39 replies to this topic

[Soma]

My fair has been thinning at an alarming rate and it is getting very discouraging. Between ridiculously sparse hair and my chronic skin condition, I am very unhappy about my physical appearance. I've perused the threads on this topic and haven't garnered a lot of hope about anything producing much of a change. I'm hoping that someone has had some success lately that they haven't written about.

From what I have read, the only viable option for significant improvement is transplant surgery. This is precluded at the moment, and the foreseable future, due to the high cost involved. What I have taken is the typical weak sauce: fenugreek extract, pumpkin seed extract, saw palmetto, tocotrienols. Of course, none of these had any discernable effect. I am currently using the well known laser comb, but this actually seems to have only exacerbated the thinning process. I am looking into ketoconazole shampoo and hoping to source 2%.

Has anybody had even a modicum of success with anything other than surgery? Thanks in advance.

Edited by Soma, 09 March 2015 - 06:58 PM.

[APBT]

I don’t have a magic bullet to offer but, IMHO, men with thinning hair and receding hairlines generally look better with a very short haircut – or buzzed.  The fluff ‘n puff, camo, or comb-over draw more attention.

 

Here’s a source for 2% Ketoconazole:  http://nootropicsmex...2-ketoconazole/

 

They also offer a “Hair Regrowth Treatment Stack”:  http://nootropicsmex...owth-treatment/

 

I can’t vouch for either, as I’ve not used the products.  

[Soma]

men with thinning hair and receding hairlines generally look better with a very short haircut – or buzzed.

I don't have the head for it. I've buzzed my hair before and it looked quite bad. I've always been jealous of guys who have a nicely shaped dome that allowed them to shave their heads.

Edited by Soma, 10 March 2015 - 01:19 AM.

[Heisenburger]

You have my sympathy. Every time I shave my head I get compliments from girls young enough to be my daughter. If you’re really that concerned about it, you probably already know that finasteride arrests the progression of MPB in 83% of all men, so the obvious first line of attack is pretty much a no-brainer. Throw some 5% minoxidil into the mix, and there’s about a ninety percent chance that you can at least keep what you have indefinitely, if not regrow a visible amount. Me, I’m 53 and happily married and don’t give a shit anymore. I also like not having to pay for haircuts or futz with my hair after I get out of the shower. Pain in the ass.

[sensei]

I have had some regrowth following high dose oral administration of C60 Olive oil.

 

I am starting on a topical C60OO and dermarolling regimen.

 

You can see pics here:

 

http://www.longecity...experiment-log/

 

 

I refuse to take finasteride or minoxidil -- it must be taken indefinitely. Any regrowth falls out when you stop taking the medication.

Edited by sensei, 12 March 2015 - 06:58 PM.

[samiamm]

Established Treatments

 

finasteride

dutasteride

minoxidil

ketoconazole

 

Promising Experimental Treatments

RU58841
CB-03-01

Growth-Factor Peptides

OC
Setipiprant

 

Physical Treatments

 

Wounding the skin, which includes

• dermarolling
• chemically wounding
• etc;

Life-Style Changes

 

ketogenic diet

avoiding creatine

 

 

 

for more in depth answers shoot me a PM

 

[nowayout]

Minoxidil is the first line of defense.  It is side-effect-free for all but a small minority of people (possibly hypochondriacs) who claim it gives them eye bags.  It is not hormonal and doesn't cause sexual side effects in anyone.  Improvement, if any, is seldom dramatic, but the risks are so low that you might as well use it. 

 

Propecia helps somewhat for many guys but has sexual side effects in a large percentage of users, which may become long term in a small percentage.  The improvement, if any, is seldom dramatic though, and often only temporary.

 

Spironolactone and ketoconazole are topical anti-androgens that may be mildly helpful.  Don't expect anything dramatic from them. 

 

 

Edited by nowayout, 24 March 2015 - 03:04 PM.

[Heyman]

Minoxidil is the first line of defense.  It is side-effect-free for all but a small minority of people (possibly hypochondriacs) who claim it gives them eye bags.  It is not hormonal and doesn't cause sexual side effects in anyone.  Improvement, if any, is seldom dramatic, but the risks are so low that you might as well use it. 

 

IMO minoxidil won't help long-term. It increases hair-density, but the hair loss continues afterwards at the normal rate. Meaning you likely offset your hair loss by about two years, but you won't stop it long-term. I have this from a diagram in a study that floated around some time ago.

 

Propecia helps somewhat for many guys but has sexual side effects in a large percentage of users, which may become long term in a small percentage.  The improvement, if any, is seldom dramatic though, and often only temporary.

 

Nothing right now improves hair dramatically. However, propecia has been shown to maintain the amount of hair you currently have for at least 10 years in about 80-90% of users in at least one study I remember. The reason the hair loss appears to continue in groups is that the 10-15% of people that are nonresponders to propecia decrease the group average over time. Can you remember why you think it is only temporary?

 

Sexual side effects happen, but the percentage is not large at all. If you control for placebo effect it might be about 2% or so if any. E.g. http://archderm.jama...rticleid=480677 or for a good review http://www.ncbi.nlm....les/PMC3481923/ which also talks about the nocepo effect. Taking a balanced look at the evidence and taking into account the general consensus with the largest studies is that finasteride-induced sexual side-effects are very rare.

 

This is quite important as of right now finasteride is the only thing to keep your hair long-term. I hope there will be a new treatment like CB-03-01 or similar that is more effective but as of right now the only thing to do long-term if you really care a lot about your hair and you notice it early enough is finasteride. Maybe Nizoral.

 

[nowayout]

Propecia helps somewhat for many guys but has sexual side effects in a large percentage of users, which may become long term in a small percentage.  The improvement, if any, is seldom dramatic though, and often only temporary.

 

Nothing right now improves hair dramatically. However, propecia has been shown to maintain the amount of hair you currently have for at least 10 years in about 80-90% of users in at least one study I remember. The reason the hair loss appears to continue in groups is that the 10-15% of people that are nonresponders to propecia decrease the group average over time. Can you remember why you think it is only temporary?

 

From my own experience (I used Finasteride for 12 years) and a number of anecdotal reports on hair loss forums.  In my case an initial (just moderate) improvement for a couple of years was followed by a subsequent resumption of hair loss - from what I have read this is common, but then maybe the guys who post are the complainers, so who knows.  I continued taking it for a number of years out of fear of what would happen when I stopped it.  I finally did stop and nothing remarkable has happened since (no speedup nor slowdown of hairloss). 

[nowayout]

Propecia helps somewhat for many guys but has sexual side effects in a large percentage of users, which may become long term in a small percentage.  The improvement, if any, is seldom dramatic though, and often only temporary.

 

Sexual side effects happen, but the percentage is not large at all. If you control for placebo effect it might be about 2% or so if any. E.g. http://archderm.jama...rticleid=480677 or for a good review http://www.ncbi.nlm....les/PMC3481923/ which also talks about the nocepo effect. Taking a balanced look at the evidence and taking into account the general consensus with the largest studies is that finasteride-induced sexual side-effects are very rare.

 

Thanks for the links, but I really don't buy it. 

 

As with SSRIs, incidence of sexual side effects is almost certainly higher than the mythical 2% reported in the studies (large or not) by the very people who were trying to get the drug approved. 

 

Also, people often don't think of reporting sexual side effects for various reasons.  I didn't realize how much lower my libido had become over the years until I stopped finasteride and suddenly got it back in spades.  In my case the onset was slow and creeping and I was still functional, so I didn't know finasteride was to blame.

 

Two of my friends also tried finasteride and stopped because of physically obvious side effects, such as dramatic changes in the consistency of semen, that eliminate the possibility of nocebo.  So that's three out of three in my circle.  If that 2% figure is right, the chances of the three of us all having side effects by coincidence is roughly 1 in 100,000.  So I find the 2% figure hard to swallow.  
 

[Heyman]

Thanks for the links, but I really don't buy it. 

 

As with SSRIs, incidence of sexual side effects is almost certainly higher than the mythical 2% reported in the studies (large or not) by the very people who were trying to get the drug approved. 

 

Also, people often don't think of reporting sexual side effects for various reasons.  I didn't realize how much lower my libido had become over the years until I stopped finasteride and suddenly got it back in spades.  In my case the onset was slow and creeping and I was still functional, so I didn't know finasteride was to blame.

 

Two of my friends also tried finasteride and stopped because of physically obvious side effects, such as dramatic changes in the consistency of semen, that eliminate the possibility of nocebo.  So that's three out of three in my circle.  If that 2% figure is right, the chances of the three of us all having side effects by coincidence is roughly 1 in 100,000.  So I find the 2% figure hard to swallow. 

 

A possible change in semen consistency seems to be related to the effect on the prostate. However, that to me is not sexual dysfunction.

 

The question is what is more trustworthy: Anecdotal evidence or studies. Your argument is basically that all research on finasteride is rigged. There are however studies not funded by Merck showing low rates of problems as well. IMO anecdotal evidence is not better for the following reason: In some research up to 30% of young men have some sexual dysfunction. Young men who mostly don't take any medication. In finasteride studies many men improve their sexual dysfunction after stopping to take - the placebo. I am not discounting your experience. You improved after stopping finasteride. But equally you should not discount the experience of people who improved after stopping a placebo. Finasteride does cause sexual dysfunction on some men, but it is not a high rate.

[sensei]

 

 

A possible change in semen consistency seems to be related to the effect on the prostate. However, that to me is not sexual dysfunction.

 

 

 

Ummm the prostate is a male sexual organ.  Simple manual stimulation of the prostate causes orgasm and ejaculation in most men.

 

Any change to the function of the prostate that impacts normal function -- is by definition -- Sexual Dysfunction

[Heyman]

 

 

 

A possible change in semen consistency seems to be related to the effect on the prostate. However, that to me is not sexual dysfunction.

 

 

 

Ummm the prostate is a male sexual organ.  Simple manual stimulation of the prostate causes orgasm and ejaculation in most men.

 

Any change to the function of the prostate that impacts normal function -- is by definition -- Sexual Dysfunction

 

 

The normal function of the prostate is not impacted - you still get an orgasm, you can still stimulate the prostate and ejaculate, there is no change in that.

 

Prostate volume / semen parameters do not change much if at all in young men in some research. (1) We are not talking about people having no semen anymore or losing their prostate, we are talking about some people in some studies having e.g. a 20% reduction in ejaculation and prostate volume - in studies on proscar these are people who had an enlarged prostate to begin with - while still being able to father children just fine.

 

I looked up several definitions of sexual dysfunction thanks to your comment. (2) (3) (4)

 

 

Sexual dysfunction, also called Psychosexual Dysfunction,  the inability of a person to experience sexual arousal or to achieve sexual satisfaction under appropriate circumstances, as a result of either physical disorder or, more commonly, psychological problems

 

Sexual dysfunction is broadly defined as the inability to fully enjoy sexual intercourse. Specifically, sexual dysfunctions are disorders that interfere with a full sexual response cycle. These disorders make it difficult for a person to enjoy or to have sexual intercourse.

 

I could not find any reference about the volume of sperm or the size of the prostate.

Edited by Heyman, 25 March 2015 - 03:45 PM.

[nowayout]

The normal function of the prostate is not impacted - you still get an orgasm, you can still stimulate the prostate and ejaculate, there is no change in that.

 

Prostate volume / semen parameters do not change much if at all in young men in some research. (1) We are not talking about people having no semen anymore or losing their prostate, we are talking about some people in some studies having e.g. a 20% reduction in ejaculation and prostate volume - in studies on proscar these are people who had an enlarged prostate to begin with - while still being able to father children just fine.

 

I could not find any reference about the volume of sperm or the size of the prostate.

 

 

Well, reduced ejaculate can cause significantly weaker and lower quality orgasms, which was my friend's complaint when all that would come out was a dry and clumpy bit of jelly.  I would consider that a sexual side effect.  He had no prostate enlargement FWIW.  My other friend got impotence from it whose temporal relationship to taking the drug was dramatic (as I can attest to since he was my boyfriend).  They were frankly not informed enough to expect any side effects, didn't speak to each other, and were not influenced by me except in the sense that I was on it and encouraging them to try it, so I wouldn't expect nocebo.   And my dysfunction was such gradual loss of libido that I didn't impute them to the drug until I stopped the drug and experienced the difference - so if you had included me in a study I wouldn't have reported side effects. 

 

As for incidence, their own pamphlet, http://www.rxlist.co...nteractions.htm, lists in one study

 

-  Impotence at 8%, which is about 4% higher than placebo, 

-  Decreased libido and ejaculate volume 3% higher than placebo

 

and in the other study

 

-  Impotence at 18%, which was 6% higher than placebo

-  Abnormal ejaculation at 7%, which was about 5% greater than placebo. 

 

Also, FWIW, the FDA in 2012 decided to require additional warnings based on post-marketing experience of cases of long term dysfunction: http://www.rxlist.co...ticlekey=157127

 

 

Now labels on both drugs will include new warnings:

• Propecia may cause loss of sexual desire, inability to ejaculate, and inability to reach orgasm. These sexual dysfunctions may continue for some time after men stop using the baldness drug.
• Proscar may cause loss of sexual desire. This may continue for some time after men stop using the drug.
• Both Propecia and Proscar may cause male infertility and/or poor semen quality. This side effect lessens or goes away after men stop taking the drugs.

 

I don't want to be alarmist - these side effects won't affect most people.

Edited by nowayout, 25 March 2015 - 06:37 PM.

[nowayout]

Just another issue to keep in mind - Propecia (finasteride) not only inhibits DHT but also inibits several other neurosteroids whose functions in the brain are not completely understood, as well as possibly affecting the long term health of the eyes.  From Wikipedia (3/25/15):

 

 

In vitro and animal models suggest subsequent 3alpha-reduction of DHT, DHP and DHDOC lead to steroid metabolites with effect on cerebral function by reducing gamma-aminobutyric acid GABAergic inhibition. These neuroactive steroid derivatives enhance GABA at GABA(A) receptors and have anticonvulsant, antidepressant and anxiolytic effects, and also alter sexual and alcohol related behavior.^[9] 5α-dihydrocortisol is present in the aqueous humor of the eye, is synthesized in the lens, and might help make the aqueous humor itself.^[10]Allopregnanolone and THDOC are neurosteroids, with the latter having effects on the susceptibility of animals to seizures. In socially isolated mice, 5α-R1 is specifically down-regulated in glutamatergic pyramidal neurons that converge on the amygdala from cortical and hippocampal regions. This down-regulation may account for the appearance of behavioral disorders such as anxiety, aggression, and cognitive dysfunction

 

[Heyman]

 

Now labels on both drugs will include new warnings:

• Propecia may cause loss of sexual desire, inability to ejaculate, and inability to reach orgasm. These sexual dysfunctions may continue for some time after men stop using the baldness drug.
• Proscar may cause loss of sexual desire. This may continue for some time after men stop using the drug.
• Both Propecia and Proscar may cause male infertility and/or poor semen quality. This side effect lessens or goes away after men stop taking the drugs.

 

This is merely a clause to protect Merck. There are several people who have to gain something by lawsuits, so that is why Merck later included this to protect themselves. It is not based on any placebo-controlled evidence.

 

I don't want to be alarmist - these side effects won't affect most people.

 

That was the only point I tried to argue. I know a few percentage of people will have an issue with finasteride, and it is in the low single digit percentages after controlling for placebo as you quoted yourself with research. In the beginning of this thread you claimed it affects a a large percentage of users.
 

 

Well, reduced ejaculate can cause significantly weaker and lower quality orgasms, which was my friend's complaint when all that would come out was a dry and clumpy bit of jelly.  I would consider that a sexual side effect.  He had no prostate enlargement FWIW.  My other friend got impotence from it whose temporal relationship to taking the drug was dramatic (as I can attest to since he was my boyfriend).  They were frankly not informed enough to expect any side effects, didn't speak to each other, and were not influenced by me except in the sense that I was on it and encouraging them to try it, so I wouldn't expect nocebo.   And my dysfunction was such gradual loss of libido that I didn't impute them to the drug until I stopped the drug and experienced the difference - so if you had included me in a study I wouldn't have reported side effects.

 

You can either claim the effects are mostly obvious, like impotence or problems with orgasm, or you can claim the effects are subtle and thus can't be detected by research. You can't have it both ways... If you wanna claim the first, these obvious side-effects would have been captured by research. If you have the opinion the side-effects are gradual and not obvious to detect (erectile problems are obvious to detect), many studies use scales. They don't rely on people reporting if they notice a difference, they use absolute scales or at least some kind of scale to measure sexual activity and desire. An example:

 

ability to have an erection when desired (five response levels), degree of participant's satisfaction with his sexual activities (four response levels), change in sexual performance (seven response levels), and frequency of sexual activities (seven response levels)

Source

 

A sample size of >18.000 men and had a placebo to control. They used the scale specifically because it allows to show more incremental or small changes. The same goes to the other study I quoted a few posts before, they asked how often people felt sexual desire. Even if you don't notice a difference in your sexual desire as it changes gradually, you would have been able to report a difference in frequency a few years later? At least I would not claim "I am horny all the time" anymore if I would nowadays only be horny half the time.

 

Regarding the study in the animal model, it is not as easy. Finasteride blocks only DHT type 2 in humans which is only found at the scalp and prostate. As far as I know, in rats finasteride affects all DHT so any comparison becomes moot. The DHT in rats brains is affected, that of humans is not. In the end what matters is actual effects on humans, and there is a placebo-controlled study with >18.000 people that also checked mental health and found no difference. So which kind of research is more relevant?
 

Edited by Heyman, 26 March 2015 - 08:48 AM.

[nowayout]

 

 

Now labels on both drugs will include new warnings:

• Propecia may cause loss of sexual desire, inability to ejaculate, and inability to reach orgasm. These sexual dysfunctions may continue for some time after men stop using the baldness drug.
• Proscar may cause loss of sexual desire. This may continue for some time after men stop using the drug.
• Both Propecia and Proscar may cause male infertility and/or poor semen quality. This side effect lessens or goes away after men stop taking the drugs.

 

This is merely a clause to protect Merck. There are several people who have to gain something by lawsuits, so that is why Merck later included this to protect themselves. It is not based on any placebo-controlled evidence.

 

No, it is nor merely a clause added by Merck to protect themselves.  The FDA required Merck to include this based on independent post-approval studies that showed these problems occurring.

[nowayout]

Well, reduced ejaculate can cause significantly weaker and lower quality orgasms, which was my friend's complaint when all that would come out was a dry and clumpy bit of jelly.  I would consider that a sexual side effect.  He had no prostate enlargement FWIW.  My other friend got impotence from it whose temporal relationship to taking the drug was dramatic (as I can attest to since he was my boyfriend).  They were frankly not informed enough to expect any side effects, didn't speak to each other, and were not influenced by me except in the sense that I was on it and encouraging them to try it, so I wouldn't expect nocebo.   And my dysfunction was such gradual loss of libido that I didn't impute them to the drug until I stopped the drug and experienced the difference - so if you had included me in a study I wouldn't have reported side effects.

 

You can either claim the effects are mostly obvious, like impotence or problems with orgasm, or you can claim the effects are subtle and thus can't be detected by research. You can't have it both ways...

 

Yes, you can have it both ways.  A drug can have immediately obvious effects in some and gradual effects in others.   

[Heyman]

No, it is nor merely a clause added by Merck to protect themselves.  The FDA required Merck to include this based on independent post-approval studies that showed these problems occurring.

There are no placebo-controlled studies showing post-finasteride syndrome - e.g. permanent sexual side-effects. It is easy for you to prove me wrong on this, just cite a single paper. The 'post-approval studies' is the following: A small number of people who are impotent and claim finasteride caused their impotence. If that is true or not, no one can tell without placebo-controlled studies. Impotence is common, about 5-20% of the younger male population has it. If a few hundred thousand people take a drug, a few of them will associate the onset of impotence with the drug.

 

 

Yes, you can have it both ways.  A drug can have immediately obvious effects in some and gradual effects in others.   

You claimed that studies do not capure the true extent of sexual side-effects as they are too gradual to be noticed. Then you went on and used 2 cases of anecdotal evidence which showed immediate obvious effects, to make your point. Either your two anecdotes do not represent the majority, or your first argument that studies do not capture side-effects because they are not obvious is invalid.

 

If I ask you how frequently you felt horny or how often you had sexual activity in the last 4 weeks, you won't say '10 times' or 'all the time' if that number is not on that level anymore after a few years. Do you agree this is how gradual changes can be measured? Because this is how some studies did it. There are also objective measures not involving people to self-report anything, e.g. this.

 

Can we agree that finasteride causes side-effects in some people but it occurs only to a minority (<10%)?

Edited by Heyman, 26 March 2015 - 05:26 PM.

[nowayout]

 

No, it is nor merely a clause added by Merck to protect themselves.  The FDA required Merck to include this based on independent post-approval studies that showed these problems occurring.

There are no placebo-controlled studies showing post-finasteride syndrome - e.g. permanent sexual side-effects. It is easy for you to prove me wrong on this, just cite a single paper. The 'post-approval studies' is the following: A small number of people who are impotent and claim finasteride caused their impotence. If that is true or not, no one can tell without placebo-controlled studies. Impotence is common, about 5-20% of the younger male population has it. If a few hundred thousand people take a drug, a few of them will associate the onset of impotence with the drug.

 

 

Yes, you can have it both ways.  A drug can have immediately obvious effects in some and gradual effects in others.   

You claimed that studies do not capure the true extent of sexual side-effects as they are too gradual to be noticed. Then you went on and used 2 cases of anecdotal evidence which showed immediate obvious effects, to make your point. Either your two anecdotes do not represent the majority, or your first argument that studies do not capture side-effects because they are not obvious is invalid.

 

If I ask you how frequently you felt horny or how often you had sexual activity in the last 4 weeks, you won't say '10 times' or 'all the time' if that number is not on that level anymore after a few years. Do you agree this is how gradual changes can be measured? Because this is how some studies did it. There are also objective measures not involving people to self-report anything, e.g. this.

 

Can we agree that finasteride causes side-effects in some people but it occurs only to a minority (<10%)?

 

 

No.  I gave two anecdotal examples of immediate side effects and one anecdotal example of gradual side effects whose true magnitude was only apparent upon discontinuation.

 

The evidence for post-finasteride syndrome was sufficiently strong for the FDA to believe it. 

[Heyman]

No.  I gave two anecdotal examples of immediate side effects and one anecdotal example of gradual side effects whose true magnitude was only apparent upon discontinuation.

 

The evidence for post-finasteride syndrome was sufficiently strong for the FDA to believe it. 

 

Why does research - even not funded by Merck - consistently show the side-effects only affect a small minority of men? Research with capable methodology to detect even gradual changes? The only placebo-controlled study looking at post-finasteride-syndrome found that people who quit placebo were more likely to still have ED at follow-up than people who quit finasteride. The FDA acknowledged in their own Q&A about the label change that the 'evidence' for pfs is merely anecdotal, a causal effect has not been established and side-effects are rare.

 

You believe that your anecdotal experience with a sample size of 3 is more reliable and trustworthy than long-term double blind placebo-controlled studies with sample sizes of >18.000. Do you understand how ridiculous that is? I'm not discounting your experience but the way you seem to extrapolate from that.

[twinkly]

I don't mean to change the direction of the discussion at hand, but, as it seems to be somewhat related to sexual functions (or lack thereof), I wonder whether or not there is any connection between hair loss and sexual activity (by no means of the chronic kind), be it sex or masturbation? The idea of the release of DHT and sexual activity gets thrown around a whole lot of the time without any scientific backing to further validate those theories. In the wake of having read some of these theories, I, as a completely healthy man with no signs of hair loss, certainly would lie if I said that I haven't found myself at a loss for what to believe. What is your take?

[Heyman]

I don't mean to change the direction of the discussion at hand, but, as it seems to be somewhat related to sexual functions (or lack thereof), I wonder whether or not there is any connection between hair loss and sexual activity (by no means of the chronic kind), be it sex or masturbation? The idea of the release of DHT and sexual activity gets thrown around a whole lot of the time without any scientific backing to further validate those theories. In the wake of having read some of these theories, I, as a completely healthy man with no signs of hair loss, certainly would lie if I said that I haven't found myself at a loss for what to believe. What is your take?

 

Is there research on sexual activity and DHT specifically? Especially DHT type 2 in the scalp? I remember a study showing e.g. creatine increasing DHT to some degree. In general people with hair loss don't have higher levels of DHT, but their follicles are more sensitive. However if decreasing DHT can stop hair loss, maybe an increase could speed it up. The question is how much and for how long is it increased after sexual activity.
 

[nowayout]

Is there research on sexual activity and DHT specifically? Especially DHT type 2 in the scalp? I remember a study showing e.g. creatine increasing DHT to some degree. In general people with hair loss don't have higher levels of DHT, but their follicles are more sensitive. However if decreasing DHT can stop hair loss, maybe an increase could speed it up. The question is how much and for how long is it increased after sexual activity.

 

The study on creatine is so widely quoted  that it has become received bro-wisdom but was too small  for any reliable conclusions to be drawn.  Another thread discusses it, but as far as I remember, it looked like regression to the mean or bad randomization - specifically, at the start of the study the creatine group had much lower DHT than the placebo group and ended with DHT at the same level as the placebo group started out with. 

 

People who are so concerned with hair loss that they would really limit sex because of it need, in my opinion, psychiatric help, not more research for them to obsess over.   But, for what it is worth, more frequent sex has been linked with better prostate health, which is something I would think is more important than hair. 
 

[samiamm]

edit for double post

 

Edited by samiamm, 30 March 2015 - 03:57 AM.

[samiamm]

"Propecia helps somewhat for many guys but has sexual side effects in a large percentage of users, which may become long term in a small percentage.  The improvement, if any, is seldom dramatic though, and often only temporary."

This is absolutely false; It does not have sexual side effects in a large percentage of the users, and the various studies Heyman provided you CLEARLY show that. Also, "PFS" has yet to be proven, it is a THEORY, and one that does not hold weight when discussing the biochemistry of the drug. Also, the drug is mainly meant for stopping loss rather than regrowth, which it does phenomenally.

 

"From my own experience (I used Finasteride for 12 years) and a number of anecdotal reports on hair loss forums.  In my case an initial (just moderate) improvement for a couple of years was followed by a subsequent resumption of hair loss - from what I have read this is common."

 

So your n=1 experience and anecdotal reports trump a decade long study showing 80+ percent of the users stayed above baseline with finasteride? Excellent.

 

I didn't realize how much lower my libido had become over the years until I stopped finasteride and suddenly got it back in spades. 

 

You took a medication which reduced 70% of serum DHT for 12 years, then hopped off and noticed a spike in libido, and you were surprised? The only interesting part here is that you took it for years without noticing this loss in libido, showing that despite fin's 70% DHT drop (assuming you were dosing at 1 mg daily) you did not experience significant sexual dysfunction.  

 

Two of my friends also tried finasteride and stopped because of physically obvious side effects, such as dramatic changes in the consistency of semen, that eliminate the possibility of nocebo.  So that's three out of three in my circle.  If that 2% figure is right, the chances of the three of us all having side effects by coincidence is roughly 1 in 100,000.  So I find the 2% figure hard to swallow.  

 

I dont even know where to start with this. 

1) "dramatic changes in consistency of semen" does not necessarily eliminate the possibility of nocebo. Also, how do we know there were, in fact, "dramatic changes in semen consistency." Because your friend said so? Did you measure his semen consistency pre and post fin use? Its that vs the safety trials provided by merck and the 3rd party testing done on finasteride efficacy and safety, which heyman linked you.

 

No, it is nor merely a clause added by Merck to protect themselves.  The FDA required Merck to include this based on independent post-approval studies that showed these problems occurring.

 

Do you know how the FDA operates? Do you know the FDA regulatory structure and how it works? You could find  the same cautionary side-effect requirements required by the FDA for a plethora of drugs taken daily 

 

The evidence for post-finasteride syndrome was sufficiently strong for the FDA to believe it. 

 

Jesus, no it is not. PFS is a THEORY and a THEORY which DOES NOT HOLD WEIGHT CURRENTLY in the context of how finasteride biochemistry works; there is NO EVIDENCE for PFS;

 

No.  I gave two anecdotal examples of immediate side effects and one anecdotal example of gradual side effects whose true magnitude was only apparent upon discontinuation.

 

Your ANECDOTAL EXAMPLES mean jack s*** in the light of the plethora of evidence Heyman has linked you.

 

You know nearly NOTHING about finasteride, and instead of educating yourself via the information Heyman has laid out for you, you argue with illogical premises every step of the way. 

 

 

and while you do raise SOME relevant and legitimate issues about finasteride, you do so against the backdrop of a very biased argument based on your own personal experience with the drug, and 2 of your friends'. 

 

 

[samiamm]

and on top of that, you're wrong about the creatine study and hairloss as well.  The study clearly showed that the creatine supplementation caused a dramatic spike in DHT which directly plays a role in MPB. But yes, youre right, the sample size was small.

 

Im a part of a forum where multiple members, interested about this study, also ran creatine with logs of hair-sheds and before/after hair density, which clearly showed the spike in DHT caused by creatine is ABSOLUTELY HARMFUL for those predisposed to MPB;

 

your information is 100% harmful to anyone looking for legitimate advice about hairloss;

 

[nowayout]

and on top of that, you're wrong about the creatine study and hairloss as well.  The study clearly showed that the creatine supplementation caused a dramatic spike in DHT which directly plays a role in MPB. But yes, youre right, the sample size was small.

 

 

The bolded statement is incorrect.  Did you actually read the text of the study?  What you call the "dramatically spiked" levels of DHT in the creatine group was the same levels that the placebo group started out with.  Also, for some unknown reason, DHT fell in the placebo group during the course of the study.  Mmmm.

 

Im a part of a forum where multiple members, interested about this study, also ran creatine with logs of hair-sheds and before/after hair density, which clearly showed the spike in DHT caused by creatine is ABSOLUTELY HARMFUL for those predisposed to MPB;

 

 

Well, you just dismissed and insulted my anecdotal evidence (and MANY others' anecdotes) about propecia, and now you are telling me I should take seriously your anecdotal evidence about creatine? 

 

You cannot have it both ways. 

Edited by nowayout, 30 March 2015 - 01:27 PM.

[nowayout]

 

The evidence for post-finasteride syndrome was sufficiently strong for the FDA to believe it. 

 

Jesus, no it is not. PFS is a THEORY and a THEORY which DOES NOT HOLD WEIGHT CURRENTLY in the context of how finasteride biochemistry works; there is NO EVIDENCE for PFS;

 

 

This went through the FDA and was found plausible enough by experts on the relevant committees to merit a required warning on the pamphlet.  The FDA doesn't just do this for every hypochondria people may pull out of their ass - in fact the FDA is known to err on the side of drug companies, if anything.  So I am not going not have the discussion with you. 

 

But do you know everything about the biochemistry of finasteride?  If so, you must be from the future, since currently it is not entirely understood.  You do know that it affects several neurosteroids besides DHT whose functions are not entirely clear, correct?  You also do seem to know that DHT levels can effect sexual function, since you told me I shouldn't have been surprised to have lower libido, didn't you?  So you are being disingenuous here.

 

Edited by nowayout, 30 March 2015 - 01:25 PM.

[samiamm]

Hahaha, I don't think YOU have read the study or understood it properly. Also, I don't believe you understand what "anecdotal" means. Either way,you're a moron, probably from propeciahelp.com, and I'm not going to waste my time arguing with you ,and anyone looking for advice on hairloss should ignore you as well