Bernstein Medical Center for Hair Restoration - 5-Alpha Reductase

5-Alpha Reductase

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Q: Does finasteride need to be taken every day? — M.B., Atlanta, GA

A: Finasteride (Propecia) is a competitive inhibitor of Type II, 5 alpha-reductase (5AR is the enzyme that converts Testosterone to DHT which then causes hair to miniaturize and eventually be lost). Finasteride is 100x times more selective in inhibiting the Type II enzyme (present in hair follicles) than the Type I enzyme (present in other body tissues). The turnover (T1/2) of the finasteride/5AR Type II complex is 30 days and the finasteride/5AR Type I complex is 15 days. This explains why finasteride does not need to be taken every day and why, after stopping finasteride, the effects may take a month or longer to begin to disappear.

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Could the 5α-reductase inhibitors (5ARIs) dutasteride and finasteride increase the risk of developing male breast cancer?

In 2012, male breast cancer was identified as a possible new risk of 5ARIs by the FDA; however, a 2013 study published in the Journal of Urology ((Bird ST, Brophy JM, Hartzema AG, Delaney JA, Etminan M. Male breast cancer and 5α-reductase inhibitors finasteride and dutasteride. J Urol. 2013 Nov;190(5):1811-4. doi: 10.1016/j.juro.2013.04.132.)) found no evidence for a relationship between male breast cancer and finasteride (Proscar®) and dutasteride (Avodart®), both of which are used to treat enlarged prostate (benign prostatic hyperplasia).

The study excluded finasteride (Propecia®), used to treat androgenic alopecia, because previous research considered a relationship between Propecia 1mg and male breast cancer unlikely.

So how did dutasteride and finasteride become implicated in the possible development of male breast cancer?

The Hypothesized Link Between Finasteride & Dutasteride and Male Brest Cancer

Going back to 1992, researchers ((Thomas DB, Jimenez LM, McTiernan A, Rosenblatt K, Stalsberg H, Stemhagen A, Thompson WD, Curnen MG, Satariano W, Austin DF. Breast cancer in men: risk factors with hormonal implications. Am J Epidemiol. 1992 Apr 1;135(7):734-48.)) had hypothesized that an increased ratio of estrogen-to-testosterone could lead to an increase risk of male breast cancer.

This hypothesis seemed to be supported when, in 2009, the Medicines and Health care products Regulatory Agency (MHRA) in England ((Niraj K Shenoy, Sangolli M Prabhakar. Finasteride and male breast cancer: Does the MHRA report show a link? J Cutan Aesthet Surg 2010; 3: 102.)) received reports of male breast cancer developing in patients using 5ARIs, which are known to alter the normal estrogen/testosterone balance. Specifically, as of November 2009, MHRA had received 50 worldwide reports of male breast cancer developing within an average of 44 months after starting treatment with 5mg finasteride for enlarged prostate. MHRA also received three reports of male breast cancer developing in men using Propecia ® 1 mg for hair loss, but because of relatively short onset times of the disease after starting treatment, the MHRA considered any link between Propecia and male breast cancer unlikely.

Even though both finasteride and dutasteride alter the normal estrogen/testosterone balance in men, the fact that 50 individuals developed male breast cancer after starting to use a 5ARI does not constitute evidence that 5ARIs contribute to the development of male breast cancer: it is possible that these 50 individuals would have developed cancer whether or not they used a 5a-reductase inhibitor.

The Study: Male Breast Cancer and 5a-Reductase Inhibitors Finasteride and Dutasteride

To ascertain whether or not a link exists between the use of 5a-reductase inhibitors and subsequent development of male breast cancer, one would want to look at two groups of men where one group has been exposed to a 5a-reductase inhibitor and where one group has not, and then one would compare the incidence of the development of breast cancer in the two groups. However, one would also need the two groups to be matched on as many known risk factors for male breast cancer as possible, such as alcoholism, gynecomastia, Klinefelter syndrome, liver damage, obesity, oral estrogen, orchiectomy and prior radiation; in short, one would want to control for all the known risk factors for male breast cancer to see if 5ARIs were contributing any additional risk.

And this is exactly what the 2013 study did. As a result, it found that 5a-reductase inhibitors were not a significant predictor of developing male breast cancer 1 to 3 years after exposure.

Because no link between 5ARIs and male breast cancer was found, the authors of the study advised doctors to prescribe finasteride and dutasteride without fear of introducing additional risk for the development of male breast cancer in their patients.

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Q: I recently visited my dermatologist regarding my hair loss, and after checking my hair he said I am showing signs of Androgenetic Alopecia (common baldness), and said if I don’t treat it, it will progress. From my research on the net, I figured he will put me on Propecia. In fact he put me on Avodart. When I told him it is not FDA-approved for hair loss, and Propecia is, he said Avodart is better and brings DHT down more, and Propecia is nothing next to Avodart. He told me to take it every day for 2 weeks, then every other day from then on as it has a long half life. From researching on the net, many hair restoration doctors rarely prescribe Avodart for hair loss due to some dangers. What is your opinion on this? — T.G., Darien, Connecticut

A: Although dutasteride (Avodart) can be more effective for male pattern hair loss, I would start with finasteride (Propecia) as many patients do great with it and the safety profile is better. The following are things I would consider before starting dutasteride:

  1. As you point out, dutasteride is not FDA-approved for hair loss.
  2. There is no data on its safety when used for hair loss. This is important since dutasteride has been only tested on an older population of patients (with prostate disease) rather than a younger population of patients needing medical treatment for androgenetic alopecia.
  3. These is no natural model for dutasteride’s combined blockage of both type 1 and 2 5-alpha reductase (finasteride blocks only type 2 5-AR and there are families that have this deficiency and have no long-term problems. This, by the way, is how the drug was discovered).
  4. The type 1 enzyme which dutasteride blocks is present in many more tissues of the body (including the brain) compared to type 2 (which is more localized to the skin).
  5. Although so far unproven, there is a concern that finasteride may produce side effects than can be persistent after stopping the medication (post-finasteride syndrome). It this does turn out to be true, the effects from dutasteride would most likely be significantly more persistent.
  6. If you start with finasteride and do have side effects, you will most surely have side effects from dutasteride; therefore, by taking finasteride first you will have avoided the potentially more problematic side effects from dutasteride
  7. You may respond well to finasteride, and so do not need to consider dutasteride
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Q: Have there been any lab studies proving that Saw Palmetto works to prevent hair loss? — A.B., Yonkers, NY

A: There have been no verifiable clinical studies that show saw palmetto can stop hair loss or cause hair to re-grow. There have been some preliminary tests showing that saw palmetto may be able to inhibit 5-alpha-reductase, but its usefulness for androgenetic hair loss has not been documented in controlled studies.

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Q: What is Saw Palmetto? — R.P., White Plains, NY

A: Saw Palmetto is a dwarf palm plant native to North America. The active ingredients can be found in the plant’s brown-black berries. It is proposed that it blocks the enzyme 5-alpha-reductase that converts testosterone to dihydrotestosterone (DHT). There is little scientific evidence that Saw Palmetto is actually effective for hair loss.

Read about the treatment of hair loss in men

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After trading anecdotes with fellow hair loss physicians about how finasteride can reduce body hair in some patients, Sharon A. Keene, M.D. took the next logical step and asked whether finasteride might have a negative effect on patients who have body hair transplant (BHT) procedures.

In a review of scientific literature on whether finasteride effects body hair growth, Dr. Keene finds that current research is inconclusive.

Finasteride, the drug in the hair loss medication Propecia, works by blocking the 5-alpha-reductase type 2 enzyme (5-AR Type 2) which is needed by the body to covert testosterone to DHT. DHT causes common baldness, by making hair follicles shrink and eventually die.

In looking at DHT’s effect on body hair growth, current research strongly suggests that it does play a key role. Males born with a deficiency of 5-AR Type 2, and thus no DHT, have reduced, or absent, body hair growth (and no loss of scalp hair).

It would seem logical then, that when finasteride is used to re-grow hair on the scalp, it would also inhibit the growth of hair on the body. However, the genetic variation among people is too great to determine exactly how much of an influence it plays.

With this uncertainty of DHT’s effects on body hair, it is impossible to say, without further study, if finasteride would have the same effect on body hairs which are transplanted to the scalp. In Dr. Keene’s conclusion, she suggests:

A patient on finasteride for at least a year who undergoes BHT is probably safe to continue it, as remaining body hairs are apparently not sensitive to the effects of this drug.

You can read the full discussion and review of current research in the January/February 2011 issue of Hair Transplant Forum International, the official newsletter of the International Society of Hair Restoration Surgery (ISHRS).

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Q: I’m concerned that finasteride might result in unwanted body hair on the arms, back, etc. Is there any truth to this? My thinking is that since finasteride blocks the enzyme 5 alpha-reductase which converts testosterone to its more active form, DHT (dihydrotestosterone), is it possible that it might actually have some effectiveness in ameliorating unwanted hair? — P.P., Stamford, CT

A: Yes, finasteride does have some ability to decrease body hair, since growth of body hair is stimulated by DHT. However, the effects of finasteride are mild and not observed by everyone, so if you have unwanted body hair you will probably need some other means to remove it such as waxing, laser hair removal or electrolysis. The important thing is that finasteride doesn’t increase body hair.

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Q: My friend is taking Avodart, he bought it over the internet. Is it safe to take? — T.G., Denver, Colorado

A: Avodart (dutasteride 0.5mg) was approved by the FDA for the treatment of prostate enlargement in men in 2002. Avodart has not been approved for the treatment of androgenetic hair loss, although physicians can use an approved medication in ways other than for which it was specifically approved. That said, the use of dutasteride certainly requires a doctor’s supervision.

Like finasteride (the active ingredient in Proscar and Propecia), dutasteride blocks the enzyme 5-alpha reductase that converts testosterone to DHT (DHT is a key hormone that causes hair loss). However, unlike finasteride, which only inhibits the Type I form of the enzyme, dutasteride inhibits both the Type I and Type II forms. This combined effect lowers circulating DHT more with dutasteride than with finasteride, but also increases the incidence of its side effects.

The Type II form of the enzyme (blocked by finasteride) is found predominantly in the hair follicle. The Type I form of the enzyme has been found in the scalp and sebaceous glands, and many other parts of the body, but its exact role in hair growth has not been determined. It is felt that dutasteride’s ability to dramatically lower serum levels of DHT is what makes it a more potent medication in hair loss.

When considering the safety of dutasteride, one should consider the following:

  • It acts on other parts of the body besides the hair follicle.
  • Unlike finasteride, where families that had a deficiency of the Type II 5-alpha reductase enzyme were followed for years without any adverse effects, there is no natural biologic model to show the safety of dutasteride.
  • Dutasteride has been approved for prostate enlargement in an older male population. It is not approved for hair loss and, in fact, the clinical trials for hair loss were discontinued, so there is no safety data for its use in younger patients. There is a greater incidence of sexual side effects with dutasteride compared to finasteride.
  • The 1/2 life of dutasteride is 5 weeks compared to 6-8 hours for finasteride. Serum concentrations of dutasteride are detectable up to 4-6 months after discontinuation of treatment.
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Q: I heard that Propecia was being used originally for shrinking the prostate, is this true? — M.D., New Hyde Park, N.Y.

A: Propecia (finasteride 1mg) is not a prostate medication that was serendipitously noted to have a side effect of re-growing hair, it is a medication that was known all along that it might be able to slow hair loss and/or to grow hair.

Although finasteride was first approved for the treatment of prostate enlargement, the researchers at Merck knew, at the outset, that there were families whose members were deficient in the 5-alpha reductase Type II enzyme and that the men in these families neither developed prostate disease nor went bald. In addition they had no long-term problems from the lack of this enzyme.

Merck used this natural model to develop a medication that could block the 5-alpha reductase Type II enzyme – the result was finasteride. Because the only approved treatment for symptoms related to prostate enlargement at the time was surgery, Merck developed finasteride as a medical treatment for this condition prior to developing finasteride as a potential treatment for men with male pattern hair loss.

This also meant that Merck would understand the safety profile of finasteride, and have it approved for a medical disease (symptomatic prostate enlargement), before developing it for a cosmetic condition.

The drug was first submitted to the FDA for the treatment of prostate enlargement as Proscar (finasteride 5mg) in 1991 and it was approved for this use in 1992. The drug was submitted for the treatment of men with male pattern hair loss as Propecia (finasteride 1mg) in 1996 and was approved for this use in 1997.

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Q: I know that I am going to be bald because my father is bald and I am losing my hair just like him. What actually causes this kind of hair loss? — J.P., Paradise Valley, Arizona

A: Although there are many different causes, the overwhelming number of people that have hair loss have what is referred to as “patterned hair loss” or “androgenetic alopecia.”

In men, it is due to a hormone called DHT, which is a by-product of testosterone produced by the action of the enzyme 5-alpha reductase. This enzyme is inhibited by the hair loss medication Propecia. See the causes of hair loss in men page on the Bernstein Medical – Center for Hair Restoration website for more information.

In women, the mechanism is a little bit more complex as another enzyme, aromatase, is involved in the metabolic pathway. See the causes of hair loss in women page on the Bernstein Medical – Center for Hair Restoration website for more information.

We know that the inheritance comes from both the mother’s and father’s side, although the actual genes causing hair loss in men and women have not yet been identified. Statistically, the inheritance from the maternal side appears to be a bit stronger, but the reason for this is unknown.

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Edwin S. Epstein, M.D.
Stuart Medical Group, Richmond, VA, USA.

SUMMARY of Dr. Epstein’s Abstract from his presentation at the International Society of Hair Restoration Surgery, 2005 – Sydney, Australia

Dihydrotestosterone (DHT) is known to be the more potent androgen in both Benign Prostatic Hyperplasia (BPH) and in Androgenetic Alopecia (AGA). Testosterone is converted to DHT by the enzyme 5-α reductase in several organs including the prostate, hair follicles, skin, liver and sebaceous glands. 5-α reductase exists in two isoforms: type 1 and type 2. Type 2 is the predominant enzyme in prostate and hair follicles. Finasteride, approved in 1992, inhibits the type 2 isoenzyme and is available in two doses: 1mg dose for AGA, and 5mg for BPH. Dutasteride, approved in January 2003 to treat BPH, is a dual inhibitor of both isoenzymes.

In current the study, men ages 21-45 received dutasteride (0.01mg, 0.1mg, 0.5mg, 2.5mg), finasteride 5mg, or placebo.

Results showed the following:

• Dutasteride seemed to have an earlier onset of effect than Finasteride
• Dutasteride 2.5mg appeared to be significantly more effective than Dutasteride 0.5mg.
• The effects of Dutasteride 0.5mg were comparable to Finasteride 5mg.

The side effect profile was difficult to interpret. All of the data is presented in such limited terms that make any interpretation difficult.

Dutasteride appears to work faster than finasteride in the treatment of androgenetic alopecia and clearly is more effective in lowering DHT levels. Because there is no human model for combined type I and II 5-α reductase inhibition (as there is with type II) long-term usage should be viewed cautiously.

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