have to stop androgenic alopecia /cardiovascular disease / metabolic associated syndrom (also for women).

As with Rapamycin, I think it has to do with dosage, duration etc…

Indeed, if finasteride IS a 5AR2 inhibitor, it is also a weak, but still a 5AR1 and 3 inhibitor. Depending on the concentration, you probably and actually certainly do have OFF TARGET. Thoses last 2 probably are, but there are also probably others.

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What???! What do you mean by “do nothing”? Do you mean you just lie on the couch all day? In that case, yes, it may lead to cardiovascular disease but it’s not because you are balding. Are you really saying that everyone who is balding is 20-30% more likely to get cardiovascular disease?

There is a relatively strong association between balding and cardiovascular disease. Whether it is directly caused by DHT (by increasing inflammation, for example) or cofounding factors (accelerated aging with the side effect of increased 5ar activity or androgen receptor density) or even reverse causation (men who go bald give up on themselves more often) is unknown. Further studies are needed.

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I just read a number of articles and studies and they agree with your statement. However, saying “if you are balding and you do nothing, you are 20 / 30% much more likely to get cardiovascular disease” is a stretch, especially if you interpret “balding” to mean any amount of balding at any age. The percentage increase varies greatly by age and amount of hair loss.
“Baldness progresses with age, affecting 30 to 40 per cent of adult men overall but rising to 80 per cent of men by the age of 80.Three of the studies monitored men for at least 11 years and found those who had lost most of their hair were a third more likely to develop heart disease. Men who went bald before middle age (55-60) had a 44 per cent higher risk. The remaining three studies showed an increased risk of 70 per cent overall, rising to 84 per cent among those who went bald before age 55-60.”
And these are associations not causative.
"Currently no one — including the study’s authors — understands what baldness and heart disease have in common.

But if you think that treating the baldness might help protect the heart, think again, said Dr. Gregg Fonarow, a professor of cardiovascular medicine at the University of California, Los Angeles. “Whether you wear a toupee or use minoxidil, it’s not going to lower your heart disease risk,” Fonarow said. “The real issue is not baldness having a direct effect on the heart, but that it’s a warning of possible heart disease”
And:
“Manson points out that hair-restoring drugs like finasteride arrest hair loss in some men by blocking the action of testosterone. But such drugs work least well in the case of severe hair loss on the crown. Also, it is unknown if these drugs can lower the risk of heart disease.”
https://news.harvard.edu/gazette/story/2000/01/male-baldness-linked-to-higher-incidence-of-heart-disease/
The bald facts: hair loss could be the first sign you have heart disease | The Independent | The Independent

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And what are your qualifications? Do you even understand what is the meaning and process behind the term “causal link” used by regulator (FDA in this case)?

Maybe just a quick reading will provide more insight and maybe you will see that you can not interpret the absence of “casual link” as simply “there is no pathway…”

Yeah what we need are rcts for high-risk people who are already on a statin where one group gets finasteride and the other group gets placebo. If the treatment group has a lower incidence of heart attacks that would point to DHT being causative for heart disease.

My qualification is basic proficiency in English as a non-native speaker. Does the following sentence, on a surface level, have any other meaning than that the FDA does not believe in persistent side effects?

In a response this week, the FDA said the group’s petition “does not provide reasonable evidence” of a causal link between Propecia and persistent sexual problems, depression or suicide .

Regarding the article you posted:

Maybe just a quick reading will provide more insight and maybe you will see that you can not interpret the absence of “casual link” as simply “there is no pathway…”

The article in question does not support your argument. All it does summarize existing algorithms developed over the years meant to assess causality between drugs and (side) effects. Given that the FDA made the assessment regarding finasteride back in 2022, all the newer guidelines had already been in place for at least 10 years.

Initially, investigators/sponsors were too cautious in their interpretation of “reasonable possibility.” They submitted reports for events that were likely to be manifestations of disease, common, probably unrelated events or study endpoints. Food and drug administration (FDA) and European medical agency (EMA) received too many suspected unexpected adverse reactions reports for which there was no evidence of “relatedness.” This necessitated regulators to push the pharma companies to have a validated system in place for causality assessment and outlined few guidelines and recommendations (e.g., methods for the assessment of individual cases guidance Council for International Organizations of Medical Sciences (CIOMS) VI (2005), guidance FDA (2010),[8] EMA guideline (2012)[9]).

So while there are obviously limitations, the guidelines already enforce stricter systems for detecting adverse events. Yet the FDA still doesn’t believe in the existence of PFS.

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Artigo completo aqui:

https://www.sciencedirect.com/science/article/pii/S0022227524000129

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