increased body fat?

[stax]

Pondle, you seem to be ignoring the facts that ive stated. So there is no point in talking to you.


Dont spread misinformation to the newbies and to others that you can trust the information Merck and Glaxo put out to the public

Newbies do not trust the word of these drug companies, they are trying to sell you the drugs, and get Doctors to prescribe you their drugs so they can make money. They have been responsible for many deaths. Do you own research, and decide for yourself. If you take Propecia or Dutasteride and notice side effects you never had before, stop the drugs. If they go away then clearly your body doesnt agree with DHT reduction. Read the Patrick Arnold article ive posted to get a better understanding of DHT's role in the human body. Im not saying that Propecia or Avodart can cause death, im simply stating you cant trust the infromation these drug companies put out to the public BECAUSE they are responsible for causing death, and they have an motive to get you on their drugs.


You as a " non expert " as you put it, choose to question the Patrick Arnold DHT article, when he has a Bachelor of Science Degree in Chemistry, and you as you said are a "non expert". I think he knows a little bit more than you on the subject, anybody on the board for that matter, and more than most people in general.




He isnt making this information up, these are TRUE FACTS. I think he has the credentials to present this information. He is definetly more trust worthy the Merck and Glaxo, the makers of the graphs you keep posting. They are trying to sell you a drug, Patrick Arnold has nothing to gain by presenting you with the information given, and the chemisty on how DHT works, how drugs like Aromasin work,ect.



And for gods sakes dont post anymore links to pages on the Propecia website. They are the same company who made Vioxx, a drug that was responsible for KILLING PEOPLE! They are NOT a trustworthy source of information.


THEY ARE THE SAME PEOPLE THAT CLAIM ONLY 2% GET SEXUAL SIDE EFFECTS WHEN IT IS CLEARLY A MUCH LARGER NUMBER THAN THAT. EVEN DOCTOR'S WHO HAVE PATEINTS ON FINESTERIDE AND DUTASTERIDE WILL TELL YOU THAT THE PERCENTAGE IS HIGHER, SUCH AS DR.LEE. SO WHY AND HOW CAN YOU BELEIVE THEIR SO CALLED GRAPHS?

The Propecia product monograph says that "finasteride has no affinity for the androgen receptor and has no androgenic, antiandrogenic, estrogenic, antiestrogenic, or progestational effects." Here's more info:
http://www.propecia.com/finasteride/pro ... drogen.jsp

Im sorry, but Merck states Gyno is a side effect, and Gyno IS a estrogenic side effect! Its even a possible progestational side effect. So that info they give is simply untrue. Also, they claim reduced sexual function is a side effects. Well when you take a pill that inhibits DHT, a potent androgen, and you get reduced sex drive from it, that IS an antiandrogenic effect!


And as i said, Dr.Proctor himself has told me over the phone that Finesteride is probabbly the best choice of anti-androgens that we have to fight hairloss.


Taken from his website:

"Antiandrogens: E.g.: Propecia (Finasteride), Cyoctal, spironolactone.

These agents have significant hair regrowth properties.. They are also useful as adjuvants to other hair loss treatment where they 1) make it work better 2) Help prevent tolerance. Every few years, a new antiandrogen will be presented as the ultimate "solution for balding". This has yet to work out. E.g., clinical trials with cyoctal, arguably the most potent topical antiandrogen, were terminated because of lack of effectiveness. Even castration, the commonly used treatment for prostate cancer, generally doesn't do a lot for balding and hair loss.
Arguably, the most promising new antiandrogen is Propecia ( finasteride), from Merck. For more on this agent, go to propecia.com. Tho the weakest antiandrogen on paper, it seems to be as effective as the others in baldness treatment. My experience is that oral finasteride works about as well as topical spironolactone, about a 50% response rate, at one year. Some individuals take even longer to respond.

BTW, I have prime patents in this area ( for growth stimulators plus antiandrogens ). In fact, because of the publication of our patents, the combination of a hair growth stimulator plus and antiandrogen is now " obvious " and thus unpatentable. I sure wish antiandrogens worked better."



There you go.

 

[Pondle]

Pondle, you seem to be ignoring the facts that ive stated. So there is no point in talking to you.
Dont spread misinformation to the newbies and to others that you can trust the information Merck and Glaxo put out to the public

All the information I've posted comes from published studies in peer-reviewed journals, drug monographs etc. My girlfriend, who is a hospital pharmacist, relies on the monographs and the SPCs created by drug companies in the course of her work. So do all doctors. Are you saying that they should just throw away their Physician's Desk References and get their info from bodybuilding and anti-ageing forums?

You as a " non expert " as you put it, choose to question the Patrick Arnold DHT article, when he has a Bachelor of Science Degree in Chemistry, and you as you said are a "non expert". I think he knows a little bit more than you on the subject, anybody on the board for that matter, and more than most people in general.

He isnt making this information up, these are TRUE FACTS. I think he has the credentials to present this information. He is definetly more trust worthy the Merck and Glaxo, the makers of the graphs you keep posting. They are trying to sell you a drug, Patrick Arnold has nothing to gain by presenting you with the information given, and the chemisty on how DHT works, how drugs like Aromasin work,ect.

"Truth by authority" is a very poor form of argument. When you suspect someone's reasoning is based on flawed evidence you have a right to question it. I question his claim that estrogen is a causative factor in BPH on the basis of the study that Bryan has posted indicating that "there was no effect at all on BPH with either dose of [an] aromatase inhibitor... That was surprising and unexpected, because of all the interest and speculation in recent years about the role of estrogen in the etiology of prostate disease. The authors of the study were quite open about their puzzlement and disappointment over the lack of results."

THEY ARE THE SAME PEOPLE THAT CLAIM ONLY 2% GET SEXUAL SIDE EFFECTS WHEN IT IS CLEARLY A MUCH LARGER NUMBER THAN THAT. EVEN DOCTOR'S WHO HAVE PATEINTS ON FINESTERIDE AND DUTASTERIDE WILL TELL YOU THAT THE PERCENTAGE IS HIGHER, SUCH AS DR.LEE. SO WHY AND HOW CAN YOU BELEIVE THEIR SO CALLED GRAPHS?

But the opinions of doctors differ. Dr Rassman seems to accept the Merck figures, as does the GP who prescribes me finasteride. I have seen no coherent critique of the clinical trials methodology, other than the intellectually vacuous "oh the drug companies are lying" schtick. BTW remember that Dr Lee sells his own range of hair loss treatments!

Im sorry, but Merck states Gyno is a side effect, and Gyno IS a estrogenic side effect! Its even a possible progestational side effect. So that info they give is simply untrue. Also, they claim reduced sexual function is a side effects. Well when you take a pill that inhibits DHT, a potent androgen, and you get reduced sex drive from it, that IS an antiandrogenic effect!

This is a semantic argument. Finasteride reduces the levels of one androgen (DHT) and increases the levels of another (T). 5ATIs are not general anti-androgens. Regulatory agencies all around the world accept this form of words.

 

[stax]

"The clinical application of this theory is discussed in US patent 5,648,350 "Dihydrotestosterone for use in androgenotherapy". The following illustrates the results:

"In 27 subjects in which the plasma DHT level was controlled, so as to modulate the administered doses, said levels have been increased to 2.5 to 6 ng/ml. There resulted a decrease in gonadotrophy as well as in the plasma levels of testosterone which exceeded at least 1.5 ng/ml (from 0.5 to 1.4 according to the case); as to the estradiol plasma levels, these decreased by 50%.

Among this group of subjects, the volume of the prostate diminished significantly, as was evaluated by ultrasound and by PSA (Prostate Specific Antigen). The mean volume of the prostates was from 31.09.+-.16.31 grams before treatment and from 26.34.+-.12.72 grams after treatment, for a mean reduction of 15.4%, the treatment having a mean duration of 1.8 years with DHT (P=0.01)."


Pondle, what does the study you are referring to that bryan posted have to do with anything? You are trying to state the Patrick Arnolds information on DHT isnt accurate because Bryan posted a study showing that Aromatase inhibitors dont have any effect on BPH? Thats a little stupid man, and i dont see where your logic comes in that Aromatase inhibitors would benifit BPH. Patrick Arnold didnt mention the use of aromatase inhibitors for BPH in his article.


Do aromatase inhibitors increase DHT to a great deal? They mainly increase T and a little probabbly converts to DHT. We are talking about DHT not being the main cause for BPH and prostate cancer, despite what the Doctors were saying. And we can clearly see that the incresed estrogen to androgen ratio is the main and more likely cause of BPH and prostate cancer.


First, DHT, the allegedly bad testosterone, appears in highest levels in young adults, which have the lowest rates of prostate problems. Second, the older men get, the lower their level of testosterone and DHT are, but yet the higher the rates of prostate problems among them are. Again, it doesn't make sense. If DHT is the main cause for prostate enlargement or cancer, why the majority of people who suffer from prostate problems are those who have lower levels of testosterone and DHT?

As men age, testosterone levels fall while estrogen levels rise.
Aging involves increased conversion of testosterone to estrogen in a process called aromatizing.



This clearly shows that DHT can have a postive effect on the Prostate, and that the increased estrogen to androgen ratio is a main factor in triggering BPH. DHT helps tip the odds in favour of an increase androgen to estrogen ratio, and antagonising the negative effects of estrogen without eliminting it. DHT seems to have a great effect on lowering Estradiol, the main estrogen involved in causing all these nasty problems, while Arimidex seems to have a smaller effect on Estradiol in men while almost abolishing Estrone in the process, which isnt very benificial.






MALE ANDRODESCENT

Male aging is associated with a steady decline in " androgens (chief male hormones: testosterone, dihydrotestosterone [DHT], androstenedione and dehydroepiandrosterone [DHEA]) and a slow steady rise in estrogens (all of these hormones are also in females at different concentrations). The physiological effects associated with male aging and accompanying changes in hormonal status include the following:


Reduced libido
Memory lapses and poor concentration
Erectile dysfunction
Heart disease
Osteoporosis
Prostate enlargement
Muscle weakness
Slower wound healing
Fatiguing quicker

After the age of 50-60, men usually experience increased difficulty in urination because of an enlarging prostate gland which compresses the urethra (the tube leading from the urinary bladder through the penis to the exit of the body). The urine flow is restricted which results in urinary retention in the bladder, greater frequency of urination, hesitancy and dribbling. In addition, the enlarged prostate makes ejaculation difficult.

There are two main concerns with testosterone supplementation: (1) will it cause the prostate to enlarge? and (2) will it cause cancer? At the moment, the first concern will be addressed. It is necessary to know what causes the prostate to enlarge, and we are faced with a classic dilemma because there are two theories.




BENIGN PROSTATE HYPERPLASIA (growth in number of cells) I HYPERTROPHY (growth in size of cells): (BPH)

The early theory of prostate enlargement holds that when testosterone enters the cells of the prostate, it is more than 95% converted by the enzyme 5-alpha reductase into the potent androgen, dihydrotestosterone (DHT) which binds to androgen receptors that stimulate the production of new prostate cells, while postponing the death of some older prostate cells. It is generally accepted that DHT is more potent than testosterone in promoting prostate growth. Normally, there is a balance between old cell death and new cell birth that keeps the prostate stable. This theory gave rise to the use of the pharmaceutical, Proscar (chemically "finasteride"), and the herbal Saw Palmetto berry extract to inhibit the 5-alpha reductase enzyme to slow DHT production.

However, it is still not clear whether DHT causes prostate enlargement because in teenagers and men below the age of 50, BPH rarely occurs despite high DHT levels in their prostates. This lack of a continuum forced researchers to seek answers other than the common concept. Their investigations led to estradiol which is relatively low in young people and progressively increases with age.

Prostate tissue obtained during surgical transurethral resection ("the TURP or roto-rooter" procedure to lessen the encroachment of the prostate on the ureter) of the prostates of men with BPH, was exposed to various combinations of hormones, drugs and sex hormone binding globulin (SHBG) in the laboratory. The results clearly showed that BPH was associated with elevated estradiol, decreased androgens, and increased SHBG. However, DHT not only did not cause new prostate growth, but DHT inhibited it by blocking the binding of estradiol to SHBG. SHBG is a complex water-soluble protein that carries fat-soluble hormones (all androgens and estrogens are derived from fat-soluble cholesterol) in the water-soluble plasma of the bloodstream. So, there's more going on here than we know.

Subsequent prostate research found that estradiol attaches to SHBG that is already bound to the cell membrane. Thereafter, insulin-like growth factor-1 (IGF-1) is synthesized, and it is thought to cause proliferation of epithelial cells in the prostate. Furthermore, elevated IGF-1 may be a predictor of prostate cancer risk. In addition, environmental chemicals that mimic estradiol are known to increase SHBG, and it is likely that they are an important cause of the epidemic of prostate enlargement and prostate cancer."



Im sorry Pondle but you cant argue with that!



It seems that DHT cause problems for some people, but the majority of the cases is decreased androgens and increased Estradiol and SHBG.





Also Finesteride IS an anti-androgen!


From Wikipedia:

Currently available antiandrogen drugs (brand names in parentheses) include:

Spironolactone (Aldactone, Spiritone), a synthetic 17-spirolactone corticosteroid, which is a renal competitive aldosterone antagonist in a class of pharmaceuticals called potassium-sparing diuretics, used primarily to treat low-renin hypertension, hypokalemia, and Conn's syndrome.
Cyproterone acetate (Androcur, Climen, Diane 35, Ginette 35), a synthetic steroid, a potent antiandrogen that also possesses progestational properties.
Flutamide (Eulexin), nilutamide (Anandron, Nilandron) and bicalutamide (Casodex), nonsteroidal, pure antiandrogens. Flutamide is the oldest and has more unwanted side effects than the others. Bicalutamide is the newest and has the least side effects.
Ketoconazole (Nizoral), an imidazole derivative used as a broad-spectrum antifungal agent effective against a variety of fungal infections, side effects include serious liver damage and reduced levels of androgen from both the testicles and adrenal glands. Ketoconazole is a relatively weak antiandrogen.
Finasteride (Proscar, Propecia) and dutasteride (Avodart), inhibitors of the 5-?-reductase enzyme that prevent the conversion of testosterone into dihydrotestosterone (DHT). Finasteride blocks only 5-?-reductase type II, dutasteride also blocks type I. They are not general antiandrogens in that they don't counteract the effects or production of other androgens than DHT.



They arent your general anti-androgens, but they still are anti-androgens regardless because the inhibit the formation of the most potent androgen in the male body, bottom line.




And yes Dr.Lee does sell his own products, but he has and will prescribe Finesteride for his patients. So its not like he's trying to make up lies here.

 

[Pondle]

First, DHT, the allegedly bad testosterone, appears in highest levels in young adults, which have the lowest rates of prostate problems. Second, the older men get, the lower their level of testosterone and DHT are, but yet the higher the rates of prostate problems among them are. Again, it doesn't make sense. If DHT is the main cause for prostate enlargement or cancer, why the majority of people who suffer from prostate problems are those who have lower levels of testosterone and DHT?

But the pseudohermaphrodites with 5AR deficiency never experience BPH... as you know they were the 'model' for the development of finasteride, which like dutasteride is used to treat BPH by shrinking the prostate, and appears to reduce the risk of prostate cancer (as does dutasteride, see chart below).

My point, which you don't appear to grasp, is that in the article Pat Arnold says, explicitly, "apparently, estrogen is a causative factor in BPH or, probably more accurately, estrogen in the presence of a minimum, permissive amount of androgen."

If - as he says - estrogen plays a role in the pathogenesis of BPH, wouldn't we expect to see aromatase inhibitors have a positive impact on this condition by reducing the levels of estrogen and increasing levels of androgens? In practice, it appears not*. Once again I refer to Bryan's quote - "there was no effect at all on BPH with either dose of [an] aromatase inhibitor... That was surprising and unexpected, because of all the interest and speculation in recent years about the role of estrogen in the etiology of prostate disease. The authors of the study were quite open about their puzzlement and disappointment over the lack of results."

*BTW the study is "Estrogen Reduction by Aromatase Inhibition for Benign Prostatic Hyperplasia: Results of a Double-Blind, Placebo-Controlled, Randomized Clinical Trial Using Two Doses of the Aromatase-Inhibitor Atamestane", Radlmaier et al, The Prostate 29:199-208 (1996).

Now I don't pretend to have any explanation of the pathogenesis of BPH, but then I'm not an urologist! All I'm doing is pointing out a potential problem with the speculation about the role of estrogen in the pathogenesis of BPH, based on the study cited by Bryan.

They arent your general anti-androgens, but they still are anti-androgens regardless because the inhibit the formation of the most potent androgen in the male body, bottom line.

As I said, a somewhat semantic argument... I'll go with the agreed line of Merck, the FDA, and the MHRA here in the UK. That line is: PROPECIA is not an antiandrogen.
— Clinical studies showed men treated with PROPECIA had increased mean testosterone and estradiol levels (approximately 15%), but these levels were within normal physiologic range.

Clearly any drug that (through an indirect mechanism) reduces the level of one androgen, while increasing the levels of the principal androgen in man (the one that is necessary for normal spermatogenesis, bone and muscle mass and male libido and potency) needs a precise descripter. Describing it as an antiandrogen doesn't seem to do it justice, especially when one considers the possibility of reflex hyperandrogenicity, so I can see why the manufacturer uses the language at issue!

But this is a silly little side issue really.

 

[stax]

pseudohermaphrodites CANNOT be compared to normal men who were born with the 5ar type 2 enzyme, these people were BORN with no 5ar2 enzyme, thus is not a far comparison. Nobody knows how this effects MANY other factors compared to normal human beings and our biology.

You keep posting things about OLDER men and PSEUDOHERMAPHRODITES, well we are not PSEUDOHERMAPHRODITES for gods sakes and we are not talking about how DHT reduction effects OLDER men for the 1000th time! You cannot model a breed that NEVER had the 5ar2 enzyme to begin with period. The human body is a LOT more complicated than that.


Such can be said because men have died because they used Finesteride and developed the more aggresive type of prostate cancer, yet you say the pseudohermaphrodites never experienced BPH. Why would men get the more aggresive type of prostate cancer on Finesteride when they are essentially of the same "biology" of the "pseudohermaphrodites" when they take Finesteride? They are inhibiting DHT, so why did they get the more aggresive type of prostate cancer?



The increased Estrogen to Androgen ratio is what STARTS the BPH process, because as i said, DHT, the allegedly bad testosterone, appears in highest levels in young adults, which have the lowest rates of prostate problems. Second, the older men get, the lower their level of testosterone and DHT are, but yet the higher the rates of prostate problems among them are. Again, it doesn't make sense. If DHT is the main cause for prostate enlargement or cancer, why the majority of people who suffer from prostate problems are those who have lower levels of testosterone and DHT?

As men age, testosterone levels fall while estrogen levels rise.
Aging involves increased conversion of testosterone to estrogen in a process called aromatizing. After the age of 50-60, men usually experience increased difficulty in urination because of an enlarging prostate gland which compresses the urethra.


As i said "The results clearly showed that BPH was associated with elevated estradiol, decreased androgens, and increased SHBG. However, DHT not only did not cause new prostate growth, but DHT inhibited it by blocking the binding of estradiol to SHBG."




You are asking why an Aromatase Inhibitor didnt improve BPH if they reduce estrogen? Thats a good question, though is off topic.


We are talking about the CAUSE of BPH and whats starts the process, not about treating it.


Does hairloss generally regrow when you take Finesteride and inhibit DHT? NO, even castrated men didnt regrow hair.


So what makes you think that inhibiting estrogen would improve BPH once its already started? Who even said that inhibiting estrogen by way of aromatase inhibitor was the proper form of treatment. DHT seems to have a lot more benifts than an aromatase inhibitor.


And if DHT was responsible for BPH, which it is not since "DHT not only did not cause new prostate growth, but DHT inhibited it by blocking the binding of estradiol to SHBG" Then why did DHT treatment reduce prostate volume?


Whats even better is that once the BPH process has started the increase in androgens from the aromatase inhibitor had no negative effect! So its VERY unlikely that androgens would be the CAUSE that STARTED BPH, when they had no further negative effect once BPH has started!


Source - Dr. John R. Lee - Harvard.
"Studies from nearly 40 years ago and more recently (1996 and published in the Proceedings of the National Academy of Science) indicate that testosterone shrinks prostate tumors and testosterone supplementation actually kills prostate cancer cells. The benefit of castration in prostate cancer stemmed from Estradiol reduction - not Testosterone reduction. And yet, castration, antiandrogen therapy, and drugs that reduce the production of testosterone are still the prevalent forms of treatments for cancer patients. Go figure...."



Gimme a break Dude!



Oh, and yes Propecia is STILL an anti-androgen, not a full blown anti-androgen, but its still an anti-male hormone, and is still partially an anti-androgen .

 

[Pondle]

my followup question for you, pondle, and the board is why does this part of the article talk about 5-ar deficient guys and its effect on their sexual development?

i thought that there is a substantial % of men who are born w/o this element in their bodies who live normal, healthy lives ...

Merck told the FDA (and here I'm quoting from a meeting of the Dermatological and Opthalmic Drugs Advisory Committee, held on November 13th 1997): "Dr. Juliana Imperato-McGinley... and others identified patients with a genetic deficiency of the enzyme steroid 5-alpha-Reductase, which catalyzes the conversion of testosterone to dihydrotestosterone. Males with genetic deficiency of 5-alpha-Reductase were born with ambiguous genitalia which virilizes at puberty. As adults, these men have a grossly underdeveloped prostate but are otherwise healthy with normal male libido and bone and muscle mass and sparse facial and body hair. Most importantly for today's presentation, these men appear to be protected against the development of male pattern hair loss.

The observation in these men with 5-alpha-Reductase deficiency, as well as other investigations, have resulted in the identification of distinct physiological roles for testosterone compared with those for dihydrotestosterone. Testosterone, the principal androgen in man, is necessary for normal spermatogenesis, bone and muscle mass and male libido and potency. Dihydrotestosterone, or DHT, does not appear to have any essential physiological role in the adult male but is involved in the production of beard and body hair, enlargement of the prostate with age and development of male pattern baldness."

The Proscar product monograph states: "individuals with a genetic deficiency of Type II 5 alphareductase... have markedly decreased levels of DHT and small prostates, and... do not develop BPH. These individuals have urogenital defects at birth and biochemical abnormalities but have no other clinically important disorders as a consequence of Type II 5?-reductase deficiency."

Bryan has read extensively about the pseudohermaphrodites - apparently there was a big piece about them in Nature - according to him, at least some of them appear to have fathered children although many are presumably infertile.

There is more information about 5-ARD at emedicine - http://www.emedicine.com/ped/topic1980.htm

WHAT THE HELL HAPPENED TO MY LAST POST? IT'S BEEN DELETED!! AND THIS REPLY TO MBEHR APPEARS BEFORE HIS MESSAGE! :dunno:

 

[mbehr22]

Stax


i really apprec all of the info...

i took finasteride for 9 mos and saw no effects - libido or body (incl hair)

now ive been on dutasteride for 2.75 months and i can tell im more like playdough than wood ... but, like i said in the orig post, im not working out like i used to

my followup question for you, pondle, and the board is why does this part of the article talk about 5-ar deficient guys and its effect on their sexual development?

i thought that there is a substantial % of men who are born w/o this element in their bodies who live normal, healthy lives ...

This transformation serves a very important biological function in these tissues. You see, DHT is a much stronger androgen than testosterone – it binds about 3-5 times more strongly to the androgen receptor. If you took away 5-AR from these tissues and blocked the formation of DHT, then you would see some dramatic changes in physiology.

A good case in point is demonstrated in male pseudohermaphroditism due to congenital 5-AR deficiency. This is a relatively rare disorder, however it is actually quite common in the Dominican Republic. In this disorder, males are born with little or no 5-AR enzyme. They have ambiguous genitalia and are often raised as girls. When puberty occurs, their testosterone levels elevate normally although their DHT levels remain very low. Their musculature develops normally like that of other adults, however, they end up with little or no pubic / body hair and underdeveloped prostate and penis. Their libido and sexual function is often disrupted also.

Hey Pondle, i see what your saying, but do you see what im saying?

http://www.mesomorphosis.com/articles/arnold/dht.htm


This is all i really have to say. These are the facts about DHT. Im not making this stuff up im stating facts. You dont seem to be acknowledging them.


Now its funny that you say treatment with T versus treatment with T and finasteride has the same positive effects on physical performance, strength, and body composition. Please post this study.


Secondly, what the hell is it with you and older men for god sakes! And HYPOGONDAL given TESTOSTERONE??? We are starting to slip off topic. But i'll say a few words anyways.



DHT isnt ANABOLIC like T is, but that just means that T can help you build more muscle tissue than DHT itself. When you build more muscle tissue your bodyfat will drop because muscle tissue burns more calories. DHT is very mildly anabolic, and plays a role in muscle hardness, when you are already at a low bodyfat percentage, so unless this the case for these men, especially for OLDER men who were HYPOGONDAL, i HIGHLY doubt it. These men probabbly had more estrogen in them than a woman their same age. SO my point is they are a lot less likely to notice the hardening effects that DHT has on your muscles. Plus the fact that these men were given Testosterone for god sakes, that probabbly helped with the side effects of DHT reduction. If i was given T with Propecia or mabye even Dutasteride, i'll bet that i would have less sides too. And i actually said i had some reduction in fatigue,ect, when i used AIMF with Propecia. AIMF lowers estradiol and increases T. But i had no luck with this on Dutasteride.


There are guys on the steroid forums that have used Propecia and Dutasteride, and on cycle they notice some reduction in aggresiveness, but for the most part side effect free. But when off cycle they have more side effects. Its obvious that the extra T they are getting from the steroids are helping with the side effects.


But we are slipping away from the main thing we are talking about, which is the effects of DHT reduction alone, WITHOUT giving somebody Testosterone via steroids or T cream, WITHOUT giving somebody an anti-estrogen,ect. These things would obviuosly help deal with the side effects while on Propecia. Dutasteride is a different story altogether.





Old men CANT be compared to young guys in their 20's. Also finasteride incresed total T yes, but not free T that really matters. And IMO the increase in estrogen is enough in a lot of people, especially younger guys, to offset the effects of the increase in T, and even LOWER total and free T eventually. But for some people T actually Lowers estrogen, but this isnt the case in many people when DHT i being inhibited.


Yes 5ar inhibitors can prevent possible prostate problems from happening, but they can also cause you to have the most aggresive type of prostate cancer IF you still get it. Thats a risk.



And yes i agree about the placebo effect, but all the side effects that these guys are having are all known FACTS about what can happen when you inhibit DHT.



Ive never had a placebo effect in my life. I didnt even know about the side effects that inhibiting DHT could cause, untill i started experiencing things that i have never experienced before as soon as i started taking Propecia. As i said i was a healthy as a horse fit, ripped, 21 year old with an incredible sex drive.


As i said before i saw my Doctor and nothing was wrong with me from a non hormonal stand point.


As i said before i quit and 2-3 weeks later all the sides were gone.


THEN i started doing a TON of research on the topic, DHT,ect, and everything i found out correlated with the sides i was having. I also read AFTER that it will take 2-3 weeks for DHT levels to come back to normal after your last dose of Propecia, as said by Bryan.


So Pondle, how is it that even though i knew NOTHING about these facts at the time i was using and quit Propecia, that EVERY side effects i had, and the time it took for all the sides to go away, EXACTLY correlated with the side effects DHT inhibiting can cause, and the time it took DHT levels to go back to normal fter quitting Propecia?


Now thats one big coinceance aint it?


Now there are crazy people on the net yes, but there are a lot of normal guys like myself, that i can tell arent crazy but having conversations with them,ect, and reading their posts, so i tend to beleive them.


And by crazies i mean these guys that say Propecia made them gay ect, when we all know that guy people are born this way, and can infact be genetic aswell. Propecia and Dutasteride never took away my sex drive at all, but it did greatly reduce my ejaculation power, oddly Propecia did this more than Dutasteride, and my sperm was watery and the loads were smaller. I know, i know, too much info lol.



And semi castration is not harsh at all, since Finesteride IS an anti-androgen, and an ANTI male homone, Dr.Proctor said it himself. You are reducing the most potent androgen in your body by 85-95% when you use Propecia or Dutasteride. DHT is more of a potent and stronger androgen than T, DHT binds to the androgen receptor 5 times as much. This to me is semi castration, especially when your dick doesnt work as good as a result.


Testosterone takes a lot of the credit for DHT, as we can clearly see when things start going south when Finesteride and Dutasterid is taken. Why is it that we dont lose hair when on Finesteride, although it increases T, and causes androgen receptor upregulation? Just as you said? Exactly because DHT is a more potent and stronger androgen.


A quote from Bryan:

" I read in a medical journal article that even under normal conditions, most DHT molecules end up binding to androgen receptors anyway, so that argument by your dermatologist doesn't make much sense to me. In other words, having more androgen receptors shouldn't make that much of a difference. The sharp reduction in the availability of DHT molecules is a more significant factor than additional numbers of androgen receptors.



Here is another post from the same thread i quoted Bryan in, by a finasteride and dutasteride user:

" everybody seems to be different. I dont believe DHT is the cause for some people. I do have male pattern baldness.. i'm thinning diffusely. Testosterone is what is responsable for pubic hair growth, but since i started propecia and the entire time i've been on dutasteride i lost pubic hair as well. I feel tired, my libido is way down when according to how finasteride SHOULD work, my libido should be sky high now.. an increase in testosterone is not supposed to make me feel as tired as i do everyday, and is not supposed to DECREASE my ejeculate volume by 75% !! and it HAS elevated my estradiol because i've lost all traces of any muscle i had, my biceps are incredibly soft! like friggin marshmallows my tummy is soft! my chest has fatty deposits. All these sides are symptoms of LOW testosterone! i also believe an excess of estrogen can cause hairloss which does make me believe that the hair that i've lost from my nape of the neck (the safe zone! the donor area) was brought on by the medication"


I can find more for you, from older guys on fitness and anti-aging forums, and also things they told me that their Doctor has seen in their patents that took finasteride and dutasteride, mostly fatigue, loss of lidido, bloat,ect.

 

[Pondle]

Apologies for re-posting much of what I said earlier. The system seemed to delete my original post! :thumbdown2:

Such can be said because men have died because they used Finesteride and developed the more aggresive type of prostate cancer, yet you say the
pseudohermaphrodites never experienced BPH. Why would men get the more aggresive type of prostate cancer on Finesteride when they are essentially of the
same "biology" of the "pseudohermaphrodites" when they take Finesteride? They are inhibiting DHT, so why did they get the more aggresive type of prostate
cancer?

Finasteride did not 'cause' aggressive prostate cancer at a higher rate than placebo, as we previously discussed. There was a probable detection bias issue.
http://jnci.oxfordjournals.org/cgi/cont ... 99/18/1366

In general it seems that 5ARIs can only reduce the risk of prostate cancer, not eliminate it. Similarly, they cannot entirely avert balding, only slow the rate dramatically. Bryan's explanation for the relative lack of efficacy of 5ARIs compared to 'being a pseudohermaphrodite' is that "an ounce of prevention is worth a pound of cure", i.e. it helps to have never been exposed to high levels of DHT! I offer no hypothesis, because I am not an urologist. :dunno:

The increased Estrogen to Androgen ratio is what STARTS the BPH process, because as i said, DHT, the allegedly bad testosterone, appears in highest levels in young adults, which have the lowest rates of prostate problems. Second, the older men get, the lower their level of testosterone and DHT are, but yet the higher the rates of prostate problems among them are. Again, it doesn't make sense. If DHT is the main cause for prostate enlargement or cancer, why the majority of people who suffer from prostate problems are those who have lower levels of testosterone and DHT?

It is indeed puzzling how androgen-related conditions like BPH and prostate cancer develop during a stage of life when androgen levels are declining in most men. However, it is important to note:
1. A slightly elevated DHT level has been found in men with BPH (cited in Prostate and renal cancer, benign prostatic hyperplasia, erectile dysfunction and basic research - an update, by D. Newling and Ch. Bangma, Seventh Congress of the Dutch Urological Association)
2. 5ARIs are capable of reducing prostate volume in cases of BPH, by reducing DHT (as is well known!)
3. Anti-androgens like flutamide can do the same.
4. Chemical castration is an effective treatment for prostate cancer.
5. "Reduction of estrogen action has not yet resulted in successful therapeutic interventions in prostate disease"

As i said "The results clearly showed that BPH was associated with elevated estradiol, decreased androgens, and increased SHBG. However, DHT not
only did not cause new prostate growth, but DHT inhibited it by blocking the binding of estradiol to SHBG."

In the Radlmaier et al study, aromatase inhibition by two different doses of atamastene raised DHT by 23% and 35% (numbers read of a graph by Bryan) respectively. This - and the reduced level of estrogen - failed to inhibit prostate growth, which the authors found "surprising and puzzling".

 

[stax]

I have a reply for you, but before i go ay further with it, i want to see that study on the aromatase inhibitor.


They used atamastene which ive never heard of, and i even typed it in google and nothing came up.


Whats up with that? Why would they use an aromatise inhibitor that doesnt even come up on a google search like Arimidex, Aromasin, Letrozole,ect? Even these are a poor choice to use for BPH ( i'll explain in my reply ), so i cant imagine how ineffective this atamastene would be.


I need to see a reference with a link to how much this atamastene lowered Estradiol, lowered SHBG, increases Testosterone, and DHT.

 

[Pondle]

Here's a link to the study abstract - http://grande.nal.usda.gov/ibids/index. ... erow=67211 or http://www3.interscience.wiley.com/cgi- ... 8/ABSTRACT

Haven't read the full Doctor, just seen Bryan's summary of the findings in various threads. Perhaps if you PM him you can get hold of the full text.

 

[Administrator]

Pondle, I am not sure what happened!

If it happens again please let us know...

Sorry about that.

Admin

 

[abcdefg]

how do people use something like dutasteride and not expect something like weight gain. High dht helps you stay lean and keep a more muscular masculine like figure. Its the most potent male hormone for a reason to make us more manly.

 

[stax]

You know what, i was going to reply, but im not even going to waste my time. There is nothing to argue about here.


All the data i provided regarding DHT a fact.

Anybody who knows anything knows this. You can look up this information in medical journals.


Any information provided by Merck is not a fact. The amount of people they claimed had side effects cannot be looked up in a medical journal as stone cold facts.


Just like the role of Testosterone is an established fact, role role of Estrogen is a fact, and the role of DHT is a fact.


If you look up on DHT, you will find all the data to be accurate.

http://www.steroid.com/Proviron.php

Here is one more DHT based drug, read about it, these are the effects and benifits of DHT.


Now EXESS and HIGHER than normal DHT levels CAN possibly cause prostate issues, but this isnt the case most of the time for men with BPH, since their Estradiol is high and there DHT and Testosterone is low. Low DHT has been found in patients prostates with prostate cancer and even in patients with the most aggresive prostate cancer. This is a fact. Exess Estradiol and low DHT/Testosterone is the main culprit.


What you want is optimal Testosterone and DHT levels in the higher end of normal range, and lower Estadiol levels, but not too low, lower end normal on the range chart. This is the hormonal profile of a young man, which never have prostate issues.


I can tell you when i was on Dutaseride with no Anti-E, i had a hard time pissing sometimes, like dribble, and when i added the Anti-E i never had that problem again.



Now those authors of the study claimed to be "shocked and puzzled" that their Aromatase inhibiter, that doesnt even show up on a google search, and cant be prescribed by doctors, didnt improve BPH in the people they treated.


Well first of all they have no business treating anybody, because if they are "shocked and puzzled" that their crappy Anti-E didnt improve BPH symptoms, they should look into another career.

I also dont find this study credible at all, it was very poorly described, and no actual numbers were given for estrogen reduction of androgen increase. Frankly i dont buy it.


They say that Estradiol and Estrone were significantly reduced, but there was only a "slight" increase in androgens. When estogen is significantly reduced, then Testosterone would increase by atleast 50%, which is alot more than slightly.



And men who are 50-60 with BPH, their Testosterone and DHT are low, while Estradiol is high and dominates.


Even a powerfull Aromatase inhibiter like Aromasin, wont increase androgens to the level of restoring them to optimal levels, and that goes for Testosterone and DHT. Thats what HRT is for.


And the problem is you dont want to totally kill estrone and estradiol, you just want them at the lower end of the scale, with optimal levels of androgens in higher end normal range.


They should have been treated with topical DHT cream or gel on the prostate.


The clinical application of this theory is discussed in US patent 5,648,350 "Dihydrotestosterone for use in androgenotherapy". The following illustrates the results:

"In 27 subjects in which the plasma DHT level was controlled, so as to modulate the administered doses, said levels have been increased to 2.5 to 6 ng/ml. There resulted a decrease in gonadotrophy as well as in the plasma levels of testosterone which exceeded at least 1.5 ng/ml (from 0.5 to 1.4 according to the case); as to the estradiol plasma levels, these decreased by 50%.

Among this group of subjects, the volume of the prostate diminished significantly, as was evaluated by ultrasound and by PSA (Prostate Specific Antigen). The mean volume of the prostates was from 31.09.+-.16.31 grams before treatment and from 26.34.+-.12.72 grams after treatment, for a mean reduction of 15.4%, the treatment having a mean duration of 1.8 years with DHT (P=0.01).


Its clear DHT is more effective than aromatise inhibitors for treating the prostate.


DHT Studies

DHT needs to be in balance with testosterone. Dr. Edmond De Vroey, the founder of the Longevity Institute, has been using DHT gel for over 20 years to maintain prostate health by applying DHT topical gel. Applied directly to skin, DHT does not convert to estrogen. Instead, topically-applied DHT decreases estrogen levels.

Dr. Ron Rothenberg, Professor of Medicine at the University of California/San Diego, concurs with me, that the sexual and strength-enhancing benefits from DHT, is not as pronounced as testosterone, or testosterone combined with herbs that metabolize estrogen.

In a clinical study by Dr. Wang and colleagues, DHT improved total androgen levels, while significantly decreasing estradiol levels, within 14 days. Estradiol is considered the most dominant estrogen.

Dr. Eugene Shippen has conducted meta-reviews, indicating that testosterone and DHT can actually protect the prostate.

Dr. Schaison has shown that patients with decreased gonad function became more virile, developed more muscle mass and improved in sexual function, with DHT topical gel.



Using DHT Gel over a 2 year period, Dr. De Lignieres reported men, age 55 to 70, improved sexual function and decreased prostate size by an average of 15%.

DHT requires a prescription and is usually only obtained in Europe, however we use an all natural cream with bioidentical hormones as applied under the scrotum, used in the morning after you shower. The well known fact is that scrotal tissue has enzymes in the skin that can increase DHT production in the presents of androgens. This cream with natural androgens allows rapid absorption of testosterone to youthful levels and conversion to DHT to help reduce estrogens.

As with all androgen replacement therapies, signs of excessive DHT levels, such as oily skin, acne, excess hair growth, aggressiveness, or too heightened sexuality, need to be monitored.



A University of Southern California study found that 8 out of 27 men taking Finasteride for enlarged prostate, developed tumors within one year, despite the drug lowering DHT by 67%. It is my view that unidentified elevated levels of estrogen in the prostate could be the problem, not DHT. While Finasteride lowers DHT, it can cause impotency. In contrast, beta sitosterol in saw palmetto may be more effective to restore urine flow, without impotency. Beta Sitosterol improves metabolism of DHT and androgen receptor binding, while Finasteride does not. Even though Finasteride can reduce DHT in the prostate up to 80%, it only decreases the prostate size by about 20%. Some 60-65% of men get no improvement with Finasteride! Over 5% of Finasteride users suffer decreased libido, impotence, and ejaculatory disorders.

It is important to note that clearing all estrogens from adult men is not good! The aim of an estrogen reduction program is to achieve optimal levels for total male hormonal balance. When “badâ€￾ estrogens are elevated, they do not permit the hormones of youth, your good estrogens, testosterone, human growth hormone, DHEA, etc., to be at proper levels, thus potentially leading to disease and premature aging, and disability.

Nick Delgado,


Ph.D., CHT, Diplomat American Academy Anti-Aging Medicine

http://ezinearticles.com/?Estrogen---Is ... &id=631051




Now whoeven wants to use Finesteride or Dutasteride, be my guest!

But just know the facts about DHT, and know that normal levels of DHT are a GOOD thing, not a bad thing.


Guys with hairloss dont have exess DHT above normal range, their hair is just sensative to DHT by genetics.

 

[Timi]

You know what, i was going to reply, but im not even going to waste my time. There is nothing to argue about here.


All the data i provided regarding DHT a fact.

Anybody who knows anything knows this. You can look up this information in medical journals.


Any information provided by Merck is not a fact. The amount of people they claimed had side effects cannot be looked up in a medical journal as stone cold facts.


Just like the role of Testosterone is an established fact, role role of Estrogen is a fact, and the role of DHT is a fact.


If you look up on DHT, you will find all the data to be accurate.

http://www.steroid.com/Proviron.php

Here is one more DHT based drug, read about it, these are the effects and benifits of DHT.


Now EXESS and HIGHER than normal DHT levels CAN possibly cause prostate issues, but this isnt the case most of the time for men with BPH, since their Estradiol is high and there DHT and Testosterone is low. Low DHT has been found in patients prostates with prostate cancer and even in patients with the most aggresive prostate cancer. This is a fact. Exess Estradiol and low DHT/Testosterone is the main culprit.


What you want is optimal Testosterone and DHT levels in the higher end of normal range, and lower Estadiol levels, but not too low, lower end normal on the range chart. This is the hormonal profile of a young man, which never have prostate issues.


I can tell you when i was on Dutaseride with no Anti-E, i had a hard time pissing sometimes, like dribble, and when i added the Anti-E i never had that problem again.



Now those authors of the study claimed to be "shocked and puzzled" that their Aromatase inhibiter, that doesnt even show up on a google search, and cant be prescribed by doctors, didnt improve BPH in the people they treated.


Well first of all they have no business treating anybody, because if they are "shocked and puzzled" that their crappy Anti-E didnt improve BPH symptoms, they should look into another career.

I also dont find this study credible at all, it was very poorly described, and no actual numbers were given for estrogen reduction of androgen increase. Frankly i dont buy it.


They say that Estradiol and Estrone were significantly reduced, but there was only a "slight" increase in androgens. When estogen is significantly reduced, then Testosterone would increase by atleast 50%, which is alot more than slightly.



And men who are 50-60 with BPH, their Testosterone and DHT are low, while Estradiol is high and dominates.


Even a powerfull Aromatase inhibiter like Aromasin, wont increase androgens to the level of restoring them to optimal levels, and that goes for Testosterone and DHT. Thats what HRT is for.


And the problem is you dont want to totally kill estrone and estradiol, you just want them at the lower end of the scale, with optimal levels of androgens in higher end normal range.


They should have been treated with topical DHT cream or gel on the prostate.


The clinical application of this theory is discussed in US patent 5,648,350 "Dihydrotestosterone for use in androgenotherapy". The following illustrates the results:

"In 27 subjects in which the plasma DHT level was controlled, so as to modulate the administered doses, said levels have been increased to 2.5 to 6 ng/ml. There resulted a decrease in gonadotrophy as well as in the plasma levels of testosterone which exceeded at least 1.5 ng/ml (from 0.5 to 1.4 according to the case); as to the estradiol plasma levels, these decreased by 50%.

Among this group of subjects, the volume of the prostate diminished significantly, as was evaluated by ultrasound and by PSA (Prostate Specific Antigen). The mean volume of the prostates was from 31.09.+-.16.31 grams before treatment and from 26.34.+-.12.72 grams after treatment, for a mean reduction of 15.4%, the treatment having a mean duration of 1.8 years with DHT (P=0.01).


Its clear DHT is more effective than aromatise inhibitors for treating the prostate.


DHT Studies

DHT needs to be in balance with testosterone. Dr. Edmond De Vroey, the founder of the Longevity Institute, has been using DHT gel for over 20 years to maintain prostate health by applying DHT topical gel. Applied directly to skin, DHT does not convert to estrogen. Instead, topically-applied DHT decreases estrogen levels.

Dr. Ron Rothenberg, Professor of Medicine at the University of California/San Diego, concurs with me, that the sexual and strength-enhancing benefits from DHT, is not as pronounced as testosterone, or testosterone combined with herbs that metabolize estrogen.

In a clinical study by Dr. Wang and colleagues, DHT improved total androgen levels, while significantly decreasing estradiol levels, within 14 days. Estradiol is considered the most dominant estrogen.

Dr. Eugene Shippen has conducted meta-reviews, indicating that testosterone and DHT can actually protect the prostate.

Dr. Schaison has shown that patients with decreased gonad function became more virile, developed more muscle mass and improved in sexual function, with DHT topical gel.



Using DHT Gel over a 2 year period, Dr. De Lignieres reported men, age 55 to 70, improved sexual function and decreased prostate size by an average of 15%.

DHT requires a prescription and is usually only obtained in Europe, however we use an all natural cream with bioidentical hormones as applied under the scrotum, used in the morning after you shower. The well known fact is that scrotal tissue has enzymes in the skin that can increase DHT production in the presents of androgens. This cream with natural androgens allows rapid absorption of testosterone to youthful levels and conversion to DHT to help reduce estrogens.

As with all androgen replacement therapies, signs of excessive DHT levels, such as oily skin, acne, excess hair growth, aggressiveness, or too heightened sexuality, need to be monitored.



A University of Southern California study found that 8 out of 27 men taking Finasteride for enlarged prostate, developed tumors within one year, despite the drug lowering DHT by 67%. It is my view that unidentified elevated levels of estrogen in the prostate could be the problem, not DHT. While Finasteride lowers DHT, it can cause impotency. In contrast, beta sitosterol in saw palmetto may be more effective to restore urine flow, without impotency. Beta Sitosterol improves metabolism of DHT and androgen receptor binding, while Finasteride does not. Even though Finasteride can reduce DHT in the prostate up to 80%, it only decreases the prostate size by about 20%. Some 60-65% of men get no improvement with Finasteride! Over 5% of Finasteride users suffer decreased libido, impotence, and ejaculatory disorders.

It is important to note that clearing all estrogens from adult men is not good! The aim of an estrogen reduction program is to achieve optimal levels for total male hormonal balance. When “badâ€￾ estrogens are elevated, they do not permit the hormones of youth, your good estrogens, testosterone, human growth hormone, DHEA, etc., to be at proper levels, thus potentially leading to disease and premature aging, and disability.

Nick Delgado,


Ph.D., CHT, Diplomat American Academy Anti-Aging Medicine

http://ezinearticles.com/?Estrogen---Is ... &id=631051




Now whoeven wants to use Finesteride or Dutasteride, be my guest!

But just know the facts about DHT, and know that normal levels of DHT are a GOOD thing, not a bad thing.


Guys with hairloss dont have exess DHT above normal range, their hair is just sensative to DHT by genetics.

can minoxidil by any Men this bad DHT make Aggressively ???
By About Sensitive Hairs and works very bad?

Because where I put on minoxidil ,there is in short Time the Hair fall out
and never come back

Timi

 

[Guest]

Well, in order to be fair, not everybody notices an increase in body fat:




It seems to be that everybody reacts different to the various treatments. You have to find out where you stand and then make a decision!

 

[Timi]

I take to time

1,25mg Proscar

and attempt finasteride topic 0,25% from Genhair (Corners)

minoxidil stoped 12Month and nothing ,worse Hairs


i must see what make my Hairs without minoxidil
when the Hair get better
later dutasteride 0,5 all 5Days ????



Timi

 

[Andrea]

Timi I repeat always the same thing...
You MUST stop any 5 alpha reductase inibitor for 1 month...
Your scalp is totally dry...
In some people Dutasteride seems to be Roaccutan...
Restore your sebum!
Don't wash your hair everyday, don't use aggressive shampoo,don't use alcholic lotions, take Omega 3,6.9 evreryday.
Bye

 

[Pondle]

Stax, I looked up some posts by Bryan on the Atamastene study. After 48 weeks of therapy, the smaller dose of the drug raised serum DHT by about 23%, and the larger dose raised serum DHT by about 35%. I don't know why the abstract describes that as "modest".

BTW I don't know why you can't find anything about the drug on Google.
http://www.andrologyjournal.org/cgi/con ... t/12/6/403

It is described as "a selective (no inhibition of adrenal function), pure (no endocrine side effects), and highly effective steroidal aromatase inhibitor, with an excellent safety profile. Based on the discussion of its clinical potential, atamestane seems to be a promising compound for the management of BPH." The latter is obviously not true, at least in humans.

I agree with you that DHT pure and simple is not a problem for male pattern baldness, as we know it is our inherited follicular sensitivity that is the key issue! As for BPH, I do not understand the pathogenesis, but then it seems that science in general does not yet fully understand it. We know that androgens are a necessary but not sufficient condition for its development: men with 5ARD and castrates do not experience it, but it develops in older men whose androgen level is declining.

If there are alternative therapies that are supposedly more effective than 5ARIs, I would like to see professional urologists comment on their utility. In the meantime, we know that 5ARIs are a standard treatment and that they are effective in treating BPH. Large scale studies (18,000 men in the 2003 NEJM study of Proscar) also demonstrate their effectiveness in reducing the risk of prostate cancer.
http://www.jr2.ox.ac.uk/bandolier/booth ... nERAM.html
http://www.jr2.ox.ac.uk/bandolier/booth ... utast.html
http://www.gsk.com/investors/presentati ... 5/late.pdf

 

[PhoenixFly]

Hey stax.

First I would like to thank you for all your information, and you wanting to help out.
You've really opened my eyes to all of this, and it has got me very worried, mostly the body fat and gyno.

Now this has given me a great dilemma, I'm hoping you could help me out? It would be great if you could give me a few tips.
My problem is that I would love to carry on using finasteride for stopping hair loss, but im wondering what I could use to counter some of these side effects and keep using finasteride, you seem to know a lot, you mentioned Aromasin, I looked that up, and it says its for women, I'm assuming men use this too? Also what else do you recommend using to stop gyno and female style fat and possibly other side effects. Is there anything else?

Thanks a lot!

 

[about2bebald]

I certainly agree with Stax point of view and information because I can relate to it. Pondle no offense but it seems like whenever somebody says the truth about propecia or has negative thing to say about it , you get very defensive and always says its not true because it doesnt say on the Product information on the brochure or in the propecia website. Are you a Sales marketer for Merck?