In a recent blog post you wrote about sexual side effects associated with propecia use, “These side effects are reversible withing one to two weeks after you stop the medication.” You then went on to say that Dr. Irwig’s study in Journal of Sexual Medicine was not a scientific study.

When you read through the FDA hearing on Propecia (FDA link) Keith Kaufman of Merck talks about the 3.8 percent of finasteride users experiencing side effects versus 2.1 percent of the placebo. He then goes onto say that these patients then completed a validated sexual function questionare. I am not a doctor but Merck basically based these figures on self reporting, should those numbers not be considered scientific?

In July the Dr. Irwin Goldstein the Editor-in-Chief of the Journal of Sexual Medicine wrote “I think of the frequent phone calls I receive from distressed men with varying degrees of hair loss who have used 5 alpha reductase inhibitors and now have newly manifested sexual and cognitive complaints that often persist despite discontinuation of the 5 alpha reductase inhibitor. Often such 5 alpha reductase inhibitor users have sought help only to be belittled, betrayed, misdirected, and sometimes misinformed. In general, these patients feel deceived becuase of the lack of information warning them of the potential side effects.”

I am one of the individuals suffering from persistent sexual dysfunction after stopping propecia and it appears pretty certain to me that in a small subset of men the persistent sexual dysfunction is due to the medication.

I am not going to get roped into an anti-Propecia agenda. I will leave that up to those who regularly comment on almost every post where the word “Propecia” appears.

My heart goes out to you if you actually have long-lasting sexual side effects, but the questions of validity ring true to your cause of sexual dysfunction. I am not in a position to judge your problem or to put the pieces together for you. That must be between you and your doctors. I am a doctor, but the posts here are just my opinions on my blog. Some may not agree with me, but that is OK! As the disclaimer on every page says, BaldingBlog is not a place for treatment advice or diagnosis. If the readers want to discuss their issues on a professional basis, they can always make an appointment and see me.

I will post an interesting excerpt from the 1997 FDA Drug Evaluation Hearing that you quote (the last sentence particularly worth noting):

“We attempted to obtain followup on all patients reporting sexually-related adverse experiences. Of the 36 patients on finasteride reporting these adverse experiences, 21 reported resolution of the adverse event while continuing finasteride therapy. Seven reported resolution following discontinuation from the study, and seven had persistence of the adverse event while continuing in the study on finasteride therapy. The pattern for patients on placebo was essentially similar, with most patients resolving either on or off drug, four patients reported persistence of the adverse event while remaining on placebo therapy.”

Dear Drs,

I was wondering which is the difference between “scalp DHT” and “serum DHT”. I guess “scalp DHT” needs “serum DHT” concentration to reach the scalp; am I right? Then, what means in the dutasteride/finasteride studies the differentiation of “scalp DHT” and “serum DHT”?

I know Avidart inhibits, 90% of serum DHT and 55% of scalp DHT, what it mean? The 55% is inhibited from the total DHT or from the 10% (respect the 90% serum inhibit)?

Thank you.

When a drug like finasteride is introduced into the body, it works its way through all of the fluid systems of your body. In theory, almost every cell in your body gets exposed to the drug and some of the cells will do something to the drug. So when you take this finasteride pill, 50% of it will remain in your blood stream after 4-6 hours, and every 4-6 hours the concentration halves.

The drug then works its way into the body fluids around the cells, and it may (finasteride does) attach to the hair follicles and the skin of the scalp. Slowly this process reverses (probably about a week), as the drug does its job on the individual hair follicles, minimizing the DHT. This DHT working, becomes less effective because of the competition for the sites in the cell. That is a very simplified way to explain how it works.

As I’ve said before, I am not a biochemist. I really do not know how scalp DHT or serum DHT are measured.

Is it true that Finasteride in Humans would reduce important Neuroactive Steroids like for example allopregnanolone? I know there was already a post about this in the past but that was about rats. In rats, Finasteride blocks both type I and II 5α-reductase whereas in humans inhibits only type II which it seems is not present in the brain unlike type I. I would appreciate your opinion about the following two studies:

Link 1: Finasteride Treatment and Neuroactive Steroid Formation (PDF file)

Link 2: The influence of low dose finasteride, a type II 5α-reductase inhibitor, on circulating neuroactive steroids

I do not think I can add much here, as I am not a biochemist. Mood changes have been associated with finasteride and depression has been reported, but I’m unclear on specifics beyond that.

The 1st link is a study of 20 men with an average age of 69.5 years that took 5mg finasteride. The 2nd link is a study of a dozen men that took the 1mg finasteride with no listed ages that I see. Both studies are small and offer nothing definitive, using words like “probably” and “might”.

This should go without saying, but finasteride is an elective medication with some rare side effect possibilities and is available by prescription only. Hundreds of other medications also come with side effect risks, and you must talk with your doctor about these risks and benefits so you can make an informed decision.