Pregnenolone cream as an anti DHT??? Progesterone Easters...

squeegee

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My buddy told me that bodybuilders started to take pregnenolone cream to lower their DHT Level. There is guys on that very forum dropped from 226 to 80 with 50 mgs a day in a matter of 6 weeks. http://forum.mesomorphosis.com/men-s-he ... 58641.html

Some speculations also :

Yea thats the point I was trying to get across! Pregnenolone breaks down into all the major steroids, especially important neural steroids as well, but most importantly, it breaks down into progesterone and DHEA. Progesterone, as many know, is an anti DHT hormone. This is why girls are, well, girls. DHT is the most potent "Male" hormone. Girls have alot of progesterone, this is why they have low DHT and carry feminine characteristics.

I have a speculation that one of the reasons many females lose hair/get thinning hair is that when they go threw menopause, they lose progesterone.

Now remember, we can't get all progesterone crazy - thats why we don't take straight progesterone. Pregnenolone causes a slight, safe rise in progesterone, which keeps DHT in check.

This is how teenage boys have T levels in the 700 - 1000 range yet have DHT levels that are middle range or at the lower end of the top 1/3 - They have plenty of pregnenolone production.

As wel age, we lose pregnenolone production, due to aging of testicles and adrenal glands. When one goes on HRT, HTPA is shut off and testes stop working, hence the pregnenolone production is shut off. Then we have a perfect recipe for skyrocketing DHT - something we DO NOT want. T goes high, converts into DHT, with no pregnenolone to shut if down, we see guys on TRT lose hair, get swollen prostates, and in some cases high DHT can cause anxiety and irritibility.

This is also why hcG is so important - we need the testicles alive and well to supplement pregnenolone production, in addition to what we add in as cream. Plus hcG is a source of LH receptor activity! So anyone who thinks that hcG is for cosmetic purposes is simply mis-informed!

As preg enters bloodstream via cream, it is converted to various hormones, one in particular is progesterone.

Progesterone is well known to prevent T conversion to DHT.

Preg cream with possible low dose proscar would have definitely kept DHT in check. Added side bonus(big one!) is that proscar acts as a 5 alpha inhibitor in prostate gland - decreases prostate size, improves urine flow/etc.

It is possible preg cream alone would have been enough. Might want to do both and adjust according to BW.

Remember most with side effects from proscar was because of already so so DHT level being driven into ground. You have the luxury that they did not have by having BW on hand to watch numbers. It is possible Preg would have done job solo.

I am now starting to fully grasp of how/why Dr John implements things the way he does. Transdermal first is a very wise move. Much superior to injects. I like the way he backloads DHEA/Preg. Did not understand such things as little as a few months ago. Making more sense in every way the more I learn. Very ingenious.

and also
New Progesterone Esters as 5?-Reductase Inhibitors
Marisa CABEZA1), Ivonne HEUZE1), Eugene BRATOEFF2), Eugenia MURILLO2), Elena RAMIREZ2) and Alfonso LIRA2)
1) Departments of Biological Systems and Animal Production, Metropolitan University-Xochimilco
2) Department of Pharmacy, Faculty of Chemistry, UNAM, Ciudad Universitaria
(Received February 26, 2001)
(Accepted May 17, 2001)
The pharmacological activity of four new progesterone derivatives: 4-bromo-17?-(p-fluorobenzoyloxy)-4-pregnene-3, 20-dione (7), 4-bromo-17?-(p-bromobenzoyloxy)-4-pregnene-3, 20-dione (8), 4-bromo-17?-(p-chlorobenzoyloxy)-pregnene-3, 20-dione (9) and 4-bromo-17?-(p-toluoyloxy)-4-pregnene-3, 20-dione (10) was determined. These compounds were evaluated as 5?-reductase inhibitors on gonadectomized hamster seminal vesicles and flank organs. The pharmacological data of this study indicate that compounds 7 and 9 having at C-17 p-fluorobenzoyloxy and p-chlorobenzoyloxy ester functions respectively showed the highest antiandrogenic effect as measured by the reduction of the weight of the seminal vesicles. In the flank organ model, the same compounds 7 and 9 exhibited a smaller diameter, 1.8 and 1.0 mm, respectively, than the commercially available finasteride 3 (2.3 mm), thus indicating a higher inhibitory effect on 5?-reductase enzyme. Steroid 7 showed a higher inhibitory activity on the conversion of T to DHT (Fig. 3) than the presently used finasteride, thus indicating a higher antiandrogenic effect. The nonsubstituted benzoyloxy ester (compound 15) showed a lower antiandrogenic activity as measured in the seminal vesicles model than the p-substituted benzoyloxy compounds.
Key words flank organ; seminal vesicle; 5?-reduction; T-conversion; C-16 substituent

New progesterone esters as antagonist of androgen receptor
http://www.westernpharmsoc.org/wpsjourn ... esters.pdf


1) Dr. Norman Orentreich, in his article: "Biology of Scalp Hair Growth", Clinics in Plastic Surgery -- Vol. 9, No. 2, 1982:

"Local Therapy {...} Progesterone was found to be a natural and significant 5aR inhibitor when tested in vitro, in the human skin microsome system, a rich source of 5aR, and in human scalp hair follicles. When a solution of progesterone in alcohol was applied to the pubic skin of normal males, it caused an average decrease of 75.2 per cent in 5aR activity after 24 hours of treatment.
 

JayB

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Side effects of high dose pregnenolone tablets or capsules
Overstimulation and insomnia. Insomnia can lead to fatigue and exhaustion. Some people feel sleepy after they take a pregnenolone supplement.
Irritability, anger or anxiety
Acne
Headaches
Possible scalp hair loss if used daily for prolonged periods
Irregularities of heart rhythm, palpitations on high doses
Unknown effects on the thyroid gland or other organs

http://72.14.205.104/search?q=cache:5MB ... d=13&gl=us
 

squeegee

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Possible scalp hair loss if used daily for prolonged periods.....because of the increase of DHEA ,nothing to worry about because everything else increase...
 
G

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Sounds pretty dumb.Stop wasting your time.Do you really think your going to find a cure that scientists havent already explored. :jackit:
 

squeegee

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Davidoff.. as far as I know you never tried once to post something constructive..you are just here to b**ch or put somebody down with stupid comments like this..LOL If you know and tried everything then what are you doing here??You are just like a big fly that annoy everyone..f*** off then. You are like a little kid that need attention and sound frustrated all the time..Grow up little hater.
 

squeegee

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nope but you still get it.
 

Rework24

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Davidoff you are a c0ck. You must live like a hermit because I can't imagine a nob like you has friends!
 
G

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Rework24 said:
Davidoff you are a c0ck. You must live like a hermit because I can't imagine a nob like you has friends!
How did you know bell end? lol :woot:
 

squeegee

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Mens Rea said:
Very interesting little thread guys.

Thought it was worth a bump.


This mirrors Chillin's theory of how to slow down baldness...

http://www.musclechatroom.com/forum/con ... ostate-101


Chillin is a notorious poster on Dr Crisler's forum. He's a bit of a genius. Have a read.


Thanks a lot for the reply! Bad ***!!
Baldness and Prostate 101
by
chilln
Published on 01-30-2011 01:36 PM Number of Views: 1247
THE DETAILED CAUSES OF MALE PATTERN BALDNESS AND PROSTATE GROWTH

Overview:

when systemic progesterone and systemic cortisol levels are too low, this causes too high DHT metabolism in hair follicles which in turn causes excess free radical damage to the hair follicles on our head in areas where the blood flow is restricted ("due to genetic predisposition"). The additional lack of blood flow to hair follicles means the free radical damage to hair follicles cannot be repaired adequately.

The same excess-free-radical-damage-due-to-excess-DHT-metabolism occurs in our prostate, inflaming our prostate causing either pain and / or constricting the urethra thus reducing urine flow.

This overview omits a lot of important details, so you MUST also read the following detailed explanation before discounting the above info.

Details:

Relatively high levels of progesterone are necessary to compete with DHT for DHT receptors. When progesterone triggers a DHT receptor, then DHT cannot trigger that receptor, and the progesterone which enters the cell triggers progesterone's actions not DHT's actions.

Relatively high levels of progesterone are necessary to upregulate the p53 tumor suppressor protein, which is postulated as one of the primary means of minimizing prostate tumors.

Relatively high levels of cortisol are necessary to oppose / downregulate DHT metabolism. Cortisol acts directly on our genes to limit the ability of T and DHT to trigger their own genetic effects.

When the cortisol-production-line hormones progesterone and cortisol are too downregulated, then cells will aromatase T into E2, and use the E2 to oppose T metabolism and DHT metabolism. To our cells, this is "Plan B". "Plan A" is to use progesterone and cortisol to oppose / downregulate T and DHT metabolism.

While using E2 to oppose T metabolism and DHT metabolism works well in cells which absorb DHT from serum, it works very poorly in cells which manufacture their own DHT (eg: prostate, and hair follicles, ie: all cells with plenty of 5? reductase). Hence these cells continue to experience too high DHT metabolism even in the presence of too high E2.

At the onset of male pattern baldness, our progesterone and our cortisol have gone too low, which would allow T metabolism and DHT metabolism to go too high, so our cells invoke their secondary defence mechanism and increase E2, and they then use E2 to oppose T metabolism and DHT metabolism.

When progesterone is relatively too low, this spells that all of the cortisol-production-line hormones (eg: preg, prog, cortisol) are downregulated to below optimum, and this is why the solution is to restore the optimal hormone levels in the cortisol-production-line.


HALTING AND POSSIBLY REVERSING MALE PATTERN BALDNESS
Addressing The Root Cause

Addressing the root cause requires boosting systemic progesterone (not necessarily by supplementating with progesterone) and boosting systemic cortisol (not necessarily by supplementing with HC, which is man made bioidentical cortisol), up to the level which balances systemic DHT metabolism.

Unfortunately for most males, boosting the cortisol-production-line also requires boosting thyroid hormones T3 and T4, because once the cortisol-production-line hormones are lowered, our cells automatically downregulate our T3 to match our reduced cortisol levels, which creates an excess of T4 (T3 is made from T4). When our hypothalamus detects excess T4, it downregulates the synthesis of T4 in the thyroid gland.

Unfortunately once our hypothalamus downregulates our T4, our body enters a very stable state with a reduced resting metabolic rate. When this occurs, boosting the cortisol-production-line hormones requires boosting our resting metabolic rate, and that requires a three phased solution approach, ie:

Phase 1: Restore preg, prog and cortisol, via supplementary transdermal pregnenolone (or prog), to as good as can be achieved without thyroid hormones.

Phase 2: Restore thyroid hormones, pref via supplementary slow-release-compounded T3 (not yet T4) and adjust both preg and T3 thyroid hormones together to achieve optimum balance as well as optimum levels of all cortisol-production-line hormones as well as optimum levels of thyroid hormones.

Phase 3: Swap out as much T3 with T4 as possible (definitely possible) and swap out as much pregnenolone with dietary cholesterol as possile (less effective with increasing age).

This is explained in Hormone Modulation Therapy 101 (HMT101) scroll down to "What process should my doctor follow...", and the details re pregnenolone supplementation are explained in Cortisol Boost 101 (CB101), scroll down to "Finding the pregnenolone and progesterone "top up" sweet spots". The details re thyroid hormone supplementation are explained in Thyroid Boost 101 (TB101), scroll down to "Dosing suggestions for T3-only, and T4-only".


HALTING AND POSSIBLY REVERSING MALE PATTERN BALDNESS
Leaving The Root Cause In Place By Reducing Hair Follicle DHT Metabolism

Option 1: Infra Red or Laser Thermal Treatment of Hair Follicles.

This increases the metabolic rate of the hair follicle cells, so they absorb more hormones including progesterone, and they allow the free radical damage to be repaired.

Option 2: Localized DHT Metabolism Reduction: Hair Follicles Only

Only Big Pharma drugs are available to achieve this, and the best of these are topical low concentration ketoconazole (eg: Nizoral) and spironolactone (eg: Aldactone)

Provided you keep the concentration low, then these do have mild systemic effects, however in many cases a small degree of systemic DHT suppression is required to help keep DHT metabolism in the prostate in check, and some people have discovered that ceasing their ketoconazole and / or spironolactone treatement results in mild prostate inflammation.

Option 3: Systemic Reduction Of DHT Metabolism: Only Use This If Systemic DHT Metabolism Is High

WARNINGS:
1) A little suppression of systemic DHT metabolism may reduce libido.
2) Too much suppression of systemic DHT metabolism will definitely reduce libido.
3) If your cortisol-production-line is too downregulated while you're undergoing systemic DHT suppression therapy, then this can "tip you over the edge" and strongly suppress your entire cortisol-production-line (the "finasteride effect"). This can happen after a week if your cortisol-production-line is too downregulated when you start systemic DHT suppression therapy, or it can occur after several years as aging will eventually downregulate your cortisol-production-line hormones over time.

How to measure systemic DHT metabolism is explained here (hint: 24 hr urinalysis of several specific metabolites is necessary):
http://musclechatroom.com/forum/show...36&postcount=4

The Big Pharma drugs available to specifically reduce DHT metabolism, without directly reacting with other hormones, are dutasteride (eg: Avodart) and finasteride (eg: Proscar, Propecia)

The natural substance isolates / extracts which specifically reduce DHT metabolism are saw palmetto (not sure if there are any others).

Of these three substances, low dose dutasteride (eg: Avodart) is able to be managed much more reliably than both finasteride and saw palmetto (more on this below), and when finasteride or saw palmetto are not managed adequately in some people, those people have experienced a severe crash of the cortisol-production-line hormones - and these people have formed self-help groups such as propeciahelp.com, mypropeciasideeffects.com, etc...

NB: all these people need to do is restore their cortisol-production-line hormones to optimum, but:
a) they don't understand what their cortisol-production-line hormones are,
b) they're prepared to undergo "quick fix" hormone modulation therapy using finasteride or saw palmetto, but they're usually not prepared to undergo the much slower but much more reliable process of boosting their cortisol-production-line hormones.


HALTING AND POSSIBLY REVERSING MALE PATTERN BALDNESS
Recovering Libido

The only option to maintain hair and recover libido is to boost the cortisol-production-line hormones (eg: preg, prog, cortisol) as much as possible, and in addition boost thyroid hormones T4 and T3 up to the limit imposed by the maximum cortisol levels.

Determining the max boost to the cortisol-production-line hormones and thyroid hormones as an iterative process (boost preg/prog/cortiso, then boost T4/T3, boost preg/prog/cortisol a little more, boost T4/T3 a little more, etc...) This will boost overall metabolism, which includes boosting systemic T and systemic DHT, yet the DHT metabolism boost within hair follicles and the prostate is kept manageable, ie: there is no excessive free radical damage to these tissues so hair follicles stay healthy and the prostate remains normal size.


WHAT SPECIFICALLY ABOUT FINASTERIDE AND SAW PALMETTO CAUSES THIS HORMONE CRASH ?

While finasteride (eg: Proscar, Propecia) lowers systemic DHT metabolism similar to dutasteride, the fact that the half life of finasteride is anywhere from 4 hours (in fast metabolizers) to as high as 12 hours (in slow metabolizers), which means the effective life of the finasteride or saw palmetto can be anywhere from 6 hours to 18 hours. This means that the amount of suppression / downregulation of DHT metabolism can be much greater than anticipated.

The problem with excessive DHT suppression / downregulation is that DHT triggers many of the same gene expression actions as T (not 100% overlap) and therefore suppression / downregulation of DHT results in downregulation of our testosterone metabolism.

Since one of progesterone's and cortisol's critical functions is to oppose T and DHT metabolism, therefore when T and DHT metabolism activity declines (includes genetic expression effects), then cells downregulate their cortisol and progesterone receptors and absorb less cortisol and less progesterone. This is because they need less "opposition" or "downregulation" of T and DHT.

The way the body achieves this negative feedback loop is by downregulating the entire cortisol-production-line (eg: preg, prog, cortisol). But once the cortisol-production-line hormones are lowered, our cells automatically downregulate our T3 to match our reduced cortisol levels, which creates an excess of T4 (T3 is made from T4). When our hypothalamus detects excess T4, it downregulates the synthesis of T4 in the thyroid gland.

Unfortunately once our hypothalamus downregulates our T4, our body enters a very stable state with a reduced resting metabolic rate. Once we've entered this very stable state with a lowered resting metabolic rate, most males who then back out their finasteride or saw palmetto can only recover their previous hormone levels (along with their previous high resting metabolic rate) very very slowly, and some will never recover their previous high hormone levels without intervention.

Once we've entered this very stable state with a lowered resting metabolic rate, the intervention required is to boost the cortisol-production-line hormones by boosting resting metabolic rate, and that requires the three phased solution approach, explained in the previous section "Addressing the root cause".


HOW DO I PREVENT MY HORMONES CRASHING WHEN SUPPRESSING DHT ?

While it's simple to explain at a high level, it's a complex process when implemented: You need to initially monitor your sex hormones and your cortisol-production-line hormones (eg: preg, prog, cortisol) and if these are too low initially then you will need to either abstain from using DHT suppressants / downregulators, or you must first optimize at least your cortisol-production-line hormones (eg: preg, prog, cortisol) until your E2 is lowered, before commencing to suppress DHT.

This process is described in the Cortisol boost 101 primer, and you can access that from the links in the Hormones 101 primer, which is a sticky on the front page of this AllThingsMale forum.


WHAT IF INCREASED SERUM PROGESTERONE DOESN'T REVERSE MALE PATTERN BALDNESS ?

That's usually because the progesterone isn't being absorbed by cells, which is usually because those cells have an overall metabolic rate which is too low.

Since the progesterone is synthesizing into some cortisol (just not enough) the reason for the too low metabolic rate in these cells is not due to inadequate cortisol. In this case it's due to inadequate thyroid hormone T4.

Once T4 levels are restored to optimum, the cells will absorb both the T4 (which gets enythesized into T3) and extra cortisol, and they will boost their overall metabolic rate to optimum, and that's when they'll start absorbing more progesterone.


WHY IS THE DHT METABOLISM IN MY HAIR FOLLICLES HIGH, YET I DONT HAVE EXCESSIVE LIBIDO, AND / OR MY ERECTION PERFORMANCE IS BELOW PAR ?

Since libido and erection performance are promoted by DHT which originates from cells which absorb DHT from serum (ie: not the prostate, not hair follicles), and since these cells are using relatively high E2 to oppose / downregulate their DHT metabolism, therefore the cells which promote libido and erection performance are doing a poor job of triggering adequate libido, and they're doing a poor job of triggering adequate erection performance.

When these cells use increased levels of progesterone and cortisol to oppose / downregulate T metabolism and DHT metabolism, then IF your thyroid hormone T4 levels rise to match the increase in your cortisol (more likely in younger males, less likely in older males), then your overall metabolic rate will increase, and this includes your systemic T and DHT metabolism but NOT your hair follicle or your prostate DHT metabolism ! Thus your libido and erection performance will remain unchanged, yet your hair will stay put, and your prostate will shrink to normal size.

HOWEVER (WARNING!) When these cells use increased levels of progesterone and cortisol to oppose / downregulate T metabolism and DHT metabolism, then IF your thyroid hormone T4 levels do not rise to match the increase in your cortisol (more likely in older males, less likely in younger males), then your overall metabolic rate will not increase, so your systemic T and DHT metabolism will not increase. Thus your libido and erection performance will decrease. In this case you must boost your thyroid hormones too. This is explained in the Thyroid boost 101 primer, which has a link in the Hormones 101 "sticky" on the first page of this AllThingsMale subforum.


PAPERS / REFERENCES

1) Confirmation of ability of progesterone to inhibit DHT in hair follicles:

Journal: European Journal of Dermatology. Volume 11, Number 3, 195-8, May - June 2001, Revues
Title: "Influence of estrogens on the androgen metabolism in different subunits of human hair follicles"
URL full text


2) Confirmation of cortisol's ability to downregulate T

Journal: JCEM
Title: Acute Suppression of Circulating Testosterone Levels by Cortisol in Men
URL abstract

and

Journal: Journal of Molecular Endocrinology, 41, 165-175.
Title: Glucocorticoids antagonize cAMP-induced Star transcription in Leydig cells through the orphan nuclear receptor NR4A1
URL full text


3A) Confirmation that hair follicles which have their own 5? reductase absorb serum T to manufacture most of their own DHT.

Journal: Archives of Dermatological Research. 1998 Mar;290(3):126-32.
Title: 5 alpha-reductase activity in the human hair follicle concentrates in the dermal papilla.
URL abstract

3B) Corrolary: Since increasing cortisol downregulates T synthesis, therefore increasing cortisol also downregulates the synthesis of DHT within hair follicle cells.

That's because hair follicle cells don't absorb much DHT directly, but instead they absorb T from serum and synthesize that into DHT via the action of 5? reductase.


4A) Confirmation that upregulation of serum DHT levels follows upregulation of hair follicle DHT levels (not to the same extent):

I don't have an obvious demonstration of this.

4B) Confirmation that downregulation of serum DHT levels follows downregulation of hair follicle DHT levels (not to the same extent):

Journal: Journal of the American Academy of Dermatology Volume 55, Issue 6 , Pages 1014-1023, December 2006
Title: The importance of dual 5?-reductase inhibition in the treatment of male pattern hair loss: Results of a randomized placebo-controlled study of dutasteride versus finasteride
URL abstract
URL detailed summary

4C) Assumption with high likelihood of being correct: Since the downregulation of serum DHT levels follows downregulation of hair follicle DHT levels (but not to the the same extent), that the upregulation of serum DHT levels follows downregulation of hair follicle DHT levels (but not to the the same extent).

While you might choose to be pedantic and dispute this assumption, if you rejected the hard fact that both progesterone and cortisol downregulate DHT in hair follicles, just because you chose to dispute this assumption, then you'd be throwing the baby out with the bathwater.


5A) Confirmation that E2 does not suppress DHT metabolism adequately in cells which manufacture their own DHT

[TO DO]


ACCURATE MONITORING OF DHT METABOLISM

Unfortunately serum DHT levels get high when DHT gets "backed up" and DHT is not being used up (ie: when DHT metabolism is low). This is quite unlike testosterone, which does not get "backed up" when T is not being used.

When DHT is being used up, more DHT needs to be synthesized, ie:
testosterone ---5? reductase---> DHT

Therefore any biomarker which can indicate the activity of 5? reductase enzymes also indicates the rate of synthesis of DHT from testosterone, and thus indicates DHT metabolism.

Via experimental research, several research teams have confirmed that the synthesis of tetrahydrocortisol ---5? reductase---> 5? tetrahydrocortisol (5?THF)

...can be monitored using 24hr urinary analysis, and the ratio of 5?THF to THF follows the 5? reductase activity, ie:

high ( 5?THF / THF ) shows high 5? reductase activity
low ( 5?THF / THF ) shows low 5? reductase activity

Taken together, these are good indicators of 5? reductase acitivity, and thus DHT metabolism. Dr Crisler seems to agree.

The following research teams confirmed that the ratio of 5?THF to THF follows the 5? reductase activity, and thus DHT metabolic activity, eg:

Title: Diagnosis of 5alpha-reductase 2 deficiency: a local experience
Journal:
Author(s):
URL Full Text

NB: 5a THF/THF normal ratio range is between 0.5 and 2.5 quoted in "Diagnosis of 5alpha-reductase 2 deficiency: a local experience".

Title: The Diagnosis of 5{alpha}-Reductase Deficiency in Infancy
Journal: blah
Author(s): blah
URL Full Text

Title: A Case of 5 alpha-reductase Deficiency in Infancy
Journal: blah
Author(s): blah
URL Full Text

Title: Early diagnosis and management of 5 alpha-reductase deficiency
Journal: blah
Author(s): blah
URL Full Text

Title: Increased 5{alpha}-Reductase Activity and Adrenocortical Drive in Women with Polycystic Ovary Syndrome
Journal: blah
Author(s): blah
URL Full Text


Copyright is retained by chilln, 2008, 2009, 2010, 2011
 

metadalll

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that was a very interesting article, seems like it should be posted on propeciahelp for all those people who say they have permanent impotence n sh*t
 
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