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Learn MoreCan blood tests reliably determine the risk of sexual side effects from hair loss drugs? Low-quality evidence (i.e., anecdotes and observational studies) suggest, in men, that low levels of free testosterone and/or high levels of sex hormone binding globulin are correlated with higher rates of sexual dysfunction. As such, some clinicians have argued that free testosterone and sex hormone binding globulin may act as proxies to determining side effect risks from hair loss drugs – though the evidence here is extremely limited. Interestingly, blood tests are a better predictor of another side effect from these drugs: gynecomastia (i.e., the growth of male breast tissue). Read on to learn how estrogen and prolactin levels might help give an early indication of your risks for this side effect.
Finasteride and dutasteride are drugs that lower the hormone dihydrotestosterone (DHT), which is a hormone that is causally linked to both benign prostatic hyperplasia and male pattern hair loss. While both drugs tend to be effective hair loss treatments for men, they do come with a risk of side effects –most commonly sexual side effects and the growth of male breast tissue (gynecomastia).
These side effects are believed to occur because of finasteride and dutasteride’s inhibitory effects on 5-alpha reductase – an enzyme that helps convert free testosterone into dihydrotestosterone. By inhibiting this enzyme, finasteride and dutasteride are able to therapeutically lower DHT levels to improve the symptoms of an enlarged prostate and/or regrow hair. However, the inhibition of 5-alpha reductase can come with undesired side effects in 5-15% of men using these drugs – mainly due to the hormonal shifts that occur throughout the body when 5-alpha reductase activity is suppressed.
Based on clinical data (so far), there aren’t yet reliable blood tests to determine someone’s risk of sexual side effects from drugs like finasteride or dutasteride. Having said that, clinical studies show that men who have low levels of free testosterone and/or high levels of sex hormone binding globulin tend to be at the highest risk of “low libido”.[1]https://pubmed.ncbi.nlm.nih.gov/25800960/
As such, some clinicians have argued (anecdotally) that patients reporting side effects from finasteride and dutasteride tend to already have hormonal imbalances associated with reduced libido prior to starting the drug. As such, these same clinicians sometimes suggest that by taking measures to (1) improve free testosterone, and/or (2) reduce sex hormone binding globulin – these men tend to see improvements to libido and, as a consequence, sport a higher tolerability for drugs like finasteride and dutasteride.
So, if you’re worried about sexual side effects from finasteride and dutasteride, there is at least some anecdotal and observational evidence suggesting that testing free testosterone and sex hormone binding globulin might help to predict your actual risk tolerance. With that said, it’s important to note that the data here remains limited.
Gynecomastia is the growth of male breast tissue. It results from prolonged, elevated levels of the hormones prolactin and/or estrogen.
When it comes to the use of finasteride and dutasteride, blood tests can likely be used to determine someone’s risk of gynecomastia from both drugs.
Gynecomastia is estimated to affect between 0.25% to 1% of healthy people using 5-alpha reductase inhibitors, with 5-year retrospective studies in men with benign prostate hyperplasia suggesting an incidence of up to 3% to 5%. [2]https://pubmed.ncbi.nlm.nih.gov/23067029/
Interestingly, those who start finasteride and/or dutasteride while already having elevated levels of prolactin and estrogen might be at a higher risk of developing gynecomastia. This is because drugs like finasteride and dutasteride can raise blood levels of both testosterone and/or estrogen by 10-20%, depending on the dose.[3]https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/020788s020s021s023lbl.pdf[4]https://journals.sagepub.com/doi/abs/10.1177/2051415820926301 Consequently, as blood levels of estrogen and/or prolactin rise, these hormones can stimulate the growth of ductal tissue and alveolar differentiation – both of which relate to the growth of male breast tissue.[5]https://www.ncbi.nlm.nih.gov/books/NBK279105/
So, for those starting the drug with borderline-high estrogen, the additional lift in estrogen levels may put someone in the “danger zone” for gynecomastia.
For peace of mind, people can always order blood tests for prolactin and estrogen prior to starting finasteride or dutasteride. Additional tests can be performed further down the line.
If levels are within range, the risk of gynecomastia is likely much lower. This can be done with a primary care physician. Those based in the U.S. (and other countries that offer direct-to-consumer lab testing), can order tests through the links below.
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While it’s up for debate if blood tests can actually predict someone’s risk of sexual side effects from finasteride or dutasteride, there is evidence that estrogen and prolactin levels pre-hair loss drugs might give some insights into the risk of developing gynecomastia. The totality of evidence suggests that finasteride and dutasteride may raise estrogen levels by 10-20%. Therefore, if your pre-finasteride levels of estrogen and/or prolactin are within 10-20% of the upper limit, it’s probably best to find ways to lower these levels before committing to the drug.
Diet, lifestyle, and environmental changes are often enough to normalize these hormones in many men.
The best predictor of hair regrowth from finasteride comes not from a blood test, but from an accurate hair loss diagnosis. After all, two-year clinical studies show that in otherwise healthy men with androgenic alopecia that presents in its standard horseshoe pattern, response rates for finasteride tend to hover around 80-90%.[9]https://www.sciencedirect.com/science/article/pii/S0022202X15529357
Recently, marketers have begun pushing genetic testing to determine someone’s response rate to finasteride and dutasteride. Preliminary data from poorly designed clinical studies suggests that perhaps there are some genes associated with higher-magnitude responses from both drugs, and also a better success rate. For instance, one study suggested that genetic “CAG repeat score” might help determine the response rate to finasteride, and that this data could be collected through blood draws.[10]https://pubmed.ncbi.nlm.nih.gov/31949455/
But again, the evidence here is limited and preliminary. Given the overwhelmingly high odds of a response to finasteride overall, we tend to place more weight on an accurate diagnosis than on genetic testings for either drug.
References[+]
↑1 | https://pubmed.ncbi.nlm.nih.gov/25800960/ |
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↑2 | https://pubmed.ncbi.nlm.nih.gov/23067029/ |
↑3 | https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/020788s020s021s023lbl.pdf |
↑4 | https://journals.sagepub.com/doi/abs/10.1177/2051415820926301 |
↑5, ↑6 | https://www.ncbi.nlm.nih.gov/books/NBK279105/ |
↑7 | truehealthlabs.com/product/prolactin |
↑8 | truehealthlabs.com/product/estradiol-e2 |
↑9 | https://www.sciencedirect.com/science/article/pii/S0022202X15529357 |
↑10 | https://pubmed.ncbi.nlm.nih.gov/31949455/ |
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