How bad is finasteride?

[milkboi]

If so then, you want to block 5ar and take testosterone? I cant see that playing out well.

Maybe you are right, but I don't see a real alternative if I don't want to lose my hair. I think taking Test with Fin would be better than Fin alone, at least the high levels of Test will provide you with a decent amount of androgenic signaling

 

[Mister]

What good alternative do we have? Minoxidil (or any other growth stimulator) alone wont stop balding

Minox + needling is a good alternative imo. Best one is just getting multiple transplants, you're in Germany so it's easy to get one in Turkey.

 

[Jayvee]

Maybe you are right, but I don't see a real alternative if I don't want to lose my hair. I think taking Test with Fin would be better than Fin alone, at least the high levels of Test will provide you with a decent amount of androgenic signaling

I would think more along the lines of stimulating blood flow rather than blocking DHT. Your protocol sounds like a recipe for high estrogen and cortisol to me. It's not Ray's ideas or finasteride. Their are heaps of options. I think even topical DHT has been shown to reduce hairloss (pretty sure I read that somewhere). Anyway research some more. Caffeine might be good too

 

[milkboi]

Minox + needling is a good alternative imo. Best one is just getting multiple transplants, you're in Germany so it's easy to get one in Turkey.

The transplants will eventually fall out again if you don't protect them against the cause of your original hair loss from what I've heard.Minox and needling might help you keep your hair for a little longer, but Finestaride seems to much more successful in the long-term (in terms of halting hair loss).

The one thing I don't buy is that androgens aren't causing hairloss btw. The more androgenic a steroid, the more shedding it induces. I don't see how anyone could deny then that decreasing AR activation in the scalp is helpful for hair loss.

 

[milkboi]

I would think more along the lines of stimulating blood flow rather than blocking DHT. Your protocol sounds like a recipe for high estrogen and cortisol to me. It's not Ray's ideas or finasteride. Their are heaps of options. I think even topical DHT has been shown to reduce hairloss (pretty sure I read that somewhere). Anyway research some more. Caffeine might be good too

Yeah, estrogen and cortisol could become an issue, you are right about that.

 

[Donttreadonme]

3 years no negative side effects on Avodart which is even stronger. Idk why this one website is so full of bias against it. Dht is a double edged sword.... when you're young its good. When you're older it has a cumulative negative effect on the prostate.

I've read some real garbage here about it being "tranny pills" and being akin to castration.... that's just plain crap. I'm also weight train and have no negative effects on muscle or strength. Considering bph basically effects every man on the planet i think it's a good idea.

Look... tomatoes also inhibit dht and no one goes around warning men against eating tomatoes.

 

[cupofcoffee]

3 years no negative side effects on Avodart which is even stronger. Idk why this one website is so full of bias against it. Dht is a double edged sword.... when you're young its good. When you're older it has a cumulative negative effect on the prostate.

I've read some real garbage here about it being "tranny pills" and being akin to castration.... that's just plain crap. I'm also weight train and have no negative effects on muscle or strength. Considering bph basically effects every man on the planet i think it's a good idea.

Look... tomatoes also inhibit dht and no one goes around warning men against eating tomatoes.

i mean taking a pharma grade anti-androgen that also inhibits progesterone and cortisol metabolism can't possibly be good for health, it's not that hard to understand. PFS is very rare so you might very well never experience side effects, which is what i hope for you, but on the long term it probably will harm health in some way. DHT's role in BPH is debatable since it's also associated with estrogen, prolactin and cortisol.

Also just because a natural compound that inhibits DHT with a fraction of the potency of fin and duta it doesn't mean they won't harm health

 

[ChemHead]

Maybe you are right, but I don't see a real alternative if I don't want to lose my hair. I think taking Test with Fin would be better than Fin alone, at least the high levels of Test will provide you with a decent amount of androgenic signaling

The fin will already raise your test levels. That won't help you. It's also not how the body works. When it comes to steroids like DHT and estradiol, they're blackbox steroids. The body carries testosterone and other weak androgens in the blood and they enter tissues and enter the cell. Once in the cell, they're in a blackbox... They're metabolized to active androgens like DHT or active estrogens like estradiol, they bind nuclear receptors and cause gene expression, and then they're further metabolized. At this point, they can leave the cell and be further metabolized and eliminated. In this way, the body's regulatory axes don't really know what's going on because the cell does its thing and the serum bloods supply never sees it.. It only sees the metabolites.

You may get away with taking fin and having relatively few side effects, but if you do have side effects, I guarantee you will not escape them by taking testosterone.

 

[GenericName86]

I'll also sign off on Finasteride being pure poison. When I first took it my hair was super thick and barely receding (if it was it wasn't really noticeable) However hair loss is in my family and against my better judgement I went along with what hair loss forums told me which was to be pre-emptive with treatment and "strike first" and what a mistake that was. I had never experienced what this "itch" was that I read all these people with mpb talking about but as soon as I jumped on fin I got constant itching along my hair line/shedding and my hair in general looked like ***t, lost the natural wave it had and just seemed thinner and flat and not to mention the brain fog.

I've discovered things like T3 or Nicotinamide Riboside, things that are pro androgen, my scalp feels really good, the itch goes away, hair looks better.

@ChemHead, I've read how you've said aromatase is important when it comes to hair, do you know if consuming foods or natural supplements that can have an inhibiting effect on aromatase like Olive leaf extract or broccoli can have negative effect aromatase expression in the follicle?

 

[Apple]

Maybe you are right, but I don't see a real alternative if I don't want to lose my hair. I think taking Test with Fin would be better than Fin alone, at least the high levels of Test will provide you with a decent amount of androgenic signaling

Why would you want taking Test with Fin ? Fin alone increases testosterone and any excessive testosterone on top of that would probably be converted to estrogens.
You may end up loosing more hair this way.

 

[ChemHead]

@ChemHead, I've read how you've said aromatase is important when it comes to hair, do you know if consuming foods or natural supplements that can have an inhibiting effect on aromatase like Olive leaf extract or broccoli can have negative effect aromatase expression in the follicle?

I'm not sure tbh. While I know that aromatase expression in the scalpel is inversely associated with hair loss (in other words, women and men who don't experience hair loss have higher levels of aromatase expression in the scalp), I'm not sure this is the whole story. I've had a feeling for awhile that there may be a mineralocorticoid involved. Whatever it is, it's a steroid that is 5a-reducible (or metabolite of a 5a-reducible steroid) and acutely spikes in concentration when taking finasteride.

Regarding food, however, anything that requires very little of your body's own energy and resources will ultimately raise your total steroid synthesis, including estrogens. Part of the reason is also because your body has more resources to eliminate steroids quickly rather than having them hang around in the main circulation where they don't belong. Lack of steroid clearance causes negative feedback in the hypothalamus and pituitary, reducing overall rate of steroid synthesis.

 

[FinVictim]

@ChemHead

Very interesting theory. Thanks a lot for sharing and all the effort you put in. If I understand correctly you would theorise the extra iodine is causing higher production of T4, thereby speeding up 5AR production, fixing PFS?
My question would be: How come supplementing thyroid hormone doesn't fix PFS or speed up recovery? Thyroid supplementation has been tried quite a lot over the years.

What is your current regimen? Can we read your story somewhere, how you got PFS and your prior history?

I have been on 200-300IU hCG eod for the last 12 months, with a few breaks in between. It helps with fatigue but does nothing to my non existent libido/emotional flatness/anhedonia.
In addition I've tried 6 weeks of mesterolone (proviron) in november - december 2021 while also on hCG but it hasn't done anything unfortunately.

I'm currently in the process of ramping up heavy resistance training. Heavy lifting seems to be a factor in most recovery stories. I've been inspired by Sibelio's thoughts and thread on PH. There's quite a lot of scientific backing for the relationship between exercise and (DH)T production. There's actually a study showing the positive feedback loop between DHT and 5AR (Pubmed ID 6218182). He theorises we've reached a homeostasis in which there is a very low 5AR activity because intracellular DHT is very low. By somehow ramping up intracellular DHT (which is very hard with exogenous DHT like proviron, but easier with exercise), we can increase 5AR activity using the positive feedback loop and reach a new homeostasis with healthy intracellular DHT levels, fixing PFS.

 

[tankasnowgod]

I've read some real garbage here about it being "tranny pills"

It's not just "here," it's one of the listed primary uses for the drug-

Dutasteride - Wikipedia

en.wikipedia.org

Dutasteride, sold under the brand name Avodart among others, is a medication primarily used to treat the symptoms of an enlarged prostate. A few months may be required before benefits occur.[4] It is also used for scalp hair loss in men and as a part of hormone therapy in transgender women.[5][6] It is taken orally.[7][8][4]

and being akin to castration.... that's just plain crap.

No, it's not. It's the main reason these drugs were developed. The entire "androgen theory of hairloss" originated because bald or balding men who were castrated regrew their hair (this comes from the work of Dr. Hamilton). Dr. Imperato-McGinely found a group of pseudohemaphrodites that also seemed resistant to baldness. Merck developed 5AR inhibitors to try and mimic these conditions. Danny Roddy goes over this in "Hair Like A Fox."

The Danny Roddy Weblog

Because some of the ideas progressed in HAIR LIKE A FOX are consistently misrepresented (or misinterpreted), I thought it might be useful to attempt to mimic a Q and A format in order to provide clarity on topics I might have failed to address clearly in the book.

www.dannyroddy.com

In 1974, Dr. Imperato-McGinely found a group of pseudohermaphrodites in the Dominican Republic that mimicked Hamilton’s baldness-resistant castrates. Her team found that the pseudohermaphrodites testosterone levels were normal, but they lacked the enzyme that converted testosterone into the more potent androgen, DHT.

"Free" Testosterone > 5-Alpha Reductase > Dihydrotestosterone (DHT)

Taken together, presumably, castrates and pseudohermaphrodites were protected from baldness because of the lack of the androgen, dihydrotestosterone.

In 1975, Merck got wind of Imperato-McGinley’s research and began working on a pharmaceutical to block the enzyme that synthesized DHT from testosterone (5-alpha reductase or 5-AR) to treat prostate disorders that affect a large number of men in old age. During this time, Merck discovered that the drug was somewhat effective at growing hair, and in 1997 Merck received FDA-approval for their "blockbuster" drug, Finasteride (marketed under the name Propecia).

 

[Jayvee]

Finasteride and Dutasteride do effect a much larger proportion of people than what is let on by the pharmaceutical industry and their short term studies. Even if DHT was responsible for hairloss (no 'evidence' in favour of this is concrete), then you wouldn't want to disrupt all the other metabolites.

I feel like the 'pro 5ar blockers' people sound like me from the past. I wouldn't hear it from anyone and believed it only affected tiny percentage of people which is so far from truth.

 

[tankasnowgod]

The Peat strategies against hair loss don't have a good track record at all

I think what you mean to say is "The Peat strategies against hair loss don't have multi-billion dollar companies constantly pumping out advertising and other propaganda telling you that they work, like finasteride and dutasteride have. "

 

[milkboi]

I think what you mean to say is "The Peat strategies against hair loss don't have multi-billion dollar companies constantly pumping out advertising and other propaganda telling you that they work, like finasteride and dutasteride have. "

I'm not looking at any advertisement on Finestaride nor on many studies. Just reading lots of anecdotal reports. If you look at r/tressless, you'll see a lot of people getting regrowth with Finestaride + Minoxidil and there is picture proof of it. I haven't seen a single pair of process pictures like that achieved with "Peaty" strategies.

 

[ChemHead]

If I understand correctly you would theorise the extra iodine is causing higher production of T4, thereby speeding up 5AR production, fixing PFS?
My question would be: How come supplementing thyroid hormone doesn't fix PFS or speed up recovery? Thyroid supplementation has been tried quite a lot over the years.

See quote from my original post:

"another important aspect in TH regulation is the existing crosstalk with androgens due to the presence of ARE in genes related to THs, such as deiodinases and TH receptors (reviewed by Flood et al., 2013). Indeed, 5α-DHT treatment increases transcription of thyroid receptor β and deiodinase 1 (Campbell and Langois et al., 2018), and FIN treatment impacts expression of TH-related genes such as deiodinase and TH receptors in S. tropicalis (Langois et al., 2010b; Langois et al., 2011)."

So, there are androgen response elements within the genes encoding for deiodinases and thyroid hormone receptors and DHT treatment increases transcription of thyroid receptor β and deiodinase 1. Moreover, treatment of finasteride impacts the expression of these genes. So, what I'm seeing here is not only a classical picture of hypothyroidism (where only thyroid hormones are insufficient), but potentially hypothyroidism on the receptor side. With pharmaceutically-induced 5AR deficiency, low synthesis of DHT can cause an under-expression of the genes for deiodinase 1 (which plays a direct role in deiodinating T4 to the active T3) and for thyroid receptor β. So, if hypothyroidism isn't being induced by lack of thyroid hormones (perhaps you may be supplementing THs?), it can also be induced by lack of thyroid hormone receptor β expression. That hypothyroidism can then cause a sort of catch-22 situation where you don't have 5AR expression (and, thus, no DHT), so you can't express TH receptors properly, and you don't have sufficient thyroid hormone stimulation of tissues, so you can't express 5AR. This is the essence of post-finasteride syndrome in my opinion.

So, again, what I think may be happening is that: even if you supplement with thyroid hormone, if you already have little or no DHT production, you won't be able to properly express thyroid hormone receptor β. You won't be properly expressing deiodinase 1 either, but that probably won't matter so much if you're supplementing thyroid hormone. So, anyway, if you have sufficient thyroid hormone, but you don't express thyroid hormone receptor β, you're still going to be hypothyroid... which means that your body will still continue not to express 5AR. Now, if you were to simultaneously supplementing thyroid hormone and DHT in a reasonably high concentration? That would probably work to restore 5AR expression.

PFS imo truly is a catch-22 situation (wiki definition for those unfamiliar: "Catch-22" is "a problem for which the only solution is denied by a circumstance inherent in the problem or by a rule.").

There's actually a study showing the positive feedback loop between DHT and 5AR (Pubmed ID 6218182).

Yes. This is also likely part of the equation in the positive regulation of 5AR expression. DHT plays a role in upregulating the enzyme that creates it to begin with. Technically, it's actually androgen receptor mediated. The only problem I have (maybe) is that it was unclear to me whether DHT positively regulated 5AR expression in normal cells or only cancerous cells. If I recall correctly, the effects of DHT binding AR on all three isoforms of 5AR was evaluated of prostate cancer cells. I believe the type 1 5AR actually went up while type 2 expression actually went down. It could be the inverse... I don't quite remember.

So, it was this feedforward regulation of DHT on 5AR expression that originally prompted me to try a course of DHT. I've tried this multiple times of the years, but unfortunately nothing improved. So, it possible (maybe even likely) that the feedforward regulation of DHT on 5AR is actually only present in prostate cancer cells, while normally functioning cells do no behave in this manner. It's also possible that thyroid hormone is more important in regulating 5AR expression. It's also possible, I suppose, that there is some independent mechanism with iodine itself that I'm unaware of. However, I think the association between hypothyroidism and 5AR deficiency and hypogonadism is pretty solid.

 

[ChemHead]

Can we read your story somewhere, how you got PFS and your prior history?

If you search for my posts on here or on HLT, you'll probably find it in multiple posts in multiple different threads. I've repeated myself quite a few times, so it should be pretty easy to find.

I'm currently in the process of ramping up heavy resistance training. Heavy lifting seems to be a factor in most recovery stories.

While I agree with this, I don't think it's a prerequisite to recovery. The last time I recovered, I didn't do any type of resistance training or physical activity. I was too tired to function, both physically and cognitively. However, within days of recovery, my body became nearly instantly more muscular looking... literally almost overnight. I was leaner and the muscle tissue that I had was more swollen/plump. After this, not only did I have the desire to be physically active, it was actually something that I needed... completely the opposite state in comparison to PFS.

 

[GenericName86]

@ChemHead are you familiar with Cordyceps at all? If so do you think it might help with PFS? I've heard it increases 5AR expression. In regards to thyroid and 5AR, I notice increase in forearm/leg hair and slight increase in chest hair when using thyroid.

 

[ChemHead]

I guess I should mention that, at this point, I would recommend a protocol for PFS that looks something like this:

- 25-50 mg DHT daily

- iodine and cofactors (selenium, ascorbic acid, niacin, riboflavin) AND/OR thyroid hormone (T4)

- some type of gonadotropin to keep the body from going into severe steroid deficiency while using DHT... so something like hCG or gonadorelin

- an androgen receptor antagonist


I know the last one may seem counterintuitive or even controversial, but androgen receptor overexpression may be playing a big role in PFS as well. Finasteride causes androgen receptor overexpression and because loss of 5AR expression is persistent in this condition, I would expect a persistence of AR overexpression. So, obviously, my logic is that temporary antagonism of AR may help stimulate 5AR expression and will likely also stimulate gonadotropin secretion.