The TRUTH about % of finasteride side effects?

[Mew]

Compare what's listed below to their "2%" claim about Propecia side effects: http://www.propecia.com/finasteride/pro ... safety.jsp

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Check it out
http://www.merck.com/mmpe/lexicomp/finasteride.html


Adverse Reactions

Note: “Combination therapyâ€￾ refers to finasteride and doxazosin.

>10%:

Endocrine & metabolic: Impotence (19%; combination therapy 23%), libido decreased (10%; combination therapy 12%)

Genitourinary: Neuromuscular & skeletal: Weakness (5%; combination therapy 17%)

1% to 10%:

Cardiovascular: Postural hypotension (9%; combination therapy 18%), edema (1%, combination therapy 3%)

Central nervous system: Dizziness (7%; combination therapy 23%), somnolence (2%; combination therapy 3%)

Genitourinary: Ejaculation disturbances (7%; combination therapy 14%), decreased volume of ejaculate

Endocrine & metabolic: Gynecomastia (2%)

Respiratory: Dyspnea (1%; combination therapy 2%), rhinitis (1%; combination therapy 2%)

<1%, postmarketing and/or case reports: Hypersensitivity (pruritus, rash, urticaria, swelling of face/lips); breast tenderness, breast enlargement, breast cancer (males), prostate cancer (high grade), testicular pain

 

[Wash n' Gone]

That is for Finasteride and doesn't mention dosage. I would imagine it is talking about the 5mg version taken by much older men as doxazosin is an alpha blocker used to treat BPH. It doesn't contradict the clinical studies at all. Surely this should be in the side effects forum any way?

 

[Pondle]

It also doesn't compare to placebo, so is somewhat misleading. I posted the MTOPS adverse reactions data in the side effects forum.

 

[abcdefg]

It says right at the top merk doesnt endorse or in no way is affiliated with this 3rd party source. How on earth did this 3rd party source come up with these percentages? If they have studies and info the rest of us dont by all means share and let it be peered reviewed. Hell I can make percentages.

It says this in one of there article references:
A Canadian trial of 472 men followed for 2 years demonstrated a statistically significant but clinically modest difference in symptom scores favouring finasteride (5 mg/d) over placebo. The group difference was 1.4 points on a 54 point scale. Adverse effects of finasteride were relatively common, notably impotence ( ARI = 10% ) and ejaculation disorder (ARI = 6%)

472 men is a pretty small sample and I like how no study ever gives information about the men it uses like age, weight, starting testosterone, and the other 20 important factors that might influence the statistical accuracy of the study. A sample size of 472 is pretty minor relative to the thousand men that were enrolled in merks own study. Its possible the smaller sample got a less accurate result due to smaller sample size no one knows. I would trust the larger study since its a much larger and over a much longer period although it is from merk.

 

[Pondle]

Looks like Mew's taking his data from the MTOPS Proscar study. What he's not showing you (deliberately? 8) ) is the comparative results for placebo, which are kinda ESSENTIAL when evaluating side effects. There's another discussion on this in the side effects forum.

 

[Mew]

No, it wasn't deliberate not to mention Placebo... just didn't have the source document at the time. But here it is:

http://www.merckfrosst.ca/assets/en/pdf ... 2_06-E.pdf

Page 4.

Regardless it is interesting to note these stats.

 

[abcdefg]

You know I never read about anyone saying finasteride might increase your risk of breast cancer or atleast change it. According to the study the link between those 2 is no known.

 

[bubka]

christ Mew, half of the side effects out actually HIGHER with the placebo than with finasteride

 

[Mew]

bubka, yes some Placebo effects are higher than finasteride -- but not the 2 most men would concern themselves with, I believe: Impotence and Libido decrease.

ALSO -- interesting to note some other points in that PDF as well:

PAGE 3:
Four patients in MTOPS reported the adverse experience breast cancer. Three of these patients were on finasteride only and one was on the combination therapy... The relationship between the long-term use of finasteride and male breast cancer is currently unknown.


PAGE 6:
"Finasteride has been found to cross the blood-brain barrier."


PAGE 7:
Although the clinical significance is unclear, a higher incidence of cataracts (4.2%, finasteride vs. 2.5%, placebo) and diabetes (2.8%, finasteride vs. 1.7%, placebo) was observed in patients receiving finasteride.


PAGE 12:
"Finasteride appeared to inhibit both C19 and C21 steroid metabolism and hence appeared to have an inhibitory effect on both hepatic [liver] and peripheral Type II 5 alpha-reductase activity. The serum DHT metabolites androstenediol glucuronide and androsterone glucuronide were also significantly reduced."

This metabolic pattern is similar to that observed in individuals with a genetic deficiency of Type II 5 alpha reductase who have markedly decreased levels of DHT and small prostates, and who do not develop
BPH.

"Finasteride has been recovered in the cerebrospinal fluid (CSF) of patients treated with a 7-10 day course of finasteride, but the drug does not appear to concentrate preferentially to the CSF."

 

[Pondle]

Why worry about developing a metabolic pattern similar to the pseudohermaphrodites with 5AR2 deficiency? They were the 'model' for finasteride and, apart from their genitalia, they appear to be otherwise healthy with normal male libido and bone and muscle mass - though perhaps not all aspects of their condition have been extensively studied. Bryan mentioned that he found a long article about them recently, was it in Nature?

I'm also not worried about finasteride crossing the blood-brain barrier, unless it has some clinical significance I'm not aware of. I understood that finasteride (at least in doses below 270mg/day, or thereabouts - Bryan posted a figure some time ago) does not block production of neurosteroids, because it has little affinity for 5AR1. Even if it did, I'm not sure whether that would be of enormous consequence. After all, women seem to do just fine with something like 1/3 of the 5AR1 of men.

The stats on cataracts & diabetes look concerning, but are those differences statistically significant?

 

[Mew]

Why worry about developing a metabolic pattern similar to the pseudohermaphrodites with 5AR2 deficiency

Perhaps because they were BORN that way and hence their development/brain/sexual function was designed to work under such conditions?

Taking already-born, normal young men and transforming their hormonal profile via Finasteride to match that of a pseudohermaphrodite, despite normal men not having been born that way (ie, their wiring was never meant to function as a pseudo) is not necessarily a good thing.

I understood that finasteride (at least in doses below 270mg/day, or thereabouts - Bryan posted a figure some time ago) does not block production of neurosteroids, because it has little affinity for 5AR1

Wrong. See below article.

I'm also not worried about finasteride crossing the blood-brain barrier

I would be, based on the below.

After all, women seem to do just fine with something like 1/3 of the 5AR1 of men

Women aren't men. It's apples vs oranges. Sure, they might be able to get by with low levels of DHT just fine -- but that's not necessarily true for some men, as we've seen with Finasteride side effects due to inhibition of DHT -- because men are NOT the same as women, hormonally speaking, and we're hardwired differently -- even the ratio of our hormones is different.

So comparing the two is a pointless argument, really. Who cares if women can get by on low DHT? Some men CANNOT, and that's the point here... although I will say, 5AR1 inhibition is obviously not preferred by Finasteride, but it has been documented to occur, however ususally at much higher doses.

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http://www.ingentaconnect.com/content/b ... 1/art00005

A New Look at the 5α-Reductase Inhibitor Finasteride

Finasteride is the first 5α-reductase inhibitor that received clinical approval for the treatment of human benign prostatic hyperplasia (BPH) and androgenetic alopecia (male pattern hair loss).

These clinical applications are based on the ability of finasteride to inhibit the Type II isoform of the 5α-reductase enzyme, which is the predominant form in human prostate and hair follicles, and the concomitant reduction of testosterone to dihydrotestosterone (DHT).

In addition to catalyzing the rate-limiting step in the reduction of testosterone, both isoforms of the 5α-reductase enzyme are responsible for the reduction of progesterone and deoxycorticosterone to dihydroprogesterone (DHP) and dihydrodeoxycorticosterone (DHDOC), respectively.

Recent preclinical data indicate that the subsequent 3α-reduction of DHT, DHP and DHDOC produces steroid metabolites with rapid non-genomic effects on brain function and behavior, primarily via an enhancement of γ-aminobutyric acid (GABA)ergic inhibitory neurotransmission.

Consistent with their ability to enhance the action of GABA at GABAA receptors, these steroid derivatives (termed neuroactive steroids) possess anticonvulsant, antidepressant and anxiolytic effects in addition to altering aspects of sexual- and alcohol-related behaviors.


Thus, finasteride, which inhibits both isoforms of 5α-reductase in rodents, has been used as a tool to manipulate neuroactive steroid levels and determine the impact on behavior. Results of some preclinical studies and clinical observations with finasteride are described in this review article.

The data suggest that endogenous neuroactive steroid levels may be inversely related to symptoms of premenstrual and postpartum dysphoric disorder, catamenial epilepsy, depression, and alcohol withdrawal.

 

[Pondle]

Why worry about developing a metabolic pattern similar to the pseudohermaphrodites with 5AR2 deficiency

Perhaps because they were BORN that way and hence their development/brain/sexual function was designed to work under such conditions?

Taking already-born, normal young men and transforming their hormonal profile via Finasteride to match that of a pseudohermaphrodite, despite normal men not having been born that way (ie, their wiring was never meant to function as a pseudo) is not necessarily a good thing.

Hmm, I think 'designed' may be a strong word in the case of a random mutation. It's not as if hormonal profiles can't be changed - women and men can undergo HRT and gender reassignment - you've seen the vids Michael Barry has posted, Buck Angel et al? Now it may be the case that there are long term negative health outcomes associated with gender reassignment, I just don't know enough about this field to comment. But we do know, based on 15 years of clinical use, that finasteride has a pretty good safety profile, and this is much less radical than HRT.

Women aren't men. It's apples vs oranges. Sure, they might be able to get by with low levels of DHT just fine -- but that's not necessarily true for some men, as we've seen with Finasteride side effects due to inhibition of DHT -- because men are NOT the same as women, hormonally speaking, and we're hardwired differently -- even the ratio of our hormones is different.

So comparing the two is a pointless argument, really. Who cares if women can get by on low DHT? Some men CANNOT, and that's the point here... although I will say, 5AR1 inhibition is obviously not preferred by Finasteride, but it has been documented to occur, however ususally at much higher doses.

The point about women is it suggests that DHT is not essential to 'non-gender specific' health outcomes (as opposed to impotence, low libido, etc etc). As I said above, male and female are not totally exclusive categories; someone can be born a man, or a woman, and change their hormonal profile quite radically. On the basis that is presumably relatively safe, I see no reason to worry about finasteride therapy, which is rather less radical!

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In addition to catalyzing the rate-limiting step in the reduction of testosterone, both isoforms of the 5α-reductase enzyme are responsible for the reduction of progesterone and deoxycorticosterone to dihydroprogesterone (DHP) and dihydrodeoxycorticosterone (DHDOC), respectively.

Recent preclinical data indicate that the subsequent 3α-reduction of DHT, DHP and DHDOC produces steroid metabolites with rapid non-genomic effects on brain function and behavior, primarily via an enhancement of γ-aminobutyric acid (GABA)ergic inhibitory neurotransmission.

Consistent with their ability to enhance the action of GABA at GABAA receptors, these steroid derivatives (termed neuroactive steroids) possess anticonvulsant, antidepressant and anxiolytic effects in addition to altering aspects of sexual- and alcohol-related behaviors.

Thus, finasteride, which inhibits both isoforms of 5α-reductase in rodents, has been used as a tool to manipulate neuroactive steroid levels and determine the impact on behavior. Results of some preclinical studies and clinical observations with finasteride are described in this review article.

The data suggest that endogenous neuroactive steroid levels may be inversely related to symptoms of premenstrual and postpartum dysphoric disorder, catamenial epilepsy, depression, and alcohol withdrawal.

How much of the total effect on neurosteroids in rodents is due to the fact that, at this dose, finasteride is inhibiting type 1 5AR as well as type 2? How much can we extrapolate to humans taking 1mg/day or 5mg/day?

Perhaps if you are prone to depression, you ought to be cautious about Propecia. However, male pattern baldness is likely to make you depressed anyway... you pays your money and you takes your choice. Personally, I'm pretty relaxed about this issue (I note that dutasteride is being tested for treating mood disorders in menstrual women). But then I'm not prone to depression!

 

[Pondle]

pondle you sound like a god damn wh*** for merck, you have too much time on your hands to know all that useless crap.

Well I do spend too much time on forums... trying to wean myself off, I do have a life beyond! 8) If people want to stick Big Pharma in the box marked "bad" that's fine with me, but Propecia saved my hair, and I got no side effects (knock on wood). In fact I'm growing my barnet long now! I even bought straighteners last week. :jump:

 

[stampede]

Mew, would you like to explain to me the benefit of having a super strong libido when you've got a horseshoe? :?

If I was an NW7 (which I would be in a couple of years if I wasn't on treatments), I would rather not have any sexual desire. I mean, it's not as if I'm going to get any now, is it?

 

[hairsucks]

I agree 100% with Rambo on that one, Only a crazy man would want hair over the use of his penis ! Stampede, that statment makes me think you need help!

I have very thin hair now on my head and shave it to the bone so I look bald as a coot but I screw at least 3 times a week and I love it.

Pondle - as if you have bought tongs! maybe the finasteride is actually turning you into a girl but your in denial because you love finasteride so much! - just messing :lol:

 

[stampede]

As long as I can pee, my penis is working just fine.

 

[Mew]

As long as I can pee, my penis is working just fine.

If you get sexual dysfunction from finasteride, that's about the only thing you'll be able to do -- especially if the sides don't go away after quitting.

Mew, would you like to explain to me the benefit of having a super strong libido when you've got a horseshoe?

Bald men do get laid despite what you might think, and they also tend to have higher sex drives than their non-balding counterparts.

Being bald is nothing compared to not being able to f*** thanks to a drug.

 

[Pondle]

Bald men do get laid despite what you might think, and they also tend to have higher sex drives than their non-balding counterparts.

Being bald is nothing compared to not being able to f*** thanks to a drug.

Some bald guys can look great, but it's not a look that would ever suit me. I'm far too skinny and boyish; I'd just look ill.

If you get persistent sides from finasteride or dutasteride, your hair is pretty much f*cked. That's a damn shame, but there is more to life than hair. Only the most troubled guys are willing to sacrifice their relationship for the sake of their scalp follicles. As for those folks taking spironolactone, well.... :freaked:

 

[IBM]

Troubled guys are those who sacrifice their hair because of their lack of women's autonomy.

In twenty first centuty we still see a lot men's will devation with fear of a possible women's scorn. Simply pathetic.

I dont think it's crazy a person think of himself first.

 

[stampede]

If you get sexual dysfunction from finasteride, that's about the only thing you'll be able to do -- especially if the sides don't go away after quitting.

Don't worry about me fella, I quit that nasty finasteride stuff after I decided that it was for pussies.

I'm now on 5 Dutasteride capsules a day :lol: :lol: :lol: