5α Reductase inhibitor Puns

As Finasteride has its post-finasteride-syndrome I was wondering if Dutasteride has that too.

I found a study which specifically looked into this:

" POST FINASTERIDE SYNDROME: IS DUTASTERIDE UNFAIRLY ACCUSED?

Objectives: Finasteride (FIN), a 5areductase inhibitor (5ARI’s), is used to treat benign prostatic hyperplasia and alopecia. Controversial research has suggested that finasteride, can result in persistent sexual and nonsexual side effects known as postfinasteride syndrome (PFS). Because of a shared mechanism of action, dutasteride voluntarily underwent an FDA label change similar to that for FIN. The aim of this study was to evaluate adverse effects associated with dutasteride by examining an FDA Adverse Event Reporting Symptoms (FAERS) database. The aim of this report was to address PFS putatively induced by dutasteride by quantifying and summarizing these FAERS reports, create a demographic of patient reports, assess the cluster of PFS symptoms, and to correlate consistency of the PFS syndrome. Materials and Methods: A FAERS database between 4/1/2011 and 10/29/2014 pertaining to all 5ARI’s received was analyzed. Every reported case was coded according to date received, case type, whether it was reported by a health professional, outcomes, manufacturer, age of patient, country, product used, adverse events, and the suspected role of the reported drug. Results: The FAERS database consisted of 3,295 cases (2,986 male and 305 either female or gender unreported). Of the 2,986 male cases, 31 were with the concomitant use of finasteride and dutasteride. There was only one reported case of dutasteride which caused “back pain.” Sexual dysfunction was reported in 16% of cases with a combination of finasteride and dutasteride. Overall, 41% incidences of PFS symptoms were reported with finasteride alone and none with dutasteride alone.

Conclusion: Use of a FAERS database demonstrated that there were no persistent sexual side effects reported over a 3.5 year period associated with the use of dutasteride alone. Although the FAERS has limitations such as self-reported data, our findings suggest that dutasteride is not associated with PFS. "

Now I was wondering, is there any upside in choosing Finasteride over Dutasteride if duta blocks more types 5α-Reductase and doesn't have that PFS?

Clearing the air, or should I say brain fog?

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Hey guys, so I've been balding since 15, known about fin since 18, but garnered the courage to take the plunge after I turned 20.

Because I was earlier scared shitless by alarmist propaganda, sometimes as extreme as just one dose of fin turned them into apathetic brain-dead wretches – the last thing I needed being a college student.

Surprisingly, neither the experiences of prescribing clinicians (dermatologists for AGA or urologists for BPH), nor clinical trials involving human subjects offers a shred of evidence for their claims; insinuating no causal link between such experiences and the use of 5ARIs.

I've put together a two-part series, and this is the first of two.

Mood-related sides like depression and anxiety, I will address in my next post.

But in this one, I'll be systematically refuting the alleged performance-related sides of 5ARIs in particular, like attention, memory, verbal fluency and energy – so you have one less reason to surrender ground to the Norwood Reaper.

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Before I start, I find it necessary to point out that all studies that practically demonstrate a deleterious effect of 5ARIs on cognition like this ( https://pubmed.ncbi.nlm.nih.gov/33249331/ ) this ( https://pubmed.ncbi.nlm.nih.gov/30836157/ ) and this ( https://pubmed.ncbi.nlm.nih.gov/29214729/ ) subjected ratsto more 5ARIs in one day than even BPH patients would take in a year. I will be referring only to high quality prospective human studies - the only type of study results that can be generalized to any of us on this sub.

• Prospective human clinical trials

First, in the short term.

Study 1( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2805481/ ) recruited both younger and older men and randomized them into four groups - 1) testosterone and estradiol were maintained at eugonadal levels for young men 2) block testosterone's conversion to estradiol (rendering greater 5 alpha reductase activity) 3) induce complete hypogonadism 4) placebo (rendering no fluctuations in hormones relative to baseline)

After having tested for measures of executive function, memory, and spatial cognition before and after

Link to study. Click "Download full-text PDF" to access the full version.

"Conclusion
The antiandrogenic effect of Minoxidil, demonstrated by significant downregulation of 5α-R2 gene expression in HaCaT cells may be one of its mechanisms of action in AGA and FPHL, which is not being emphasized well in the dermatology literature."

You can simply check the results of 5a-R2 inhibition on Wikipedia page 5a-reductase

We can't express our massive endless gratitude to:

• r/FDA and r/WorldHealthOrg for their approval of Minoxidil without clear understanding of the mechanism of action and prompt reaction on adverse effects reports
• Johnson & Johnson and Perrigo for the warning labels on their products
• Various Dermatology associations, academies and institutions for their published studies and observations on the safety of Minoxidil
• All journals, newspapers, scientists for their conclusions about safety of Minoxidil
• All barbers and dermatologists for their prescriptions and recommendations. All urologists, endocrinologists, cardiologists that denied the possibility of side effects and didn't send reports to the relevant drug safety regulation institutions.
• Each online comment from drug advocating accounts that disprove the possibility of side effects and claim the drug safety without any justification.

Who will be responsible for the actions that caused severe persistent health disorders, ruined families and lifes?

An abstract from:

https://journals.aace.com/doi/10.4158/EP12108.RA?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed

"Until recently, the adverse effects of 5a-reductase inhibitor therapy were thought to be very minor and well tolerated . New information, however, suggests that these drugs may impair sexual function, including sexual desire, erectile and orgasmic function.

Recent studies in animal models suggested that these agents alter penile tissue histoarchitecture and nitric oxide synthase function in penile tissue and thus can contribute to erectile dysfunction (82-83). It is particularly important to note that in a subset of patients, the effects of these drugs are long lasting and may be irreversible (84).

An association between use of these inhibitors and depression is also noted (84), suggesting potential adverse effect on the brain. Also, studies in animal models have shown that these agents affect tissue histoarchitecture of the prostate (85,86) and clinical trials suggest that these drugs do not reduce the incidence of aggressive and high-grade tumors.

A number of case reports have suggested that 5a-reductase inhibitor therapy is associated with angioedema, cataract and intraoperative floppy-iris syndrome, pseudoporphyria, T cell-mediated acute localized exanthematous pustulosis, gynecomastia and male breast cancer.

The recently introduced warnings on the drug labels also suggest a need for increased awareness of the potential irreversible side effects of these agents (FDA)."

Studies: (82) https://www.ncbi.nlm.nih.gov/m/pubmed/21834872/

(83) https://www.ncbi.nlm.nih.gov/m/pubmed/22568670/

(84) https://www.ncbi.nlm.nih.gov/m/pubmed/21122055/

(85) https://www.ncbi.nlm.nih.gov/m/pubmed/19200255/

(86) https://www.ncbi.nlm.nih.gov/m/pubmed/15270776/

Ran into this study while doing research on dut, http://jamanetwork.com/journals/jama/fullarticle/1105045. It was done by a well respected endocrinologist Shaleneder Bhasin. The main thing it concludes is that dut has no significant effect upon muscle mass, and secondarily it concludes that there was no significant difference between the two groups in terms of sexual health either (semen, ejaculation strength etc.). However, it does still clearly state that the role of DHT is still very poorly understood.

TLDR; This study shows some evidence that DUT is safe particularly for retaining muscle mass.

inb4 anti-fin ppl hate on this post, I'm just trying to find decent research on 5-ar inhibitors and share it with people. I understand this is just one study (and potentially could have flaws), but its some what recent (2012) and done by a seemingly well respected doctor.

Seeing as Benign Prostatic Hyperplasia (BPH) seems to be a disease that all men will eventually get (given one lives long enough), will taking Avodart (dutasteride) in one's 20s or 30s be an effective prophylactic measure against prostatism?

Also, although it comes with various risks, there might be other benefits such as hair loss prophylaxis and increased testosterone.

I guess what i'm asking is, theoretically speaking is it worth it for a healthy adult male free of co-morbidities to take dutasteride as a preventive measure?

Disclaimer: I'm not looking for medical advice, I'm just fascinated by this idea.

Hi all, I'm curious if any members of this community can shed some light on an ongoing debate among hairloss sufferers regarding the popular 5AR inhibitor, finasteride, which is commonly used to treat male pattern hairloss and prostate issues. There's concern among users that finasteride lowers the potentially important neurosteroid allopregnanolone, which can lead to adverse cognitive side effects, and unfortunately, this appears to be corroborated by what little research has been performed (https://www.ncbi.nlm.nih.gov/pubmed/19655698).

What I find odd, however, is that finasteride supposedly only inhibits type II and III 5AR isozymes in non-negligible quantities, while having little effect on type I activity (which apparently is the type predominately found in the brain). The study I've linked tested allopregnalone levels in the blood of patients before and after finasteride administration and observed a dramatic decrease over a four-month window, so my question is how did this happen and what are its implications for the cognitive functioning? Could allopregnanolone synthesis in peripheral tissues be responsible for the large drop in serum measurements if synthesis in the brain is, in fact, largely unaffected? And even if that is the case, would altered serum levels have a significant effect on the brain regardless? Thanks.

does this inhibitor exist at all in the natural foods?

The title basically.

Thank you.

Saw this posted on Longecity.org

I'm about to take this stuff internally but I read a few people saying that it can cause "post-Finasteride syndrome" from lowered DHT like effects like depression, anxiety, impotence, erectile dysfunction, decreased libido due to the fact it's an 5α-Reductase Inhibitor.(at least what I read online it's a 5α-Reductase Inhibitor)

https://en.wikipedia.org/wiki/5%CE%B1-Reductase_inhibitor

User "Hyperflux" posted in the other GHK-CU thread that he was having these effects and they weren't going away.

How many of you have experienced such effects and did they go away over time?

https://www.longecity.org/forum/topic/104986-ghk-cu-and-potentially-dangerous-5%CE%B1-reductase-inhibition/

I’m getting close to my 2 week doom period and I’m living in fear at this point (it gets to a point of constant SI for me).

Found some interesting research I wanted to share/ see if anyone knew anything about-

So 5a reductase inhibitors can prevent a luteal phase increase in allopreganolone - we’re talking drugs like dutasteride (a cousin of finasteride/propecia that blocks 5a reductase I AND II) and saw palmetto.

It was also done in a few case studies here. Also mentions PMDD w/ Comorbid PCOS for my homies cursed like me.

Has anyone tried dutasteride or saw palmetto?

I’m going to plan on trying saw palmetto if I can’t find contra indications for chronic illnesses - so far I havent found downsides to saw palmetto (& seems to be good for pcos too which is a win for me).

Praying for a miracle ~

DOI: 10.1080/J157v05n01_03

URL: https://www.tandfonline.com/doi/abs/10.1080/J157v05n01_03

Thank you in advance!

Thanks!

PLEASE, IF YOU'RE ALREADY TAKING FINASTERIDE STOP READING HERE (I don't want to cause you nocebo effect) UNLESS YOU KNOW A LOT ABOUT BIOLOGY. If your case is the latter, please, help me with this.

I have been thinking of starting Finasteride and I was to jump into the drug but recently I saw these studies and to say it in a humorous way my penis just shrinked like when you take a really cold shower, if you know what I mean. I'm fucking scared but at the same time I don't want to lose my hair: http://www.asiaandro.com/archive/1008-682x/5/33.htm https://www.ncbi.nlm.nih.gov/pubmed/22375859 and https://www.ncbi.nlm.nih.gov/pubmed/23876578

That freaks me out. What do you think? They say that's probable that DHT prevents important parts of the penis from getting damaged (fibrosis, etc).

According to this, and if you can extend rat (and rabbit) results to humans, everyone taking Finasteride should be affected by those morphological changes. Maybe they are to slight that most don't notice? Even if they don't suffer from ED their penis tissues should be more deteriorated and maybe they probably would experience ED years before they would naturally experience it.

At the same time I think 'everyone in Hollywood, TV, sports, etc is taking this drug' so I don't know what to do. I got the prescription and even the pills but I'm scared shitless... The least I want is to regret my decision in the future because of premature ED.

I know that Finasteride inhibits only 5a-reductase type II and III but in rats it also inhibits type I. Could that be related to the penis tissue damaging in rats while we apparently don't see much ED in humans?

I hope someone here know about biology and can help me with this because I don't think Minox alone is gonna keep my hair.

If you don't know the answer I would REALLY APPRECIATE that you could tell me an online (free) doctor or some webpage when some physicist can answer to these questions online.

So I was looking into finasteride and other 5-alpha reductase inhibitors and saw that it can increase the risk of dementia. So lets say I take it until I am 60 and then stop taking it will my odds of getting dementia still be higher. Or will the lower dht levels already have fucked my hippocampus (part of your brain) because of the lower dht.

Berberine appears to be a 5-alpha-reductase and androgen receptors inhibitor. (not sure what "inhibit androgen receptors" means)

I have trouble interpreting scientific studies (not being very good at chemistry and english isn't my first language).

But does anyone know how to interpret these different studies?

Does this make berberine a potential treatment?

"Berberine Improves Benign Prostatic Hyperplasia via Suppression of 5 Alpha Reductase and Extracellular Signal-Regulated Kinase in Vivo and in Vitro" :

https://www.frontiersin.org/articles/10.3389/fphar.2018.00773/full

"Berberine Ameliorates Prenatal Dihydrotestosterone Exposure-Induced Autism-Like Behavior by Suppression of Androgen Receptor" :

https://www.frontiersin.org/articles/10.3389/fncel.2020.00087/full?report=reader

"Berberine Suppresses Androgen Receptor Signaling in Prostate Cancer" :

https://mct.aacrjournals.org/content/10/8/1346.short

"Berberine inhibits androgen synthesis by interaction with aldo-keto reductase 1C3 in 22Rv1 prostate cancer cells" :

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4955188/

Hello World,

Can anyone provide me with some information about possible interactions (or recommendatios in general) of mRNA vaccine and 5-alpha reductase inhibitors (e.g. finasteride)? I'm trying to find something about this topic for the last three days, but can't find anything.

I'm asking this because I was scheduled to get Moderna vaccine on 5th of May. When I told the physician that I take finasteride (1 mg/day for 7 years now) she told me that I cannot get the jab. The reason that she gave was that she checked on the Internet (sic!) That finasteride is a steroid and these drugs tend to supposedly weaken the production of antibodies. If I want the vaccine I should stop taking the drug for at least 15 days before the first dose.

I'm not sure if I'm right but is it possible that she didn't understand what finasteride accutaly is and what purpose it serves/ what is its mode of action? I know steroids for their antiinflammatory action but I not sure if 5-alpha reductase inhibitors work the same way?

Any thoughts on that? Stay safe.

I would like to preface that I am not posting this in search of medical advice. However, I am looking for more information in order to make a decision that COULD have impacts on my health.

Questions:

1. In what way do 5α-reductase inhibitors affect the brain?

2. I am aware of potential sex-related side effects of 5α-reductase inhibitors, but would they be exacerbated by a history of TBIs/concussions?

3. If saw palmetto and finasteride are both 5α-reductase inhibitors, do they necessarily have the same mechanisms of action - conversely if you take a similar dosage of the two and don't experience any noticeable side effects, is unlikely that you will experience side effects with the other?

4. Would people with a history of TBIs/concussions be necessarily more at risk of developing things like brain fog, depression, dementia, etc. from the use of 5α-reductase inhibitors? How and why?

I apologize for the lengthy post. My questions are primarily related to the brain, but if this is the wrong subreddit for this, please let me know. Thank you in advance for your help - answering as many of these questions as you can would be appreciated!

Background information about me: I am a 20-year-old male university student who has noticed a receding hairline over the past two years. My father and maternal uncle and grandfather are all bald, and my father also started balding in his late teens. My receding hairline is the only thing that I see when I look in the mirror or when I am on Facetime or Zoom calls, which is why I recently reached out to a doctor about Finasteride (I was prescribed to take 1/4 Proscar tablets (1.25mg Finasteride) daily, but have not yet picked up my prescription/started to take the pills.

I have had two minor concussions (no loss of consciousness, although the second one took months to recover from, likely due to stress and poor management of the concussion in the early days) at the ages of 14 and 17. I have been taking saw palmetto orally for the past ~3.5 years on the recommendation of my mother without understanding the mechanism behind it (as I was just a teenager, taking my mother's word - I only found out what a 5α-reductase inhibitor was in the past week). Within those 3.5 years, there was a 3-month period this year where I stopped taking it (simply because it ran out) and no significant changes were noticed. I have had depressive periods in my life in my teen years (although I seemed to have depressive tendencies bef

I notice that a lot of natural aromatase inhibitors also inhibit 5 alpha reductase. Are there any that just inhibit aromatase? If so, what are your experiences with them?

i know both testosterone and dht decrease with age, but what about the conversion of T to DHT. Does it decrease or increase?