Spencer Kobren Speaks With Dr. Michael S. Irwig About Post Finasteride Syndrome (PFS)

good work.

Great interview, thanks Spencer and Dr. Irwig. Unfortunately I dont think it really answered many questions, but it was good to hear Dr. Irwig's opinion on the subject.. Im looking forward to more broadcasts about this subject!

The complex pathways thing really freaks me out from using this product, I dont think ill be taking this product any time soon, not worth risking 10 years without proper sexual function for a few years with a bit of extra density.

Especially with future treatments. Man dont get me wrong but i would be pissed about all recognitions when i got a decent head with hair but my schlong wouldnt work any more

You see, this is the problem with alot of people looking on at this subject. They are immediately aggreived by lack of clear proof to hang their coats on.

As Dr Irwig said, we aren't going to stick a needle into men's heads but there are studies on animals vouching for what men are experiencing. We can't really take men's penisis off and study how finasteride has messed with erectile muscles and tissues either.

That's just how it is and personally i think MERCK are hiding under this stone of medical restriction as are the naysayers.

The best thing we have right now is top guys like Irwig showing profound concern for the various PFS sufferers out there.

Spencer, I love how you try to undermine this guys study by asking with a tone of insinuation if any of these side effects might have been manifested merely by the users prior fear of getting a sexual side effect. What do you have stock in Merck or something? Why is everyone so afraid to tell it like it is? Time to see the light guys! This story is only going to snowball larger and LARGER, because it's TRUE.

That being said, thanks for at least giving this guy the airtime to say what he has to say.

Much respect to Spencer but I don't want to hear an interview on a drug like this. I want to hear about new treatments that actually work, with real science directed at hair loss, without horrible side effects like these.

Seriously, you people need to stop saying Spencer is financially involved with Merck! Hes said countless times that he isnt! Dr. Crisler is the one that started that crazy rumor, and we all saw how mentally unstable he turned out to be.

That’s just crazy talk. Any good interviewer would ask that question, what’s wrong with some of you people? Talk about being paranoid. Kobren get’s the most in-depth interview with Irwig on the net, something that I am grateful for and the haters still bitch. Before this interview I hadn’t a clue that the entire study was based on a questionnaire and conducted by phone. http://www.psy-world.com/asex_print.htm This is an important element that no one is talking about. I was under the impression that there was much more to the study. I’m not as worried as before, but I still think it’s good to shed light on this topic.

An easy to use experimental design that could resolve this issue quickly.

My issue with this study is that an underlying assumption of the stated aim is that otherwise healthy men do not spontaneously develop permanent sexual dysfunction. Sexual dysfunction is relatively common, and it can strike at random. It does not necessary have to result from a drug, and in fact it often happens for no apparent reason.

The only way to show that these men actually developed persistent sexual side effects from propecia is to compare the percentage of users reporting persistent sexual side effects to the percentage of men in general who spontaneously develop the sexual side effects randomly during the duration of the study.

Ie, if a study shows that 2% of men who take propecia for 12 months develop persistent sexual side effects, but 1% of men develop the same side effects independently without using propecia, then propecia actually causes Post finasteride syndrome. If this were reversed, then propecia actually exerts a protective effect (and this is possible!).

It is claimed by Irwig that he can't do a proper study which actually demonstrates that persistent sexual side effects result form the use of propecia for MPHL, because it would require substantial resources. In fact, this is not the case. Below I present an experimental design that would answer this question once and for all. It would not require extensive resources, and one researcher could complete this quickly.


What Irwig should of done was interview 400 people who reported any sexual side effect whilst using propecia. Out of those 400, he should have made a note of those whose side effects continued after stopping the drug.

Let the variable X = (the number of propecia users experiencing PFS) / (the number of propecia users who have had any sexual side effect)


Since other studies have already indicated that there is about a 2% rate of sexual side effects, Irwig would have been able to use a statistical method to estimate the rate of Post Finasteride Syndrome to a reasonable degree.

The estimated rate of PFS = X / (2/100)
= X / 50


Since the rate of spontaneous sexual dysfunction is known through other studies, it is possible, and fairly easy to verify the hypothesis that propecia causes Post Finasteride Syndrome. You just compare the percentage of users reporting persistent sexual side effects to the percentage of men in general who would be expected to spontaneously develop the sexual side effects randomly during the duration of the study.


If the estimated rate of PFS is greater than the expected rate of sexual side effects during period covered by study, and this can't be accounted for by chance, then the hypothesis is proved. Otherwise it is disproved.

This is not that hard to do, and I highly encourage researchers in the field to either take this approach or try something similar.

River - Your proposed research design is not viable for several reason. I will list the most important.

1. The rate of spontaneous development of ED is not known, especially within men in their 20's. I have only seen one study that examined young men in Japan and it showed the frequency of moderate to severe ED in men in their 20s was 0.0%. It was slightly higher for mild cases. Feel free to prove me wrong if you can find any study that proves otherwise as I have been vigorously looking for this myself.

2. You cannot combine figures from one study and use them in another. All studies have intrinsic biases and borrowing from several studies would make the conclusion false. Not just weak as in Irwig's study, but false. The clinical trials put the rate of sexual AEs at 2%, but other studies have this number well into the double digits.

3. There is a concurrent emergence of cognitive problems that emerges with PFS that makes it not equivalent to normal ED. There is also the emergence of the common complaint that semen volume is significantly decreased with a decrease in viscosity and increase in transparency. You could not compare these to your generic complaints of attempting to achieve an erection.

Your thought process was logical, but the idea is not completely practical for those reasons plus more.

This is ANYTHING but simple buddy.

It's not even about percentages or numbers. Irwig hasn't even attempted to try ascertain how big or large this subset is. Too difficult at this moment in time.

Also, you think a simplistic calculation of comparing pecentages of non-finasteride users vrs finasteride users having spontaneous sexual dysfunctinon would suffice...

Reality: There are FAR too many variables: For example, in many cases these guys who develop these "spontaneous" issues had just happened to be on finasteride for a month. Some longer. How one could begin to calculate the liklihood of one individual developing sexual dysfunction in the same time frame (as i said, sometimes days or weeks) as finasteride treatment, i just don't know. A study without this type of information would be massively inaccurate.

This doesn't even account for types of sexual dysfunction. In finasteride cases there seems to be a strange trend emerging where many guys are presenting with unique symptoms such as low FSH, low 3-adiol-G, Vitamin D deficiency and seemingly androgen resistent (i.e. very low response to high doses of TRT: unprecedented!!). These thing are entirely different than the average case so for one to lump all cases of sexual dysfunction together would be completely misguided...


The prevailing reality that many top endos are now finding out is that guys who have taken 5AR inhibitors such as Finasteride, Dustasteride, Accutane and even Saw Palmetto, are in a whole different bracket than the normal guy complaining of ED. Therefore, the devil lies in the detail. I would also add - the TRUTH lies in the detail. These patterns prove PFS and I've no doubt they'll emerge over the next decade as accepted facts.

To kaypeeoh

TO KAYPEEOH

In case you see this message which I hope you do, SSRIs are not necessarily the answer to solving the neurosteroid imbalance caused by finasteride. SSRIs typically have very common sexual side effects as well, but they tend to be reversible much more often than from finasteride. Please be sure to consult with a trusted doctor before you experiment with this type of thing on your own, even though I know you are a veterinarian.

Perhaps you should read this article on the prevalence and medical management of erectile dysfunction in Asia. (Shows prevalence rate of 2 to 88% of men, depending on age/ and other factors)


Actually, you can combine figures from one study and use them in another. It's done all the time, and it is regarded as scientific if it is done right. The science of epidemiology, or population health, is completely dependent on this. For example, read "Asthma and Risk of Erectile Dysfunction-A Nationwide Population-Based Study", and examine how they derive their data. (http://www.ncbi.nlm.nih.gov/pubmed/21426497)

I'm not concerned about the types of permanent ED resulting from the use of propecia, only determining whether it actually occurs.

You would be surprised how easy it is to calculate the liklihood of one individual developing sexual dysfunction in the same time frame as finasteride treatment. That is really not an issue at all.

Your assertion that there are too many variables relates to the problem of the perfect being the enemy of the good. It would be great to have a double blind control trial, but it is not necessary to characterize every case of ED suffered by every propecia patient to investigate this issue. It is only necessary to have a sufficient population size such that you can test your hypothesis to a reasonable confidence level.