The TRUTH about % of finasteride side effects?

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Pondle

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stampede said:
Don't worry about me fella, I quit finasteride after I decided that it was for pussies.

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

HARDCORE :king:
 

Mew

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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

Hopefully that's a joke, but if not... good luck with that, hope you don't come down with some neuro-degenerative disease in the future.
 

Pondle

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Mew said:
Hopefully that's a joke, but if not... good luck with that, hope you don't come down with some neuro-degenerative disease in the future.

What would be the causal mechanism for that, Mew? I remember in a previous thread someone mentioned that the prevalence of Alzheimer's is very similar in both men and women (this may not be accurate, I haven't seen any studies)... despite women having only 2 - 20% of male DHT levels, and something like 1/3 of the 5AR1.
 

hairsucks

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IBM said:
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.

Please elaborate ?
 

joseph49853

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Mew said:
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.

Amen. I admire you for not backing down from your position.

More faith is placed in these limited clinical trials than simple logic and reason. Most people quoting these studies, and mimicking this pseudo techno-jargon, probably also don't fully understand the history of the FDA, and why it's currently broken.

Post-FDA-approval, you then have those limited Medwatch funds pitted against billions (upon billions) of corporate dollars spent during pro-drug marketing campaigns and media blitzes. Again, I hope many of you aren't looking toward the mostly failed Medwatch system in relation to many of these over-hyped drugs.

Just how many confirmed instances of suppression of this real-world data and information from within do we need? This was more recently exemplified in a senior FDA official's removal for his voicing concerns over Avandia. But then, even a simple black box warning (as was suggested) would be bad for Glaxo's sales of Avandia, but Merck's Propecia/Proscar.
 

joseph49853

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hairsucks said:
IBM said:
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.

Please elaborate ?

Place your finger lengthwise between your top and bottom lip. Now fully enunciate and form a b-sound, while quickly moving your finger up and down. :)
 

Pondle

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Rambo said:
Thats a pretty stupid statement , There are alot of ways to keep your hair without sacrificing your balls like alot of you damn freeks.

There's nothing with the proven long term efficacy of Propecia.

There's minoxidil... but it doesn't halt the balding process, merely provides a temporary growth stimulus. And the response rate has traditionally been poor, although the foam is claimed to 'work' for 85% of men.

There's RU... but it's not been commercialised for treating male pattern baldness. You have to buy it from China and mix it up yourself. There are mixed reports from people who have actually done this.

There's Revivogen... but it's not been through a rigourous clinical testing process. Again, there are mixed reports from users. Likewise for Tricomin.

I can't think of anything else!
 

Mew

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What would be the causal mechanism for that, Mew? I remember in a previous thread someone mentioned that the prevalence of Alzheimer's is very similar in both men and women (this may not be accurate, I haven't seen any studies)... despite women having only 2 - 20% of male DHT levels, and something like 1/3 of the 5AR1.

Again, we're NOT comparing women to men here, its apples vs oranges as mentioned in a previous thread (ratio of hormones). So remove women from your equation, because they play NO ROLE in this argument.

The other causal mechanism is, as also mentioned in a previous thread, that Finasteride, and ESPECIALLY Dutasteride (since it is a DUAL inhibitor, ie 5ARI and II) DO BLOCK THE PRODUCTION OF NEUROSTEROIDS IN THE BRAIN via inhibition of the 5AR pathway.

If you choose to ignore this fact, by all means go ahead and keep lying to yourself about it if it makes you feel better. This is ESPECIALLY concerning since Dutasteride blocks 5ARI, which is found in significant amounts in the human brain.

In particular, the blockade of allopregnanolone, which is a neuroprotective steroid, and resultant interference with the GABA-A signalling pathway via 5AR inhibitors, has been shown to alter aspects of behaviour in both humans and rodent models.

If you don't think the longterm inhibition of important and vital bodily processes/pathways/neurosteroids/metabolites may not have a negative effects on one's health down the road, specifically in the domain of neurology, you are quite frankly just being plain ignorant of the risks.

-------------

Here is one man's synthesis of some of the research out there on this topic:

http://www.bio.net/bionet/mm/neur-sci/2 ... 58929.html

"The latest research in mice raises a disturbing question about the
safety of FDA approved 5AR inhibitors like finasteride
(Proscar/Propecia) and especially dutasteride (Avodart) when it comes to
managing long-term risk for neurodegenerative diseases like Alzheimer's.
This is because these drugs not only reduce levels of DHT but also wound
allopregnanolone production in the process.

To summarize the new findings on allopregnanolone (see attached below),
Niemann-Pick type C is a rare lysosomal storage disorder/childhood
neurodegenerative disease in which brain cells accumulate fat and die
due in part to severely disrupted neurosteroidogenesis. A mutant gene
for lysosomal acid sphingomyelinase disturbs cholesterol synthesis
throughout the body and results in the accumulation of sphingomyelin.
Progressive loss of neurosteroid synthesis may contribute to
neurodegeneration. Replacing lost allopregnanolone substantially
increases the survival of mice with this type of disease by mitigating
the damage and delaying the onset of symptoms. Results were best when
administered as early as possible in the animal¹s life.
Allopregnanolone may be effective with managing other neurodegenerative
disorders. Other important neurosteroids like pregnenolone are also
diminished in Niemann-Pick type C but what's interesting here is how
valuable allopregnanolone is by itself.
<http>. NPC
model mice may have amyloid-beta accumulations similar to those in
Alzheimer's [PMID 14982851, 14982829] and may represent a good model for
studying general aspects of neurodegeneration.

5 alpha reductase (5AR) is an enzyme which comes in two forms, type I
and type II. It not only converts testosterone (T) to
dihydrotestosterone (DHT, a ketone), it also converts progesterone to
allopregnanolone and deoxycorticosterone (Doctor) to tetrahydroDOC (THDOC),
both allosteric enhancers of the GABA(a) receptor (e.g., they increase
the effectiveness of inhibition signals relayed along GABA channels in
nerves). The second stage of this conversion is performed by
3alpha-hydroxysteroid oxidoreductase.

This pathway has widespread influence in the body. Progesterone is the
precursor to allopregnanolone. Monthly drops in women¹s progesterone
prior to their periods is a factor in PMS and epileptic seizure.
Progesterone lozenges ameliorate seizures. Both estrogen and
progesterone are important for TMJ remodeling [PMID 10670598]. Men with
epilepsy can benefit from aromatase inhibitors which block the
conversion of testosterone to estrogen via aromatase [PMID 15123030].
Allopregnanolone can block cocaine induced seizures [PMID 12921865].
Complete 5AR inhibition shortens inhibitory currents in GABA(A) channels
both via allopregnanolone [PMID 12559121] and
5alpha-dihydrocoticosterone (THDOC) [PMID 11978855].

SSRIs (antidepressants like Zoloft) have been shown to upregulate levels
of progesterone and allopregnanolone (THP) [PMID 12957330] as well as
neurogenesis [PMID 14872203, 15001810, 14512209]. In animal models it¹s
the hippocampal neurogenesis that accounts for the behavioral effects of
SSRIs [PMID 12907793]. Conversely, inescapable stress which reduces
hippocampal neurogenesis also causes depression [PMID 12838272].

Levels of allopregnanolone can also be regulated by 3alpha-HSDs
(3alpha-hydroxysteroid dehydrogenase) - enzymes which are identical in
function to 5AR, except they convert T back from DHT instead of the
other way around. 3alpha-HSDs are responsible for downregulating levels
of DHT in the prostate and unusual inhibition of 3alpha-HSD would
increase DHT levels, decrease allopregnanolone and incline a male toward
impaired GABA functioning, acne, baldness, BHP and prostate cancer.
Stimulating 3alpha-HSD might be more effective than 5AR inhibition for
treating androgen disorders (although elevated exposure to either
progesterone or allopregnanolone can become anxiety-provoking instead of
calming; there are gender differences to this effect [PMID 12606703]).

Certain synthetic progesterones may interfere with allopregnanolone
synthesis. Medroxyprogesterone acetate (MPA), an ingredient in some
birth control pills and hormone replacement therapies, doesn¹t convert
into allopregnanolone and causes anxiety, aggression and depressed sex
drive in mice compared to combinations of natural hormones
<http>.

This overview should drive home just how important allopregnanolone may
be to human health. Finasteride is a 5AR type II inhibitor which
reduces DHT levels by up to 70%. Dutasteride inhibits both type I and
type II 5AR achieving a reduction of up to 94% of DHT. Type I is the
only 5AR expressed in the brain. Its long term inhibition was never
studied when dutasteride was approved by the FDA. Blocking DHT
synthesis in the brain like this also blocks allopregnanolone production
there. While other tissues like bone also express 5AR, finasteride has
been specifically studied on bone growth and has had no effect. Will
this also be true for neurodegenerative disorders which take decades to
develop? Will 5AR inhibitors be safe for individuals with epilepsy,
TMJ, neuropathy, alcoholism, tinnitus, metals poisoning or other
GABAergic illnesses?

If it's true that dramatic 5AR inhibition contributes to long term
neurodegeneration then what other therapeutic agents are available for
dealing with excessive DHT?"
 

stampede

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Mew said:
If it's true that dramatic 5AR inhibition contributes to long term
neurodegeneration then what other therapeutic agents are available for
dealing with excessive DHT?"

Well that's the thing, isn't it?

There aren't any. Unless we get really silly and start taking spironolactone/cyproterone etc.

So unless we want to go bald, we have to accept the risks of the treatment we're on.
 

Mew

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Well that's the thing, isn't it?

There aren't any. Unless we get really silly and start taking spironolactone/cyproterone etc.

So unless we want to go bald, we have to accept the risks of the treatment we're on.

Wrong. Read the rest of the article, he presents some alternatives.
 

stampede

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He mentions this 3alpha-HSD stuff, which converts DHT back to testosterone. Which is nice.

But where do I get hold of it and does it actually work, that's the thing? :?
 

Mew

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You're getting confused, that's not even a "treatment", it's a metabolic pathway.

Here:

"Understanding why male hormonal disorders like BHP, prostate cancer and
baldness have become common in "advanced" economies is important to
answering this question. One contributing factor is the bad mix of fats
consumed in the American diet (high in trans-fats, hydrogenated oils,
bad omega-6 and -9's and low in omega-3). Another factor is high
glycemic index diets which contribute to insulin resistance and androgen
signaling disorders like polycystic ovarian syndrome. High levels of
insulin lower levels of sex hormone-binding globulin, a substance which
binds to testosterone and lowers the amount of "free" androgens
available to bind to the receptor (see [PMID 14527633],
<http>). These
androgen driven disorders are all complex genetic disorders which can
develop from many different angles. For instance, in a small study,
prematurely balding men could be divided into two groups: the first
group (about a third of the men) had a hormonal/insulin profile similar
to women with polycycstic ovarian syndrome (low SHBG, hyperinsulemia,
high free androgens and insulin resistance) whereas the second group had
no similarities or only lower SHBG [PMID 15209536]. How you react to
pathologically elevated levels of DHT is determined by your genetic risk
and your environment.

While dietary factors like fat and sugar consumption are important , the
major actor on DHT throughout our evolutionary history has been a
substance called equol. Equol is a derivative of the soy metabolite
daidzein produced by bifidus bacteria in the gut. It directly binds to
dihydrotestosterone and deactivates it [PMID 14681200]. Most male
mammals produce ample amounts of equol to regulate excessive DHT
production. High levels of equol in men lowers the risk for prostate
cancer [PMID 14681200, 14720329] and improves blood cholesterol [PMID
14679315].

By taking antibiotics, you usually increase your risk for chronic
inflammatory disorders. In this case, killing your gut bacteria leaves
abnormally high levels of free DHT floating around in your blood
stimulating your androgen receptors beyond what your body is used to.
Over a lifetime, this brings out your genetic risk for androgen-driven
disorders like the ones I keep mentioning. Destroying your gut bacteria
with antibiotics probably also increases the risk for allergies, asthma,
arthritis and other inflammatory disorders (see
<http>,
<http>, PMID
15120189) - not to mention it can give you a bad yeast infection like
you see in chronic sinusitis.

How can you obtain equol if you no longer make your own?

That's the problem. You can't. The only versions manufactured and sold
today are racemic - meaning both the left and right isomers of the
molecule are produced in a mixture. Only one form is naturally made and
used in the human body. The other is not well studied. Another
limiting factor is that finasteride and dutasteride are patented while
equol can't be - it's a natural product which has been around too long.
Contact manufacturers and let them know there is a market for this
therapeutic substance and that it's worth conducting clinical trials.

If 5AR inhibitors do pose long term risks and you absolutely have to
take them, it may be possible to lessen the neurological damage with
things like acetyl-l-carnitine, minocycline, l-theanine, taurine,
curcumin, green tea (EGCG), CoQ10, nicotinamide/niacinamide, creatine,
ketogenic diets, so on and so forth (each of which carries with it its
own complicating factors)"
 

Pondle

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Mew said:
What would be the causal mechanism for that, Mew? I remember in a previous thread someone mentioned that the prevalence of Alzheimer's is very similar in both men and women (this may not be accurate, I haven't seen any studies)... despite women having only 2 - 20% of male DHT levels, and something like 1/3 of the 5AR1.

Again, we're NOT comparing women to men here, its apples vs oranges as mentioned in a previous thread (ratio of hormones). So remove women from your equation, because they play NO ROLE in this argument.

The other causal mechanism is, as also mentioned in a previous thread, that Finasteride, and ESPECIALLY Dutasteride (since it is a DUAL inhibitor, ie 5ARI and II) DO BLOCK THE PRODUCTION OF NEUROSTEROIDS IN THE BRAIN via inhibition of the 5AR pathway.

If you choose to ignore this fact, by all means go ahead and keep lying to yourself about it if it makes you feel better. This is ESPECIALLY concerning since Dutasteride blocks 5ARI, which is found in significant amounts in the human brain.

In particular, the blockade of allopregnanolone, which is a neuroprotective steroid, and resultant interference with the GABA-A signalling pathway via 5AR inhibitors, has been shown to alter aspects of behaviour in both humans and rodent models.

If you don't think the longterm inhibition of important and vital bodily processes/pathways/neurosteroids/metabolites may not have a negative effects on one's health down the road, specifically in the domain of neurology, you are quite frankly just being plain ignorant of the risks.

I fail to understand why you reject the male-female comparison, Mew. Apples and oranges? Surely male and female brains are not that different, biochemically? After all, we are dealing with two sexes, not two species. What about men who have gone through gender reassignment? Which reference group should we compare their health outcomes to?

I entirely accept that the role of neurosteroids is imperfectly understood, and the long term consequences of dutasteride use are unknown. The question for me, though, is what level of neurosteroidal inhibition is 'dangerous' and in what way.

I presume (it's a presumption, I don't know) that if women don't have the same level of 5AR1 and DHT as men, then they have a lower level of certain neurosteroids, and if the relative level of those neurosteroids play an important role in some neurological health outcomes, one would expect women to have relatively worse neurological health outcomes than men, unless there is some other compensatory biochemical mechanism in the female brain that is not present in the male brain...???? :?

A good test, I suppose, would be whether men that have undergone HRT and gender reassignment have worse neurological health outcomes than men (and/or women). I've never seen any data on this, though.

Another issue would be whether the 5AR deficient pseudohermaphrodites have worse neurological health outcomes... again, as far as I understand it, no clinical abnormalities of this sort have been reported for this group.
 

stampede

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Mew.

If you're happy with a bald head, good for you man. You're free of the evil Propecia, go and live your life :)

Why would you want to hang around a board with people who take the nasty stuff? Get out there and show your horseshoe to the world :)
 

Pondle

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I think the problem is that we're dealing with supposition, extrapolation and speculation. There's no data on the neurological significance of long term use of finasteride or dutasteride; none of us are experts in biochemistry or neurology; we're looking up studies, making deductions and interpretations from animal models that have different metabolisms and physiologies. Our interpretations and deductions may easily be flawed, one way or the other.
 

joseph49853

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stampede said:
Mew.

If you're happy with a bald head, good for you man. You're free of the evil Propecia, go and live your life :)

Why would you want to hang around a board with people who take the nasty stuff? Get out there and show your horseshoe to the world :)

Stampede, if you hadn't noticed this forum is called "Dealing with Side Effects." The one you're looking for is two doors down and to the right. That's the happy panacean forum that will allow you to sleep soundly at night, not this one.
 

stampede

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To stop taking your medication is not what I'd term "dealing" with side effects.

I deal with my side effects, not by chickening out of taking my medicine, but by dealing with problems as they arise. For example, I have arimidex on hand should I start getting any pectoral feminisation, or start retaining water etc. And I go to the gym to keep off all the weight.
 

stampede

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Sure thing man :lol:

You'll have issues when you have no hair. And I'd drop that hippy natural regimen right now, you may as well save your money for all the hats you're gonna need...
 
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