Finasteride, Low Sperm Count, Pregnancy And Child Deformities
This is an excerpt from the FDA website from 2010 on finasteride (https://www.accessdata.fda.gov/drugsatfda_docs/label/2011/020788s018lbl.pdf). Dr. Ed Epstein, from the Bosley Medical Group is a urologist by training and has kept up on the latest information on the impact or lack of impact of the drug finasteride on risks for an unborn fetus. “I am not aware of new studies on amounts of finasteride in semen or vaginal absorption data” that reflect increased risks for fetal abnormalities induced by finasteride other than what is written in the FDA white paper referenced above.
Some doctors are concerned that patients who go on finasteride should get semen analysis to keep track of semen levels in case these level dropped while a patient was on the drug finasteride. Dr. Epstein said: “Concerning getting semen analysis on child bearing age men starting finasteride, I totally disagree. Typically a male infertility workup is suggested after one year of unprotected intercourse. The subgroup of men who have low sperm counts on finasteride are those with preexisting conditions and appear to respond to discontinuation of finasteride.”In other words, he feels that a young man should not worry about either low semen counts caused by finasteride, but that they could always stop the drug and if there was a causal relationship, it would reverse. He also suggested than men with low sperm counts while on finasteride, probably had it before they started the drug and should get any low sperm count evaluated by an expert.
The FDA while paper referenced above showed that studies on semen in sperm were either not present or when present were so low as it not cause a risk to a pregnant woman or a woman who is expecting to become pregnant. “Semen levels have been measured in 35 men taking finasteride 1 mg/day for 6 weeks. In 60% (21 of 35) of the samples, finasteride levels were undetectable (<0.2 ng/mL). The mean finasteride level was 0.26 ng/mL and the highest level measured was 1.52 ng/mL. Using the highest semen level measured and assuming 100% absorption from a 5-mL ejaculate per day, human exposure through vaginal absorption would be up to 7.6 ng per day, which is 750 times lower than the exposure from the no-effect dose for developmental abnormalities in Rhesus monkeys and 650-fold less than the dose of finasteride (5 ?g) that had no effect on circulating DHT levels in men”Another opinion can be found here: https://www.medpagetoday.com/Endocrinology/Infertility/41424
Dr. Rassman. This is a very serious question:
-Why we are in 2016 and people with MPB don’t have a better and a safer alternative to Finasteride?
While well-intentioned, your urology expert did not clarify this area well for the non-medical reader. I am a physician-scientist who has been in the drug development industry for over 30 years, so I would like to add.
This is not an FDA “white” paper but the official FDA package insert (i.e.. label) that comes with every Propecia prescription given to a patient by a pharmacist. In other words, your readers should know that this is given to everyone receiving this drug – and should be read as a starting point. The FDA web site is a publicly available website (www.fda.gov). The above FDA label cited is from 2010; the current (2014) label is available at
https://www.accessdata.fda.gov/drugsatfda_docs/label/2014/020788s024lbl.pdf
While package inserts summarize important studies, the scientific literature has space to describe them in more detail. The best, controlled study on effect of finasteride on sperm parameters (and discontinuation) has been published and is at:
https://www.ncbi.nlm.nih.gov/pubmed/17299062
Most importantly, the issue of how a drug affects sperm (whether it lowers sperm count and contributes to infertility) is different, of course, than the issue of whether a drug causes birth defects (“teratogenicity”). The expert statement “I am not aware of new studies on amounts of finasteride in semen or vaginal absorption data that reflect increased risks for fetal abnormalities induced by finasteride other than what is written in the FDA white paper referenced above” is incomplete. Again, this is not a ”white paper” again, it is a package insert (i.e., drug label). However, finasteride is classified as a “Pregnancy class X” drug by the FDA to signify that it produces significant birth defects in woman exposed to the drug. This is indisputable and is based on the extensive animal research required before a drug can be used in humans – and is the basis for the massive warning on the label (package insert) prohibiting use and exposure in women. What the urology expert is getting at is the continued misunderstanding among bloggers that a terataogenic drug (a drug that can cause birth defects when taken by pregnancy women) may cause birth defects when taken by a man whose sperm then is transferred to a pregnant women. AT PRESENT, NO EVIDENCE EXISTS SHOWING THAT PATERNAL (MALE) EXPOSURE DIRECTLY INCREASES RISK OF BIRTH DEFECTS FROM ANY DRUG, INCLUDING DRUGS THAT ARE HIGHLY TERATOGENIC IN WOMEN (eg ACCUTANE, etc). In the case of finasteride, it may just be related to the low vaginal exposures from animal experiments mentioned in the blog or to something else. And if new evidence was ever to prove different, the first place would be the FDA label and scientific literature, all publicly available.
A nice summary of the teratogenicity studies that was required as part of the basis of approval of Propecia can be found at:
https://www.accessdata.fda.gov/drugsatfda_docs/nda/97/020788_propecia_toc.cfm