Potential side effects from Finasteride. Is Dutasteride any better?

I was interested in taking Finasteride to see if it helped with hair loss and also to limit localized DHEA to DHT conversion in my body (side stepping Testosterone to DHT conversion). I was prescribed 5mg daily, which is a lot, but I thought it would make side effects very apparent.

For me Finasteride was very stimulating physically and drove me to burn an extra 500 calories daily in exercise to wear myself down enough to sleep. It also gave me anxiety and insomnia. I only took 5mg doses for a couple of days before quartering the tablets into 1.24mg doses. Even at that dosage it was still too stimulating.

When I told my doctor about my issues with Finasteride and asked about trying Dutasteride, they said they operate the same way, so the issues I was having would be the same. Eventually I switched doctors and was prescribed 0.5mg Dutasteride – guess what? The side effects were entirely different in my case, and much more tolerable on Dutasteride. Personally Dutasteride makes me a little bit more tired during exercise and lowers my mood a little. Localized tissue production of DHT spikes during exercise, so that seems straight forward, and depression is a common side effect of both Finasteride and Dutasteride.

1. The first clue that Finasteride and Dutasteride are not flavors of the same thing is the dosage difference. Additionally the half life of Finasteride is 6-8 hours where as the half life of Dutasteride is 5 weeks.

Dutasteride is approved for the treatment of male androgenetic alopecia in South Korea and Japan at a dosage of 0.5 mg per day.[6][17] It has been found in several studies to improve hair growth in men more rapidly and to a greater extent than 2.5 mg/day finasteride.[6][18][19] The superior effectiveness of dutasteride relative to finasteride for this indication is considered to be related to the fact that the inhibition of 5α-reductase and consequent prevention of scalp DHT production is more complete with dutasteride.[18][1][20] This may be because of stronger binding to 5α-reductase type II relative to finasteride, rather than dual inhibition as type I is not typically found in scalp follicles.[21] Dutasteride is also used off-label in the treatment of female pattern hair loss.[22][23]


2. Dutasteride is also a more complete blocker than Finasteride.

Dutasteride belongs to a class of drugs called 5α-reductase inhibitors, which block the action of the 5α-reductase enzymes that convert testosterone into DHT.[41] It inhibits all three forms of 5α-reductase, and can decrease DHT levels in the blood by up to 98%.[1][42][43]


3. Finasteride is also found to be a potential treatment for ADHD, which probably explains why it was so stimulating to me.

Methods: Open‐field behaviors were evaluated by exploratory and motor behaviors. Dopamine and its metabolites were assayed by liquid chromatography‐mass spectrometry. Tyrosine hydroxylase mRNA and protein expressions were determined by real‐time qRT‐PCR and western blot, respectively.

Results: It was found that in adolescent male rats, administration of finasteride at doses of 25 and 50 mg/kg for 14 days dose dependently inhibited open‐field behaviors, reduced contents of dopamine and its metabolites in frontal cortex, hippocampus, caudate putamen, nucleus accumbens, and down‐regulated tyrosine hydroxylase mRNA and protein expressions in substantia nigra and ventral tegmental area. However, there was no significant change of these parameters in early developmental rats after finasteride treatment.

Conclusion: These results suggest that finasteride inhibits dopaminergic system and open‐field behaviors in adolescent male rats by inhibiting the conversion of testosterone to dihydrotestosterone, and imply finasteride as a potential therapeutic option for neuropsychiatric disorders associated with hyperactivities of dopaminergic system and androgen.


4. The adverse/long term side effect profile of Finasteride is very different than Dutasteride. Update: as was pointed out in the next reference, it’s possible Dutasteride is simply less popular/well studied as an explanation for different adverse/long term side effects.

Finasteride may cause persistent adverse sexual, neurological and physical effects in a subset of men.[13][14] This has been called post-finasteride syndrome, characterized by reported sexual and physical symptoms such as loss of libido, erectile dysfunction, ejaculatory disorders, reduction in penis size, penile curvature, reduced sensation, male breast enlargement, muscular atrophy, fatigue and severely dry skin. People with post-finasteride syndrome may experience depression and anxiety, cognitive impairment and suicidal thoughts.[14]

Post-finasteride syndrome may also have reduced levels of neurosteroids such as allopregnanolone in their cerebrospinal fluid. One study found that 1.4% developed persistent sexual dysfunction.[13]

A 2019 Reuters investigation showed that Merck found evidence of persistent side effects in their original clinical trials and did not disclose it in their warning label.[51][52] They uncovered court filings which demonstrated that Merck misrepresented Propecia’s safety record following clinical trials in the mid-late 1990s.[51]

In one deposition, Charlotte Merritt, who oversaw regulatory activity for Propecia, acknowledged that Merck changed Propecia’s label for sexual adverse events in 2002, four years after Propecia hit the market. The label changed from “resolution occurred in all men who discontinued therapy with Propecia ” to “resolution occurred in men who discontinued therapy with Propecia”. Merritt testified that Merck eliminated the word “all” due to evidence from the clinical trials of adverse events that did not resolve following discontinuation of use.[52] In another deposition, Paul Howes, the head of marketing for Propecia acknowledged that Merck was aware that warnings of sexual side effects, particularly persistent to permanent side effects, would have a devastating impact on sales.[52]


5. Post-Finasteride syndrome is well documented, and there doesn’t seem to be a post-Dutasteride syndrome equivalent. I have no citation for this because I simply cannot find any reference to it. Please post in the comments if you can find a citation of a post-Dutasteride syndrome specifically.

Update 20210207: As noted by Redditor u/usernames_are_taken_ , Dutasteride has more interactions with medications and very possibly does have the same long term adverse reactions as Finasteride; and is simply less popular/well known.

Medically reviewed comparison: https://www.healthline.com/health/enlarged-prostate/dutasteride-finasteride-comparison#dutasteride-vs-finasteride

Comparison of long term health effects: https://pubmed.ncbi.nlm.nih.gov/32202088/

So dutasteride interacts with a bunch of medicines while fin isn’t known to interact with many, and dutasteride has the same side effects. Dutasteride is also slightly worse for your health long-term with an increased risk of type 2 diabetes, fatty liver disease, etc.

I believe the perceived difference is the nocebo effect for dutasteride is much less strong since it’s less talked about, while everyone on fin knows about “post finasteride syndrome” which has never been found to exist in studies.

So dutasteride is what you should go on if fin hasn’t worked for you in a year of use. It shouldn’t be the first one tried.


Finasteride Details:


Dutasteride Details:


6. Finasteride and Dutasteride Health Risks

5α-dihydrotestosterone (5α-DHT) is the most potent natural androgen. 5α-DHT elicits a multitude of physiological actions, in a host of tissues, including prostate, seminal vesicles, hair follicles, skin, kidney, and lacrimal and meibomian glands. However, the physiological role of 5α-DHT in human physiology, remains questionable and, at best, poorly appreciated. Recent emerging literature supports a role for 5α-DHT in the physiological function of liver, pancreatic β-cell function and survival, ocular function and prevention of dry eye disease and kidney physiological function. Thus, inhibition of 5α-reductases with finasteride or dutasteride to reduce 5α-DHT biosynthesis in the course of treatment of benign prostatic hyperplasia (BPH) or male pattern hair loss, known as androgenetic alopecia (AGA) my induces a novel form of tissue specific androgen deficiency and contributes to a host of pathophysiological conditions, that are yet to be fully recognized. Here, we advance the concept that blockade of 5α-reductases by finasteride or dutasteride in a mechanism-based, irreversible, inhabitation of 5α-DHT biosynthesis results in a novel state of androgen deficiency, independent of circulating testosterone levels. Finasteride and dutasteride are frequently prescribed for long-term treatment of lower urinary tract symptoms in men with BPH and in men with AGA. This treatment may result in development of non-alcoholic fatty liver diseases (NAFLD), insulin resistance (IR), type 2 diabetes (T2DM), dry eye disease, potential kidney dysfunction, among other metabolic dysfunctions. We suggest that long-term use of finasteride and dutasteride may be associated with health risks including NAFLD, IR, T2DM, dry eye disease and potential kidney disease.


7. If Dutasteride is so effective, why isn’t it prescribed more for hair loss instead of Finasteride?

However, while dutasteride has been shown to be effective, it’s also worth noting that finasteride is currently the only prescription medication approved by the FDA for treating male pattern baldness. That means finasteride has undergone — and passed — the FDA’s rigorous drug approval process and shown that it’s safe and effective for the treatment of hair loss in men.


8. What about the increased risk of prostate cancer for Finasteride and Dutasteride?

The most recent development in this line of research came in 2019, when researchers found no increase in the number of men who’d died of prostate cancer between the finasteride and control groups.


9. What about increased sexual dysfunction on Finasteride and Dutasteride?

Just like with finasteride, individuals taking dutasteride may experience negative sexual side effects like decreased libido, erectile dysfunction and problems ejaculating.

In one study, researchers found that 5.1 percent of men who used dutasteride stopped taking it due to some sort of sexual dysfunction as a result of their treatment.

In addition, the study also found that 3.5 percent of men taking dutasteride also experienced tenderness in the breast or gynecomastia — the enlargement of breast tissue.

There have been reports of a slight increased risk (1.8 percent with 5mg Finasteride dosage versus 1.0 percent placebo) of High Grade Prostate Cancer for men over age 55 years old. Again, this is at a much higher dosage (5mg versus 1mg ) than we prescribe for hair loss.


10. What is this reference of DHEA to DHT conversion in the introduction talking about?

Circulating dehydroepiandrosterone (DHEA) is converted to testosterone or estrogen in the target tissues. Recently, we demonstrated that skeletal muscles are capable of locally synthesizing circulating DHEA to testosterone and estrogen. Furthermore, testosterone is converted to 5alpha-dihydrotestosterone (DHT) by 5alpha-reductase and exerts biophysiological actions through binding to androgen receptors.


DHEA and other adrenal androgens such as androstenedione, although relatively weak androgens, are responsible for the androgenic effects of adrenarche, such as early pubic and axillary hair growth, adult-type body odor, increased oiliness of hair and skin, and mild acne.[12][13][14] DHEA is potentiated locally via conversion into testosterone and dihydrotestosterone (DHT) in the skin and hair follicles.[4] Women with complete androgen insensitivity syndrome (CAIS), who have a non-functional androgen receptor (AR) and are immune to the androgenic effects of DHEA and other androgens, have absent or only sparse/scanty pubic and axillary hair and body hair in general, demonstrating the role of DHEA and other androgens in body hair development at both adrenarche and pubarche.[15][16][17][18]


A new understanding of the endocrinology of menopause is that women, at menopause, are not only lacking estrogens resulting from cessation of ovarian activity but have also been progressively deprived for a few years of androgens and some estrogens originating from adrenal DHEA and androstenedione (4-dione). In fact, serum DHEA decreases by about 60% between the maximal levels seen at 30 years of age to the age of menopause. This decreased secretion of DHEA and DHEA-S by the adrenals is responsible for a parallel decrease in androgen and estrogen formation in peripheral tissues by the steroidogenic enzymes specifically expressed in each cell type in individual target tissues.


11. Tangential: Energy storage in the body.

In my case, even with a serum Testosterone and DHT well under castration levels, my athletic performance and muscle gains were still high. Even before HRT with a peak Testosterone level of 320 ng/dL I was heavily muscled particularly in the upper body while living a mostly sedentary lifestyle. Although I’ve had no genetic testing to confirm (frankly my only memory of a reference to this was in a BBC documentary where a participant in an over eating study gained no additional body fat but instead had increased muscle mass; please comment if you know what I’m talking about and can find a citation); I also ate a terrible diet that never resulted in much fat gain, but after a big meal I would notice my muscles would bulk up even more the next day.

They found that the in vivo muscle fuel oxidation (Krebs cycle flux) was higher in trained than in untrained individuals. Using the ATP synthesis flux to Krebs cycle flux ratio as a marker of mitochondrial coupling,62,63 lower energy efficiency was observed in trained vs untrained individuals. Such results are in line with the observation that after intense endurance exercise, in vitro muscle energy efficiency was decreased in humans.64 Similarly, Rosenbaum et al.65 showed that maintenance of reduced or elevated body weight results in respective decrease or increase in energy expended in physical activity.


If in my case there isn’t a genetic component then a chronic and dramatic lifestyle starting at a young age may explain my experiences. I started writing software at age 10 and spent 14+ hours a day sitting, mostly at a computer (and still do). I’m 37 years old now for reference at the time of this writing.

At age 16 I started body building and at one point my arms were 16 inches in circumference. Around the same time I was also doing Tae Kwon Do training throughout the week for a few months. I had a lifestyle with periods of extreme sedentary sitting, coupled with intense exercise on and off. I have maintained this extreme rest and intense exercise flip flop most of my life. For example in the past 7 years I built a 1750sqft metal workshop, then a 560sqft addition on our house, then rebuilt a 1550sqft barn – doing most if not all the physical work by myself, while still doing software development on a computer. Typically this was an every other day cycle of rest and exercise.

Interestingly even while on HRT with castration level T/DHT, I noticed that these activities were only slightly more difficult even after months of inactivity on projects (being even more sedentary). Little muscle loss was occurring and athletic performance and muscle gain were still high. After starting Dutasteride my body is finally struggling more with this lifestyle and rebound; though, after almost 1 month of Dutasteride my athletic performance seems to be rising again in terms of cardiovascular, though less with muscle gain and rebound than pre-Dutasteride.

This is all very biased self reporting, but interesting if not hyperbolic.


Getting back to the point of this article (sorry for the tangents), if you have an incompatibility with Finasteride, or have little efficacy with hair recovery, it may be worth giving Dutasteride a shot. The adverse and long term side effect profiles are not identical, and in my personal experience Finasteride was intolerable while Dutasteride is very tolerable.

Also, if you are Transfeminine and struggling with Feminization; it may be worth giving Dutasteride or Bicalutamide a shot due to localized DHEA to DHT production stunting progress. Note that DHT is a much more potent Androgen than Testosterone and serum levels may not provide a full picture of DHT activity in localized tissues.

If you are not Transfeminine I would not recommend giving Bicalutamide a shot, as it will increase levels of Testosterone as your body attempts to overcome Androgen Deprivation. On the note of Androgen Deprivation; I would also make that a consideration with long term use of Bicalutamide; which blocks Testosterone and DHT signals. Personally the side effects of Bicalutamide were intolerable and I also had concerns about a complete deprivation of Androgen signals in my body for any extended period of time.

Personal: Sexual Side Effects

Surprisingly the only thing that has caused sexual dysfunction or reduced libido for me since starting HRT/AA (antiandrogen) medications is a lack of hormones. For the period of time while I was high on Estradiol then switched to 1/3rd the previous dose, I had some erectile issues and reduced libido. My body corrected for this within 30 days and I was back to business as usual. I have not experienced erectile problems even at castration levels of T/DHT, other than also having a low Estradiol profile at the same time.

Dutasteride has caused some tiredness and initially for a couple of weeks erections were a little weaker; however, by the 3rd week I was again back to normal. Your mileage may vary! This seems to be very atypical in the Transfeminine community to be so sexually functional with low androgen activity… my only theory to explain the difference may again be my strangely high athletic abilities regardless of hormone profiles.

One last interesting note before I shut up; Bicalutamide caused me to be incredibly horny for the week I was on it. One day that stuck out I had sex twice within 8 hours, then masturbated another 3 times within 24 hours. Again this is already well under castration level (20ng/dL) levels of serum Testosterone/DHT. (my serum DHT has corresponded to about 18% of serum Testosterone; which is within average)

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