Mechanism of finasteride side effects

[Dave001]

Tailback: You're right, I'm not a native English speaker .. but you got my point obviously.

OK. I didn't mean to sound rude. It would sound obfuscatory from a native speaker.

I was mainly referring to the statement that "excess T gets converted to E".

Uh, when was there any question of the metabolic pathways of testosterone to estrogens?

Go to a well equipped library to verify these outlandish claims. :wink:

I've read a thing or two about steroid enzyme conversions. Have you? :wink: Your description of steroid metabolism was far too convoluted for specific objections. It was your attempt to ascribe clinical effects to biochemical mechanisms that was specifically at question. Causal relationships are not nearly so simple.

BTW, there are many andro- steroids; e.g., androstanes, androstanols, androstenes, androstadienes, androstatrienes, androstenols. Spelling counts. There is no "androstentiole" or "androstendiole," both of which were included in your convoluted description of steroidal enzyme pathways. There is however, an androstenedione, androstenediol, and androstanediol, all of which are endogenous androgens. You probably meant androstenedione though, because it sounds like you were trying to paraphrase from the following study:

Niiyama, S., R. Happle, et al. (2001). "Influence of estrogens on the androgen metabolism in different subunits of human hair follicles." European Journal of Dermatology 11(3): 195-8.

I will give you the benefit of the doubt and assume that it's language barrier problem, because most of what you've written is patently absurd. E.g.,, "Androstentiole [sic] immediately attaches [sic] to the estrogen receptors and is metabolized via testosterone..." Perhaps you meant to say that androstenedione is converted to estrone by 17beta-hydroxysteroid dehydrogenase, which can further metabolize estrone to estradiol.

 

[hairschmair]

If peak mental and physical performance is of importance to you, you'd be much better served by a topical antiandrogen such as spironolactone.

Theory is all well and good but it doesn't explain how after 6 months of finasteride I have seen no effect on my libido, mental or physical performance.

What "theory" are you referring to? Whether or not the effect is severe enough to be noticed subjectively is not an issue that was addressed by my comment.

Theory: "General principles derived from a body of scientific data to explain a natural occurrence." I didn't mean theory as in an uncomfirmed hypothesis.

Your post was about how potent DHT is, where it acts, and so forth, with the conclusion that you can not maintain peak libido, mental and physical performance, while inhibiting it.

I have not noticed any changes in any of these areas, which lead to my questioning whether the theory ("General principles derived from a body of scientific data to explain a natural occurrence") you present perhaps has some missing components, yet to be discovered, that can explain why inhibiting DHT can have little to no effect.

Hope that clears things up

 

[Dave001]

Your post was about how potent DHT is, where it acts, and so forth, with the conclusion that you can not maintain peak libido, mental and physical performance, while inhibiting it.

I have not noticed any changes in any of these areas, which lead to my questioning whether the theory ("General principles derived from a body of scientific data to explain a natural occurrence") you present perhaps has some missing components, yet to be discovered, that can explain why inhibiting DHT can have little to no effect.

Nope. There is no question that androgens affect performance in those areas. But, as I said, "[w]hether or not the effect is severe enough to be noticed subjectively is not an issue that was addressed by my comment."

 

[hairschmair]

Fine, but whether something is noticeable or not noticeable is essential to this discussion. You could say that eating too many potatoes will affect mental, physical and libido negatively, by some mechanism.

Theory says: "DHT is a very potent androgen"

In practice some people are taking dutasteride and reducing their DHT by practically 100%, and can still function sexually, even with only the "not so potent" Testosterone around.

I'm thinking there's more to this.

 

[Dave001]

Fine, but whether something is noticeable or not noticeable is essential to this discussion. You could say that eating too many potatoes will affect mental, physical and libido negatively, by some mechanism.

Theory says: "DHT is a very potent androgen"

It is NOT a theory. The potencies of DHT and testosterone have been quantified MANY times.

In practice some people are taking dutasteride and reducing their DHT by practically 100%, and can still function sexually, even with only the "not so potent" Testosterone around.

I'm thinking there's more to this.

Side-effects are on a continuum. Androgens are not like cocaine or amphetamines; the effects can be subtle. Imperceptible changes are often the most insidious, especially over the long-term.

An extreme example: what was the time difference between the gold and bronze medal for the men's 100 meter in the last Olympics? About 0.02 seconds, right? I think fourth place was about 0.04 seconds from first. Do you think someone would be able to "feel" something that slowed him down by 0.05 seconds in the 100 meter?

 

[TA45]

Propecia

Hello, my name is Tim. I have diffuse thinning and a slowly receding hairline. Tried Propecia 2 x's in the past and could not deal with the side effects. I even tried 1/5 Proscar every other day and still couldn't do it. So I am trying it again except I'm taking anout 1/10 proscar pill every three days. I understand this is a very weak treatment due to the low dose but I really have no other choice. Do you think it may help? Can't do the Minoxidel either. Ugh-Tim

 

[Old Baldy]

Fine, but whether something is noticeable or not noticeable is essential to this discussion. You could say that eating too many potatoes will affect mental, physical and libido negatively, by some mechanism.

Theory says: "DHT is a very potent androgen"

It is NOT a theory. The potencies of DHT and testosterone have been quantified MANY times.

In practice some people are taking dutasteride and reducing their DHT by practically 100%, and can still function sexually, even with only the "not so potent" Testosterone around.

I'm thinking there's more to this.

Side-effects are on a continuum. Androgens are not like cocaine or amphetamines; the effects can be subtle. Imperceptible changes are often the most insidious, especially over the long-term.

An extreme example: what was the time difference between the gold and bronze medal for the men's 100 meter in the last Olympics? About 0.02 seconds, right? I think fourth place was about 0.04 seconds from first. Do you think someone would be able to "feel" something that slowed him down by 0.05 seconds in the 100 meter?

Dave: I've read that many men (suffering from male pattern baldness) have higher levels of DHT in the scalp (maybe serum levels also?).

Questions:

(1) Does it follow if a man has higher scalp levels of DHT than he probably has higher serum levels of DHT?

(2) If we reduce, let's say 70 percent of DHT levels by using finasteride., does it follow that there is still enough DHT remaining to "prevent" noticable "side effects"?

(3) If the answer to (2) is "yes", could that be why I'm not noticing ANY side effects from using finasteride.?

(I tried to word question (2) better but I hope I conveyed my question well enough? What I'm asking in (2) above is, reducing DHT levels in men with higher levels than average, might leave enough DHT, relative to average levels, to prevent side effects.) God, this is still worded badly, I hope you can figure out what the heck I'm trying (badly) to ask.

 

[chewbaca]

After permanent rise in Testes level, if u stop DHT inhibition through propecia, will the hair loss get more severe a there is so much Testes floating about and naturally more of it will be converted to DHT?

can someone please answer my Q?

 

[hairschmair]

The rise in Test is not permanent.

 

[Dave001]

Dave: I've read that many men (suffering from male pattern baldness) have higher levels of DHT in the scalp (maybe serum levels also?).

Questions:

(1) Does it follow if a man has higher scalp levels of DHT than he probably has higher serum levels of DHT?

Not necessarily, but circulating DHT doesn't appear terribly important, apart from its role as an indicator of local DHT production. DHT primarily affects the tissues in which it is locally produced (from 5 alpha-reductase).

(2) If we reduce, let's say 70 percent of DHT levels by using finasteride., does it follow that there is still enough DHT remaining to "prevent" noticable "side effects"?

Not necessarily, because it's not simply a matter of preventing a "DHT deficiency". In general, higher levels of DHT yield improvements in performance (of certain parameters), but at what point that effect begins to diminish, or to what level DHT must drop below to before side effects become noticeable, isn't known. It probably varies.

But again, a figure like 70% doesn't really tell us much, because it is locally produced DHT that is the most important. Most of that 70% comes from the prostate. In other words, inhibiting 5 alpha-reductase in e.g., the CNS, would be expected to produced more "mental" side effects than the corresponding reduction of circulating DHT. Speaking of the CNS, type 1 is supposedly the predominant isozyme of 5 alpha-reductase in the CNS.

(3) If the answer to (2) is "yes", could that be why I'm not noticing ANY side effects from using finasteride.?

I don't think so. It's a lot more complicated than that, and there are many variables, including feedback mechanisms and such that make it impossible to know for sure.

 

[Old Baldy]

Thanks for the info. Dave. I'm glad that the CNS is more influenced by Type I. VERY glad. Thanks again!