Finasteride, Dutasteride and Gynecomastia
Please do not regard information presented on this site as medical advice. These are purely information we compile and gather on the internet and may or may not be accurate.
Gyno is short for gynecomastia (male breast tissue formation!)
5 alpha reductase (5AR) such as Finasteride (Proscar/Propecia) and dutasteride (Avodart) have been shown to increase both testosterone and estrogen while lowering serum levels of DHT. Some suggested that this increase in estrogen may compromise its effectiveness in treating hair loss. More importantly, the increase in estrogen creates side effect called Gynecomastia or breast enlargement in some men, along with increased body fat and loss of libido.
Based on discussions from forum members, the best way to counter gynecomastia is with:
a) Arimidex (Anastrazole) - Estrogen blocker
b) Super Miraforte (natural Estrogen Blocker)
"This combination reduces excess estrogen, raises free testosterone, and potentiates the hair growth effects of 5-alpha-reductase inhibitors. It also increases libido and reduces body fat, both potential problematic areas of concern for those using Propecia alone."
As for Arimidex dosage, some forum members recommend half a tablet twice per week. It is as "safe" a drug as you can get as ".
"If all of the above fail to increase free testosterone and lower excess estradiol, then ask your doctor to prescribe the potent aromatase inhibiting drug Arimidex (anastrozole) in the very low dose of one-half (0.5 mg) mg, twice a week. Arimidex is prescribed to breast cancer patients at the dose of 1 to 10 mg a day. Even at the high dose prescribed to cancer patients, side effects are rare. In the minute dose of 0.5 mg twice a week, a man will see an immediate drop in estradiol levels and should experience a rise in free testosterone to the optimal range."
Final note: Normal Estradiol range for a male is 15-30 pg/ml. High Estrogen levels in males (above 30 pg/ml) blocks the production and effect of testosterone throughout the body, dampens sexuality, and increases the risk of prostate and cardiovascular disease.
Also note that these reference ranges indicate that it can be normal for a man to have no estrogen. The fact that most aging men have too much estrogen does not mean it is acceptable for a man to have NO (or virtually no) estrogen. Estrogen is used by men to maintain bone density and abnormally low estrogen levels may increase the risk for prostate cancer and osteoporosis."
Gynecomastia discussion from the archives (please email us and quote archive URL http://www.hairsite7.com/m574dutas24/_disc574/00000046.htm if you wish to retrieve contents)
Study which shows that "Gynecomastia produced by Propecia is transient and disappears if the treatment is discontinued." - email us or fill out the inquiry form on this page and quote archive URL reference http://www.hairsite4.com/dc/dcboard.php?az=show_topic&forum=10&topic_id=60&mode=full if you wish to read the contents.
UNILATERAL GYNECOMASTIA INDUCED BY 1 mg ORAL FINASTERIDE. REPORT OF 3 CASES
1Ferrando J, 1Grimalt R, 1Alsina M, 1Bulla F, 2Manasievska E. Depts. of Dermatology. 1Hospital Clínic. University of Barcelona. Spain. 2Centro Medicinal Kumanovo. University of Skopje. Macedonia.
Since 1998 1 mg oral finasteride (PropeciaTM) has been widely used for treament of male androgenic alopecia (MAGA). Side effects have been described in less than 2% of cases (transitory impotence, libido decrease or ejaculation disorder) and they did not imply treatment discontinuation. Five clinical trials submitted by Merck to the FDA refer those data, but only quoted a “breast enlargement and sensitivity, occasionally reported”. We had the opportunity to observe painful unilateral gynecomastia in three males under 1 mg oral finasteride regimen.
Three males aged 18 to 29 with grades II to IV of the Hamilton/Norwood classification developed unilateral gynecomastia after 2 to 6 months on treatment with 1 mg oral finasteride (one case with ProscarTM, 1/5 of tablet per day, two cases with PropeciaTM). In two cases the diagnosis was confirmed by mamography and in the third case by aspiration-biopsy. In all cases gynecomastia disappeared between 2 to 6 months after the treatment was discontinued.
Five mg oral finasteride (ProscarTM) used for treatment of benign prostatic hypertrophy can produce gynecomastia, so it would not be rare to find that effect with PropeciaTM. Gynecomastia is mainly caused by alterations of estrogen/androgen ratio. Finasteride decreases circulating dihydrotestosterone levels, increasing serum estradiol, so it could produce gynecomastia.Gynecomastia produced by PropeciaTM is transient and disapears if the treatment is discontinued.
Pathogenesis and diagnosis of gynecomastia -
by Dr. Braunstein
DEFINITION — Gynecomastia is defined histologically as a benign proliferation of the glandular tissue of the male breast and clinically by the presence of a rubbery or firm mass extending concentrically from the nipple(s). Fat deposition without glandular proliferation is termed pseudogynecomastia (often seen in obese men). These two entities may be distinguished by having the patient lie on his back with his hands behind his head. The examiner then places his or her thumb and forefinger on each side of the breast, and slowly brings them together.
In true gynecomastia, a ridge of glandular tissue will be felt that is reasonably symmetrical to the nipple-areolar complex.
In pseudogynecomastia, the fingers will not meet any resistance until they reach the nipple.
Gynecomastia can usually be detected when the size of the glandular tissue exceeds 0.5 cm in diameter.
The most important differentiation is between gynecomastia and breast carcinoma. Carcinoma is much less common, is generally unilateral, is eccentric in location rather than symmetrical to the nipple, is hard or firm, and may be associated with skin dimpling, nipple retraction or discharge, and axillary lymphadenopathy . Less common conditions leading to breast enlargement include neurofibromas, lymphangiomas, hematomas, lipomas, and dermoid cysts.
Physical examination method to distinguish gynecomastia, due to enlargement of the glandular tissue, from pseudogynecomastia, due to excessive adipose tissue. The thumb and forefinger are placed on opposite sides of the breast and slowly brought together towards the areolar-nipple complex. Gynecomastia is appreciated as a concentric, rubbery-to-firm disk of tissue, often mobile, located directly beneath the areolar area. Pseudogynecomastia presents no discrete mass, and other masses due to disorders such as cancer tend to be eccentrically positioned. Adapted from Braunstein, GD, Hosp Pract 1993; 28:37. See graphic illustration at HairSite forum.
Drugs commonly associated with Gynecomastia (fill out the inquiry form on this page and quote archive link http://www.hairsite.com/hair-loss/forum_entry.php?id=88&page=0&category=5&order=time if you wish to retrieve the contents).
Gynecomasty: histological aspects in a surgical material
TI - Gynecomasty: histological aspects in a surgical material.
AU - Andersen JA; Gram JB
SO - Acta Pathol Microbiol Immunol Scand [A] 1982 May;90(3):185-90.
In a consecutive and unselected series of 83 patients operated upon for gynecomasty, the histological and related clinical aspects were studied. It was convincingly demonstrated that gynecomasty begins in an active proliferating phase and ends in a fibrous inactive phase. Contrary to previous authors we found it justified that the formation of lobules, indistinguishable from what is seen in the reproduceable age in the female breast, is not necessarily related to the administration of exogenic hormones. In five (6.5%) cases, typical multicentric foci of intraductal epithelial hyperplasia were demonstrated--of the atypical hyperplastic or early intraductal carcinoma type. It was concluded that the clinical significance of such morphological changes must not be overestimated.
Detailed Arimidex and Gynecomastia information, (archive url is http://www.hairsite4.com/dc/dcboard.php?az=show_topic&forum=10&topic_id=7149&mode=full)
Arimidex and Gyno info
Here's the Arimidex summary from the archives:
Arimidex general info
1)Arimidex is not an estroten blocker but an aromatase inhibitor
2) Quick reference on a good Arimidex dosage, + arimidex is BETTER than nolvadex:
3) Reference with good overview and commentary
4) Posts against using Arimidex
4a) Bryan's analysis: caution against using arimidex because of beneficial role of estrogen in mpb:
5) Why Arimidex works
6) Posters who said Arimidex doesn't work:
7) Posters who said Arimidex / Liquidex works
http://www.hairsite7.com/m563finas17/_disc563/0000025e.htm (not hair related results)
7a) Arimidex shedding
9) Arimidex / liquidex Side effects
http://www.hairsite7.com/m563finas17/_disc563/00000194.htm (side effects for women only)
10) Liquidex vs Arimidex
11) Dosage reference: 1/2 tablet (0.25mg) twice a week
12)Alternative to Arimidex - Clomid: Follow this thread
Excerpts from Mesomorphosis.com
What does "anti-estrogen" mean? How are anti-estrogens like Cytadren, Clomid, and Nolvadex different from each other? Is Proviron an anabolic steroid, or not?
Anti-estrogens are drugs which act to reduce estrogenic activity in the body. This can be done either by reducing the amount of estrogen, or by reducing the activity of whatever estrogen is present.
Competitive aromatase inhibitors, such as Cytadren, Arimidex, and probably Proviron, bind to the same binding site on the aromatase enzyme that testosterone does. By doing this, they allow less testosterone to bind to aromatase. So, less testosterone is converted to estradiol (estrogen).
Here’s an important thing: the effectiveness of competitive inhibitors decreases as the amount of the normal substrate increases. Suppose that you had equal amounts of inhibitor and normal substrate in the blood, and they bound to the enzyme equally well. Then the inhibitor would at any moment be taking up half the sites that the normal substrate otherwise would, so it would reduce conversion rate by 50%. But if the amount of substrate is increased 10 times while the amount of inhibitor remains the same, then the inhibitor would be outcompeted by the more numerous substrate molecules. It would therefore be rather ineffective.
For example, with more testosterone molecules available, and similar binding strengths, the enzyme will mostly bind testosterone. It will then mostly be working to produce estrogen. To obtain the 50% reduction we had before, then the amount of inhibitor would also have to be increased 10 times.
To be really effective, the inhibitor must either be present in higher concentration than the normal substrate, or must bind more tightly.
With Cytadren or Proviron, it takes quite a lot of inhibitor to outcompete high testosterone levels. With Arimidex, rather little, even 1 mg/day, can be sufficient because it binds so strongly.
The other general approach is estrogen receptor antagonism. If a molecule binds strongly to a hormone receptor, but does not activate that receptor and makes it unresponsive to the normal hormone, then it is a receptor antagonist. Clomid (clomiphene) and Nolvadex (tamoxifen) follow this approach. These drugs are very similar structurally. They are both what are called triphenylethylenes, and are not steroids. The differences are relatively minor, but seem to affect an important characteristic of these compounds: drug metabolism.
Both tamoxifen and clomiphene are metabolized to other related compounds which can be estrogenic or anti-estrogenic. Both act as estrogens in bone tissue, perhaps after metabolism, which is a very useful property for female patients, for whom these drugs are usually intended. (Otherwise, an anti-estrogen could lead to osteoporosis.) Tamoxifen seems particularly prone to acting as an estrogen in the liver, which may account for reduced IGF-1 levels seen when this drug is taken.
Users generally seem to agree that when tamoxifen is used, gains are a little less than what otherwise would be expected. (Let’s not take this too far though: many people have made great gains while using tamoxifen as an anti-estrogen. And it’s always hard to say what "would" have been the case if a drug had not been included.) I’ve heard nothing but good about clomiphene, though.
Proviron, an anabolic steroid, is particularly interesting. I suspect that it not only acts as an antiaromatase but in an unknown DHT-like anti-estrogenic manner. This might involve estrogen receptor downregulation for example. In any case, aromatase inhibition and/or Clomid don’t seem to give the same effect on appearance and muscle hardness as when Proviron is included.
How much of these agents is needed for effective estrogen suppression?
Again, it depends on the dose of anabolic/androgenic steroids (AAS) and it depends what type of AAS is being used.
With Primobolan or trenbolone there is no need for these drugs.
With nandrolone, an aromatase inhibitor will be of no use, because aromatase is not used in the aromatization of nandrolone. A rather small amount of estrogen receptor antagonist can be useful. 12.5 to 25 mg Clomid would be plenty for 400 mg/week Deca.
With testosterone, stacking of an aromatase inhibitor and an estrogen receptor antagonist will give the best results. Cytadren use should not exceed 250 mg/day in my opinion. This alone would not be sufficient for say 1 g/week or more of testosterone. With such a dose, ideally one would add in 50 mg/day Clomid. Proviron at 100 mg/day could substitute for the Cytadren. Or Cytadren and Proviron can be used in combination, 125/50 or higher, together with 50 mg/day Clomid.
For lower doses of testosterone, proportionally less antiestrogens can be used.
Arimidex is very effective but extremely expensive. 1 mg/day of this is at least as effective as 250 mg/day Cytadren. If a milligram per day cannot be afforded, use of half a milligram would allow Cytadren use to be cut in half, which may be desirable.
How does Clomid "stimulate" testosterone production at the end of the cycle?
It really doesn’t. Rather, by acting as an estrogen receptor antagonist, it reduces the inhibition that results from elevated estradiol levels. This helps return LH to normal levels, which helps testosterone to return to normal levels (if the testicles have not atrophied).
How does hCG help?
Acts as an LH receptor agonist, thus substituing for LH. It does nothing to help the hypothalamus and pituitary. Thus, it can be effective during the cycle to help avoid testicular atrophy, but is not best used in the taper when one is attempting to restore LH production. Increases in natural testosterone, stimulated by the hCG, will act to inhibit LH production. Thus, you can see where hCG use is counterproductive in the taper itself.
Can Clomid, taken throughout a cycle, completely eliminate inhibition?
I do not believe so. There is also androgenic inhibition mediated by the androgen receptor, which has nothing to do with the estrogen receptor. Androgenic inhibition is unavoidable and cannot be helped by estrogen receptor antagonists. However, use of Clomid throughout a cycle can definitely reduce the degree of the inhibition and allow a speedier recovery at the end of the cycle.
Is it safe to take Clomid for so many weeks? I heard it should only be taken for 2 weeks.
The two week idea comes from the fact that medically its main use is to help women with fertility problems. Because of the menstrual cycle, there are only certain times of the month when there is any chance of ovulation. It is pointless, then, for these women to take the drug for more than two weeks at a time. Some have misconstrued this to apply to males.
Men have taken the drug in clinical studies for a year continuously. It is a rather safe drug.
Why do you say not to use more than 250 mg/day of Cytadren?
Cytadren has two main therapeutic activities. At high doses, such as a gram per day, it is a very effective inhibitor of the enzyme desmolase, which is required for all steroid production, and is rate limiting for the production of cortisol. So the drug is very useful for treating patients with Cushing’s Syndrome, who produce abnormally high levels of cortisol.
It is also an inhibitor of aromatase, and it is a better aromatase inhibitor than a desmolase inhibitor. About 250 mg/day is sufficient for fairly good inhibition of aromatase, resulting in only fairly low levels of desmolase inhibition.
As dosage increases, aromatase inhibition does not improve much, but desmolase inhibition increases greatly.
Even at 250 mg day, there is still significant desmolase inhibition. Other side effects, such as lethargy, may bother some individuals even at this dose.
Why is desmolase inhibition bad? I have read that cortisol is the enemy of our muscles, and we want to reduce it.
Those articles are written by people trying to sell you alleged cortisol-reducing supplements.
While abnormally high levels of cortisol are indeed muscle wasting, abnormally low levels of cortisol do not result in extra muscle growth, and cause joint problems.
You’ve talked about tapering off Cytadren. Why?
There is a feedback mechanism for production of cortisol. Low levels of cortisol enhance release of corticotropin releasing hormone from the hypothalamus, and ACTH from the pituitary. Both will result in higher production of cortisol.
So moderate inhibition of desmolase will temporarily reduce cortisol, but soon it will be back to normal as this feedback mechanism compensates.
If you then suddenly discontinue the drug, then these elevated ACTH levels will result in abnormally high cortisol for a time, until the body adjusts again. This can be avoided simply by tapering down over about a week.
Should Cytadren be taken all at once, or in divided doses?
Because the half life is only 6 or 8 hours, if the drug is taken only once, then through part of the day there will be little drug in the system, and little anti-aromatase activity.
I think the best approach is to use half the dose on arising (or an hour or two afterwards) to get blood levels from a somewhat low level up to the desired maintenance level. This would then be followed by quarters of the dose at 7 or 8 hour intervals twice after that.