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Learn MoreDutasteride is one of the most powerful treatments for male pattern hair loss, offering faster and greater regrowth than finasteride with comparable or even lower rates of sexual side effects. This comprehensive guide explains how dutasteride works, how it compares to finasteride in clinical trials, the true risks and benefits, optimal dosing, and what long-term research suggests about its safety and effectiveness.
Oral finasteride is one of the most widely prescribed treatments for androgenic alopecia (AGA). The drug is a type II 5a-reductase inhibitor, which means it helps reduce dihydrotestosterone (DHT) – the major hormone implicated in pattern hair loss.
At the same time, finasteride isn’t the most powerful DHT-reducing drug available. In fact, there’s a drug that can reduce up to 50% more DHT than finasteride. It’s called dutasteride – and for those who are interested in unlocking another level of hair regrowth, it might be the right choice for them.
So, how much hair regrowth can we expect from dutasteride? Does dutasteride outperform finasteride? How does this drug stack up in terms of side effects? And is there anything else we should know before making the “leap” to a more powerful DHT reducer?
This ultimate guide uncovers the answers.
Interestingly, despite dutasteride’s stronger DHT-reducing effects, this drug doesn’t seem to come with an increased risk of cognitive or sexual side effects – at least when compared to finasteride. In fact, some research indicates that dutasteride might be a better option altogether.
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Dutasteride is a drug used most commonly in the treatment of benign prostate hyperplasia. But it’s also used off-label as a treatment for male pattern hair loss.
Dutasteride is a dual 5α-reductase inhibitor, meaning that the drug inhibits both the type I and type II isoforms of the 5α-reductase enzyme. This makes it unique from finasteride, a drug that only inhibits type II 5-alpha reductase. And since dutasteride inhibits more 5-alpha reductase, it can reduce DHT levels much more effectively than finasteride. Specifically, dutasteride appears to reduce systemic DHT levels by 92-96% and scalp DHT levels by 51-79%; whereas finasteride reduces systemic DHT by 60-70% and scalp DHT by 50-60%.
When it comes to hair regrowth, short-term studies suggest that dutasteride is anywhere from 2-5 times more effective than finasteride (depending on the dose). However, the studies comparing dutasteride and finasteride are generally over six-month periods. This may not make for a fair comparison, as finasteride tends to take two years to achieve its full effect.
Despite being more effective, dutasteride doesn’t seem to come with an increased risk of side effects relative to finasteride. In fact, in some instances, dutasteride’s risk of side effects is actually lower than that of finasteride… despite a more substantial decrease in systemic DHT. While it’s debated why this is the case, one explanation might involve dutasteride’s molecular weight, which is much heavier than finasteride, so much so that the drug cannot likely cross the blood-brain barrier.
If you opt for dutasteride, research suggests that for treating pattern hair loss, a dosage of 0.5 mg daily is best. At this dose, dutasteride seems to outperform finasteride and not result in long-term DHT suppression after stopping the medication. At higher dosages (i.e., 2.5 mg daily), DHT can remain suppressed for 6+ even after stopping treatment.
Dutasteride is a drug used to treat a variety of androgen-related problems in men. It’s branded as Avodart®, and it’s most commonly prescribed for the treatment of benign prostate hyperplasia (BPH). But since it’s such a powerful DHT-reducing drug, many doctors will prescribe it “off-label” to treat male pattern hair loss, or androgenic alopecia (AGA).
There are dozens of ways to reduce DHT levels – from lowering overall testosterone to inhibiting enzymes to blocking androgen receptors to increasing DHT metabolism (to name just a few). Some of these methods are safe; some of them are dangerous; some of them aren’t studied well enough in humans to consider trying.
The good news? Dutasteride reduces DHT through one of the better studied (and safer) ways… and similarly to finasteride. It inhibits the enzyme that converts testosterone into DHT: the 5-alpha reductase enzyme.
Dutasteride differs from finasteride in one key way: it reduces more DHT than finasteride. This is because dutasteride inhibits both type I and type II 5-alpha reductase, whereas finasteride inhibits only the type II 5-alpha reductase enzyme.
Both isoforms of 5-alpha reductase – type I and type II – help convert free testosterone into DHT. However, both function at different pH levels, and both are found in different tissue locations throughout the body:[1]Gerst, C., Dalko, M., Pichaud, P., Galey, J.B., Buan, B., Bernard, B.A. (2002). Type-1 steroid 5 alpha-reductase is functionally active in the hair follicle as evidenced by new selective inhibitors … Continue reading
When it comes to skin tissues near and within hair follicles, the type I isoform dominates… at least in terms of the quantity of enzymes present. But interestingly, it’s the type II isoform that tends to get all of the attention when it comes to male pattern hair loss (AGA).
This is because type II 5-alpha reductase activity in the scalp seems to be a prerequisite for male AGA. This was confirmed back in the 1970s, when studies showed that men born without the genes that make type II 5-alpha reductase also never lose their hair to AGA later in life.[2]Imperato-McGinley, J., Miller, M., Wilson, J.D., Peterson, R.E., Shackleton, C., Gajdusek, D.C. (1991). A cluster of male pseudohermaphrodites with 5-alpha-reductase deficiency in Papua New Guinea. … Continue reading
In fact, these studies were what built the basis for finasteride – a drug that is now the most popular (and most studied) FDA-approved treatment for AGA. After all, finasteride is a type II 5a-reductase inhibitor, and it’s this specific enzyme that seems directly implicated in DHT-related hair follicle miniaturization.
Dutasteride does the exact same thing as finasteride – except it also inhibits both the type I and type II isoforms of 5-alpha reductase. And, since the body’s total DHT levels are closely linked to the sum of type I and type II isoform activity, dutasteride can technically reduce more DHT than finasteride – around 50% more (depending on the tissue being measured).
Maybe.
Several studies have demonstrated that dutasteride reduces DHT levels more than finasteride– at least in tests done on serum (i.e., blood) levels of DHT.[3]Bramson, H.M., Hermann, D., Batchelor, K.W., Lee, F.W., James, M.K., Frye, S.V. (1997). Unique preclinical characteristics of GG745, a potent dual inhibitor of 5AR. The Journal of pharmacology and … Continue reading In fact, a study found that while finasteride reduces serum DHT levels by ~70%, dutasteride reduces them by ~90% (depending on the dose):[4]Clark, R.V., Hermann, D.J., Cunningham, G.R., Wilson, T.H., Morrill, B.B., Hobbs, S. (2004). Marked Suppression of Dihydrotestosterone in Men with Benign Prostatic Hyperplasia by Dutasteride, a Dual … Continue reading

Figure 1: Change in DHT from baseline. Dutasteride vs. finasteride.[5]Clark, R.V., Hermann, D.J., Cunningham, G.R., Wilson, T.H., Morrill, B.B., Hobbs, S. (2004). Marked Suppression of Dihydrotestosterone in Men with Benign Prostatic Hyperplasia by Dutasteride, a Dual … Continue reading
But do these results also hold for scalp DHT – the region where DHT reduction matters most?
At least so far, the data suggests yes. Scalp biopsy studies on men taking dutasteride versus finasteride show that at certain dosages, dutasteride reduces much more DHT.[6]Olsen, E.A., Hordinsky, M., Whiting, D., Stough, D., Hobbs, S., Ellis, M.L., Wilson, T., Rittmaster, R.S., Dutasteride Alopecia Research Team. (2006). The importance of dual 5alpha-reductase … Continue reading
Again, this makes logical sense. After all, type I and type II 5-alpha reductase are found inside and surrounding our hair follicles. And since dutasteride reduces both of these enzymes, this drug should technically reduce more scalp DHT than finasteride.
Thus, it’s totally rational to presume that since:
Then all else equal, dutasteride should be a more effective hair loss drug.
But is this what the clinical research suggests? In order to answer this question, we’ll need to evaluate dutasteride’s hair-regrowing abilities against its risk profile: its reports of side effects, and how this does (or doesn’t) differ from finasteride.
While there have been a handful of studies that have researched dutasteride, there are only four studies that provide data relevant to this question. We’ve compiled these studies as well as their methodologies, results, and conclusions into the chart below.
|
Studies Comparing the Effectiveness of Dutasteride and Finasteride |
|||||||
|
High quality study? |
Daily dosages used | Length of study | Average hair count changes with dutasteride (%) | Average hair count changes with finasteride (%) | Any other notable results? |
Superior treatment? |
|
| Study #1.[7]Olsen, E.A., Hordinsky, M., Whiting, D., Stough, D., Hobbs, S., Ellis, M.L., Wilson, T., Rittmaster, R.S., Dutasteride Alopecia Research Team. (2006). The importance of dual 5alpha-reductase … Continue reading |
Yes, randomized, placebo-controlled |
Dutasteride:
0.1 mg, 0.5 mg, 2.5 mg Finasteride: 5 mg |
24 weeks | 0.1 mg: 8.6%
0.5 mg: 10.1% 2.5 mg: 11.3% |
8.3% | The amount of patients who achieved at least 10% increase in hair count increases with dutasteride dose. In other words, as dose increased, so did the amount of patients who achieved at least 10% increase in density |
Dutasteride 0.5 mg and 2.5 mg |
| Study #2.[8]Shanshanwal, S.J.S., Dhurat, R.S. (2017). Superiority of dutasteride over finasteride in hair regrowth and reversal of miniaturization in men with androgenetic alopecia: A randomized controlled … Continue reading |
Yes, randomized controlled trial |
Dutasteride: 0.5 mg
Finasteride: 1 mg |
24 weeks | 11% | 2% | 24% increase in the number of thick, terminal hairs with dutasteride vs. 4% with finasteride |
Dutasteride |
| Study #3.[9]Harcha, W.G., Martinez, B.J., Tsai, T-F., Katsuoka, K., Kawashima, M., Tsuboi, R., Barnes, A., Ferron-Brady, G., Chetty, D. (2014). A randomized, active- and placebo-controlled study of the efficacy … Continue reading |
Yes, randomized, placebo-controlled trial |
Dutasteride: 0.02 mg
0.1 mg 0.5 mg Finasteride: 1 mg |
24 weeks | 0.02 mg: 2.3%
0.1 mg: 8% 0.5 mg: 11.7% |
7.5% | 0.5 mg dosage of dutasteride was superior to 1mg finasteride in increasing hair thickness. |
Dutasteride at 0.5 mg |
| Study #4.[10]Choi, G-S., Sim, W-Y., Kang, H., Huh, C.H., Lee, Y.W., Shantakumar, S., Ho, Y-F., Oh, E-J., Duh, M.S., Cheng, W.Y., Bobbili, P., Thompson-Leduc, P., Ong, G. (2022). Long-Term Effectiveness and Safety … Continue reading |
Yes, multicenter long-term retrospective study |
Dutasteride: 0.5 mg/day
Finasteride: 1 mg/day |
≥3 years (mean 3.4 years) | Hair count data not reported (too sparse; BASP classification used instead) | N/A | Dutasteride is significantly superior across BASP basic, basic M, and V types. |
Dutasteride |
Here’s what these results tell us about dutasteride:
The most interesting finding, though? Despite the fact that 2.5 mg of dutasteride reduces scalp DHT by almost 30% more than 0.5 mg, this doesn’t necessarily translate to more hair regrowth. In fact, the difference in efficacy between the two doses doesn’t even reach statistical significance.
This suggests that even when we reduce DHT to a greater degree and where it’s most important (the scalp), we don’t necessarily see evidence that this increases efficacy. In other words, maybe reductions to scalp DHT don’t always correlate to increased hair regrowth. Maybe there is a degree of pattern hair loss that stems directly from serum DHT, not just scalp DHT. Dr. George Cotsarelis (of PGD2 fame) has mentioned this before in interviews. Hopefully, with more research, we’ll have a clearer answer.
Nonetheless, these trials still tell us that dutasteride, at various doses, is more effective than finasteride – and anywhere between 2- and 5-fold more effective (depending on the doses).
The one caveat to all but one of these comparative studies is that they were conducted over a 24-week period. This makes it difficult to discern just how effective dutasteride versus finasteride is… mainly because finasteride is notoriously slow at regrowing hair.
For instance, studies show that men taking finasteride generally just start to see improvements around the 3-6 month mark.[11]Price, V.H., Menefee, E., Sanchez, M., Ruane, P., Kaufman, K.D. (2002). Changes in hair weight and hair count in men with androgenetic alopecia after treatment with finasteride, 1 mg, daily. Journal … Continue reading These studies also show that finasteride takes 2+ years to take full effect on our hair, with scalp hair counts increasing an average of 10% over this two-year period before plateauing.
That’s 96 weeks for finasteride to demonstrate full efficacy, not 24 weeks – the length of time for all studies comparing dutasteride to finasteride. If, for unforeseen reasons, dutasteride efficacy plateaus after six months, then maybe finasteride catches up in the long run. If dutasteride continues its trajectory at the same pace as finasteride, then maybe it’s actually 2- to 5-times more effective than finasteride… and we just don’t know it yet.
In any case, we can surmise that:
Regardless, there’s still one piece to the puzzle we haven’t examined yet: the incidence of side effects.
After all, if dutasteride is 200%-500% more effective than finasteride, but it also comes with a 200-500% increase in side effects… that may defeat the point of using it. After all, for those dealing with hair loss, we’re always trying to find treatments that strike the right balance between effectiveness versus the risk of side effects.
This begs the question: given that dutasteride reduces more DHT and seems much more effective than finasteride, does it also come with an increased risk of side effects?
The answers might surprise you.
We already know that dutasteride reduces serum DHT by larger amounts than finasteride. So, does this come with a higher risk of sexual side effects?
Several studies have attempted to answer this question. Here’s what they have to say:
|
Incidence of Side Effects |
|||||||
| Average incidence of total side effects among dutasteride group vs. finasteride group | Decreased libido (%) | Ejaculation disorders (%) | Erectile dysfunction (%) | Breast enlargement (%) | Breast tenderness (%) | Total serum DHT reduction | |
|
Study #1 |
4.6% vs. 2.6% | Dutasteride
0.1 mg: 3% 0.5 mg: 1% 2.5 mg: 13% Finasteride 5 mg: 4% |
Dutasteride
0.1 mg: 4% 0.5 mg: 1% 2.5 mg: 1% Finasteride 5 mg: 3% |
Dutasteride
0.1 mg: 0% 0.5 mg: 0% 2.5 mg: 0% Finasteride 5 mg: 1% |
N/A | N/A | Dutasteride
0.1 mg: 69.8% 0.5 mg: 92% 2.5 mg: 96.4% Finasteride 5 mg: 73% |
| Study #2 |
10% vs 10% |
N/A |
N/A | N/A | N/A | N/A |
N/A |
| Study #3 |
11.5% vs. 13.4% |
Dutasteride 0.02 mg: 8.1% 0.1 mg: 6.9% 0.5 mg: 4.9% Finasteride 1 mg: 6.7% |
Dutasteride
0.02 mg: 2.2% 0.1 mg: 4.8% 0.5 mg: 3.3% Finasteride 1 mg: 3.9% |
Dutasteride
0.02 mg: 4.3% 0.1 mg: 3.7% 0.5 mg: 5.4% Finasteride 1 mg: 5.6% |
Dutasteride
0.02 mg: 0% 0.1 mg: 0.5% 0.5 mg: 0.5% Finasteride 1 mg: 0.6% |
Dutasteride
0.02 mg: 0.5% 0.1 mg: 0.5% 0.5 mg: 0% Finasteride 1 mg: 0% |
N/A |
| Study #4 | 7.6% vs. 10.5% | Dutasteride: 1.2%
Finasteride: 0.7% |
N/A | Dutasteride: 0.4%
Finasteride 0% |
N/A | N/A |
N/A |
When we examine this data, here’s what we find:
Moreover, here are some other findings from these studies that are not reported within that table:
Again, these side effects are only derived from clinical trials conducted over the course of 6 months. So, these studies alone don’t really tell us what might happen over longer periods of use. And considering that, much like finasteride, dutasteride likely has to be taken for a lifetime to sustain its effectiveness – this really matters.
So, is there any insight as to what the incidence of side effects might be after 6 months?
Well, when we examine the research, we find that the incidence of side effects actually decrease over time with dutasteride use. For example, one four-year trial employing a daily 0.5 mg dose demonstrated that the incidence of side effects decreased from 6% in year one to a marginal 0.4% by year four.
We could argue that this shift is simply a consequence of our olfactory wiring + change blindness – whereby we have a tendency to only notice changes (i.e., new smells) when they first arrive, and whereby if changes occur too slowly, we generally won’t notice them at all.
At the same time, we could also argue that with long-term use of dutasteride, our bodies simply rewire and find ways for testosterone (and other hormones) to replace the roles previously fulfilled by DHT. This is generally how the body works – there are dozens of “fallback” mechanisms in case a vitamin, mineral, or hormone is missing. In other words, we’re more durable than we think.
It’s puzzling that dutasteride seems to come with an equivalent (or lower) risk of side effects… and that over time, these side effects seem to decrease more than with finasteride. This is in spite of dutasteride reducing much more DHT than finasteride. What could explain these paradoxical findings?
Well, one could argue that maybe DHT reduction isn’t necessarily as great of a predictor of side effects as we think. But, there is one additional explanation for these findings, and one that’s much more interesting to explore…
It’s the actual structure of the dutasteride molecule itself… and the fact that the size of this molecule might greatly reduce the drug’s accessibility to certain organs within our body. Specifically, the brain.
The blood is the ultimate transporter for nutrition. It’s also the transporter for oral drugs.
During circulation, the blood will deposit various compounds into cells, where they then elicit their specific effects. However, in the brain, it isn’t quite as simple. This is because of a membrane called the blood-brain barrier (BBB).
This membrane is comprised of cells that maintain tight cellular junctions. In other words, these cells are packed in close together with minimal space between each cell. As such, only very small compounds or compounds that can bind to specific entry receptors on the BBB can pass through the membrane into the brain.
In terms of molecular size, a given compound has to be smaller than 400 daltons (a measurement of mass) to traverse past this membrane. If any larger? The compounds cannot theoretically enter the brain through blood transportation. Therefore, these molecules may not be able to elicit their specific effects on the brain.
So, what does this have to do with dutasteride and finasteride? And why might this explain the difference in the incidence of side effects?
Interestingly, while both finasteride and dutasteride act similarly with respect to DHT reduction, they are actually quite different on a molecular level – particularly regarding their molecular weight.
While finasteride is only 372 daltons, dutasteride is 528 daltons.
The biggest difference here? Finasteride is small enough to pass through the tight junctions of the blood-brain barrier (BBB). Dutasteride isn’t.
As such, finasteride may elicit effects on the brain itself, which may precipitate major effects on sexual and mental side effects. In contrast, dutasteride may have less of a direct effect on the brain… or a reduced capacity to effect androgen metabolism in the brain relative to finasteride.
Again, this is all hypothetical, and the science is still very much debated. For instance, this study on mice found that dutasteride does influence androgen metabolism in the brain (although that study also found that dutasteride had neuroprotective effects on mice, helping to stave off Parkinsons).[12]Litim, N., Morissette, M., Caruso, D., Melcangi, R.C., Di Paolo, T. (2017). Effect of the 5α-reductase enzyme inhibitor dutasteride in the brain of intact and Parkinsonian mice. The Journal of … Continue reading
At the same time, with dutasteride use, some reduction in brain androgen activity is technically to be expected… even if dutasteride doesn’t technically enter the brain. Why? Because 5-alpha reductase can be transported via the blood (where dutasteride does elicit an effect). And if blood entering the brain has less 5-alpha reductase activity, then this would also change androgen activity in the tissues where that blood eventually gets transported (i.e., the brain).
In any case, our suggestion here is that dutasteride itself has a harder time entering into brain tissues, and that this is why it may confer to a lower risk of side effects (despite more DHT reduction) than finasteride.
So, despite the fact that dutasteride has a more powerful effect on both systemic DHT than finasteride, the lower or on-par incidence of side effects may simply be due to dutasteride’s molecular weight… and how this dampens the drug’s ability to enter brain tissue.
Thus, it appears we can derive faster, more substantial hair regrowth in AGA… all with the same or even lower risk of side effects. Moreover, we can even leverage dosages to both maximize regrowth and minimize the risk of side effects.
It goes without saying that dutasteride is a drug that is appropriate only for one specific kind of hair loss: androgenic alopecia (pattern hair loss). It also goes without saying that this drug is studied almost exclusively on men. Therefore, men with pattern hair loss are the best candidates.
So, for men with pattern hair loss, what’s the best dose?
Well, revisiting data from the three studies comparing dutasteride to finasteride, we see that larger doses of dutasteride are generally no more effective than a dosage of 0.5 mg. And based on the safety data, this appears to be one of the safest doses, too.
Specifically, the studies show that 0.5 mg can increase hair counts by anywhere between 10 and 11.5% in 6 months, with just a 1.3% overall risk of sexual side effects. In contrast, finasteride’s risk of side effects ranges from 2-13% with regrowth rates only around 7-8%.
So, a daily dose of 0.5 mg of dutasteride orally seems to both maximize hair regrowth and minimize the risk of side effects. Moreover, it does so in a safer and more effective manner than both 1 mg and 5 mg doses of finasteride.
Finally, a 0.5 mg daily dose is also a dose that allows for our DHT levels to bounce back within six months after stopping the drug. Because of dutasteride’s longer half-life, it tends to exert a longer effect in the body. At higher dosages, it seems as though DHT levels remain suppressed for the majority of users, at least for six months of quitting. A 0.5 mg daily dose prevents this from happening, allowing DHT to return to 80% of baseline levels after six months of cessation, and likely 100% baseline levels a few months thereafter.
If you’d like an example of a long-term dutasteride user, look no further than Ashton Kutcher.[13]Team Coco. (2018). Ashton Kutcher’s Hair Is Starting To Go | CONAN on TBS. Available at: https://www.youtube.com/watch?v=Wv9gu1zJdRo (Accessed: November 2025)
During his 2018 interview with Konan, he revealed that he had used the drug for years, only hopping off to father his children (born in 2014 and 2016). It seems to have worked wonderfully for him. Just look at his hairline in 1998 versus today. While there’s no information about whether he has returned to using dutasteride, it also doesn’t seem like his hairline has changed much over the past several years anyway.
Finasteride is one of the most powerful and frequently used therapies for AGA. However, emerging research indicates that dutasteride may have a clear advantage over finasteride, at least in terms of (1) scalp DHT reduction, (2) hair regrowth, and (3) side effects.
Specifically, a 0.5 mg daily dose appears to increase hair density by anywhere between 10 and 11.5% over the course of 6 months, which happens to be the hair count increase expected from 2+ years of finasteride use. Moreover, dutasteride seems to achieve this without greatly increasing someone’s risk of cognitive or sexual side effects. In fact, the incidence of side effects with dutasteride seems to decrease over time, with one study demonstrating just a 0.4% incidence of side effects with four years of use.
While higher doses (up to 2.5 mg) do increase the response rate to the treatment, they don’t appear to increase the average amount of hair someone regrows. Moreover, they also increase the likelihood of long-term DHT suppression post-treatment. As such, a 0.5 mg daily dose seems like the best approach when utilizing this drug for hair regrowth.
Considering these overall advantages, cost-effectiveness, and accessibility, dutasteride shows considerable promise for men with AGA.
If you’re interested in taking dutasteride or swapping out your oral finasteride, talk with your doctor about the research. If you’re a good candidate for the drug, ask them to prescribe you a 0.5 mg daily dose, and please keep us posted with your results!
References[+]
| ↑1 | Gerst, C., Dalko, M., Pichaud, P., Galey, J.B., Buan, B., Bernard, B.A. (2002). Type-1 steroid 5 alpha-reductase is functionally active in the hair follicle as evidenced by new selective inhibitors of either type-1 or type-2 human steroid 5 alpha-reductase. Experimental Dermatology. 11(1). 52-58. Available at: https://doi.org/10.1034/j.1600-0625.2002.110106.x. |
|---|---|
| ↑2 | Imperato-McGinley, J., Miller, M., Wilson, J.D., Peterson, R.E., Shackleton, C., Gajdusek, D.C. (1991). A cluster of male pseudohermaphrodites with 5-alpha-reductase deficiency in Papua New Guinea. Clinical Endocrinology. 34(4). 293-298. Available at: https://doi.org/10.1111/j.1365-2265.1991.tb03769.x. |
| ↑3 | Bramson, H.M., Hermann, D., Batchelor, K.W., Lee, F.W., James, M.K., Frye, S.V. (1997). Unique preclinical characteristics of GG745, a potent dual inhibitor of 5AR. The Journal of pharmacology and experimental therapeutics. 282(3). 1496-1502. Available at: PMID 9316864 |
| ↑4, ↑5 | Clark, R.V., Hermann, D.J., Cunningham, G.R., Wilson, T.H., Morrill, B.B., Hobbs, S. (2004). Marked Suppression of Dihydrotestosterone in Men with Benign Prostatic Hyperplasia by Dutasteride, a Dual 5α-Reductase Inhibitor. The Journal of Clinical Endocrinology & Metabolism. 89(5). 2179-2184. Available at: https://doi.org/10.1210/jc.2003-030330 |
| ↑6, ↑7 | Olsen, E.A., Hordinsky, M., Whiting, D., Stough, D., Hobbs, S., Ellis, M.L., Wilson, T., Rittmaster, R.S., Dutasteride Alopecia Research Team. (2006). The importance of dual 5alpha-reductase inhibition in the treatment of male pattern hair loss: results of a randomized placebo-controlled study of dutasteride versus finasteride. Journal of the American Academy of Dermatology. 55(6). 1014-1023. Available at: https://doi.org/10.1016/j.jaad.2006.05.007 |
| ↑8 | Shanshanwal, S.J.S., Dhurat, R.S. (2017). Superiority of dutasteride over finasteride in hair regrowth and reversal of miniaturization in men with androgenetic alopecia: A randomized controlled open-label, evaluator-blinded study. Indian Journal of Dermatology, Venereology and Leprology. 83(1). 47-54. Available at: https://doi.org/10.4103/0378-6323.188652 |
| ↑9 | Harcha, W.G., Martinez, B.J., Tsai, T-F., Katsuoka, K., Kawashima, M., Tsuboi, R., Barnes, A., Ferron-Brady, G., Chetty, D. (2014). A randomized, active- and placebo-controlled study of the efficacy and safety of different doses of dutasteride versus placebo and finasteride in the treatment of male subjects with androgenetic alopecia. Journal of the American Academy of Dermatology. 70(3). 489-498. Available at: https://doi.org/10.1016/j.jaad.2013.10.049 |
| ↑10 | Choi, G-S., Sim, W-Y., Kang, H., Huh, C.H., Lee, Y.W., Shantakumar, S., Ho, Y-F., Oh, E-J., Duh, M.S., Cheng, W.Y., Bobbili, P., Thompson-Leduc, P., Ong, G. (2022). Long-Term Effectiveness and Safety of Dutasteride versus Finasteride in Patients with Male Androgenic Alopecia in South Korea: A Multicentre Chart Review Study. 34(5). 349-359. Available at: https://doi.org/10.5021/ad.22.027 |
| ↑11 | Price, V.H., Menefee, E., Sanchez, M., Ruane, P., Kaufman, K.D. (2002). Changes in hair weight and hair count in men with androgenetic alopecia after treatment with finasteride, 1 mg, daily. Journal of the American Academy of Dermatology. 46(4). 517-523. Available at: https://doi.org/10.1067/mjd.2002.120537 |
| ↑12 | Litim, N., Morissette, M., Caruso, D., Melcangi, R.C., Di Paolo, T. (2017). Effect of the 5α-reductase enzyme inhibitor dutasteride in the brain of intact and Parkinsonian mice. The Journal of Steroid Biochemistry and Molecular Biology. 174. 242-256. Available at: https://doi.org/10.1016/j.jsbmb.2017.09.021 |
| ↑13 | Team Coco. (2018). Ashton Kutcher’s Hair Is Starting To Go | CONAN on TBS. Available at: https://www.youtube.com/watch?v=Wv9gu1zJdRo (Accessed: November 2025) |
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