What is Gyno?
Gynecomastia, or gynaecomastia, is the development of abnormally large mammary glands in males resulting in breast enlargement, which can sometimes cause secretion of milk. The term comes from the Greek gyne (stem gynaik-) meaning “woman” and mastos meaning “breast”.
The condition can occur physiologically in neonates (due to female hormones from the mother), in adolescence, and in the elderly. In adolescent boys the condition is often a source of distress, but for the large majority of boys whose pubertal gynecomastia is not due to obesity, the breast development shrinks or disappears within a couple of years.
The causes of common gynecomastia remain uncertain, although it has generally been attributed to an imbalance of sex hormones or the tissue responsiveness to them; a root cause is rarely determined for individual cases.
Breast prominence can result from hypertrophy of breast tissue, chest adipose tissue and skin, and is typically a combination. Breast prominence due solely to excessive adipose is often termed pseudogynecomastia or sometimes lipomastia.
Gynecomastia should be distinguished from work hypertrophy of the pectoralis muscles caused by much exercise, e.g. swimming.
Physiologic gynecomastia (also called Turcios Disease) occurs in neonates, at or before puberty and with aging. Many cases of gynecomastia are idiopathic, meaning they have no clear cause.
Potential pathologic causes of gynecomastia are: medications including hormones, increased serum estrogen, decreased testosterone production, androgen receptor defects, chronic kidney disease, chronic liver disease, HIV treatment, and other chronic illness.
Gynecomastia as a result of spinal cord injury and refeeding after starvation has been reported. In 25% of cases, the cause of the gynecomastia is not known.
Medications cause 10-20% of cases of gynecomastia in post-adolescent adults. These include cimetidine, omeprazole, spironolactone, imatinib mesylate, finasteride and certain antipsychotics.
Some act directly on the breast tissue, while others lead to increased secretion of prolactin from the pituitary by blocking the actions of dopamine (prolactin-inhibiting factor/PIF) on the lactotrope cell groups in the anterior pituitary.
Androstenedione, used as a performance enhancing food supplement, can lead to breast enlargement by excess estrogen activity. Medications used in the treatment of prostate cancer such as antiandrogens and GnRH analogs can also cause gynecomastia. Marijuana use is also thought by some to be a possible cause; however, published data is contradictory.
Increased estrogen levels can also occur in certain testicular tumors, and in hyperthyroidism. Certain adrenal tumors cause elevated levels of androstenedione which is converted by the enzyme aromatase into estrone, a form of estrogen. Other tumors that secrete hCG can increase estrogen.
A decrease in estrogen clearance can occur in liver disease, and this may be the mechanism of gynecomastia in liver cirrhosis. Obesity tends to increase estrogen levels.
Decreased testosterone production can occur in congenital or acquired testicular failure, for example in genetic disorders such as Klinefelter Syndrome. Diseases of the hypothalamus or pituitary can also lead to low testosterone.
Abuse of anabolic androgenic steroids (AAS) has a similar effect. Mutations to androgen receptors, such as those found in Kennedy disease can also cause gynecomastia.
Although stopping these medications can lead to regression of the gynecomastia, surgery is sometimes necessary to eliminate the condition.
Repeated topical application of products containing lavender and tea tree oils among other unidentified ingredients to three prepubescent males coincided with gynecomastia; it has been theorised that this could be due to their estrogenic and antiandrogenic activity.
However, other circumstances around the study are not clear, and the sample size was insignificant so serious scientific conclusions cannot be drawn.
Treating the underlying cause of the gynecomastia may lead to improvement in the condition.
Patients should talk with their doctor about revising any medications that are found to be causing gynecomastia; often, an alternative medication can be ft avoids gynecomastia side-effects, while still treating the primary condition for which the original medication was found not to be suitable due to causing gynecomastia side-effects (e.g., in place of taking spironolactone the alternative eplerenone can be used.)
Selective estrogen receptor modulator medications, such as tamoxifen and clomiphene, or androgens or aromatase inhibitors such as Letrozole are medical treatment options, although they are not universally approved for the treatment of gynecomastia.
Endocrinological attention may help during the first 2-3 years. After that window, however, the breast tissue tends to remain and harden, leaving surgery (either liposuction, gland excision, skin sculpture, reduction mammoplasty, or a combination of these surgical techniques) the only treatment option.
Many American insurance companies deny coverage for surgery for gynecomastia treatment on the grounds that it is a cosmetic procedure.
Radiation therapy is sometimes used to prevent gynecomastia in patients with prostate cancer prior to estrogen therapy. Compression garments can camouflage chest deformity and stabilize bouncing tissue bringing emotional relief to some. There are also those who choose to live with the condition.
Possible treatment for Gyno using Letro:
SERM - Selective estrogen receptor modulator. These drugs work by binding to the estrogen receptors and flooding them in a sense, making it difficult (but not impossible by any means) for estrogen to bind to the receptors and thus prevent the onset of estrogen related side effects.
Most common forms: Tamoxifen (Nolvadex), Clomiphene (Clomid)
AI - Aromatise Inhibitor. These drugs work by inhibiting the aromatization of estrogen. This means that in effect AI’s prevent androgens from converting to estrogen, again, making it difficult (but not impossible) for estrogen to reach receptor sites.
Most common forms: Anastrozole (l-dex, a-dex), Exemestane (aromasin), Femera (letrozole). For our purpose of reversing gyno we are interested in Letro.
Letro and your sex drive:
Letrozole will suppress your sex drive. This is another reason why it is so important to act on preventing gyno as soon as possible. Since we all know that Test should be run in every cycle this will cancel out the effect of sex drive suppression.
Running letro to prevent gyno:
If you decide to run estrogen protection while on cycle (and it’s suggested that you do unless you are aware that you do not require it), you can run either a SERM or an AI.
Letro will be the most powerful AI you can use, it will inhibit 98+% of estrogen using a dose as low as .25mg and even lower. This is why I suggest you do not use a dose higher than .50mg while on cycle just trying to prevent estrogen related side effects.
You will want to start running the letro approximately 2 weeks before you begin your cycle to allow it to fully stabilize in your blood. It’s been said that letro takes up to 60 days to stabilize, I don’t know if I buy into this for the reason that some have reversed gyno after using letro for only 1 week. Still to be safe, it’s recommended to start it before your cycle as stated above.
If you do decide to run letro there is absolutely no need to run another AI or SERM. Do not make the mistake of thinking more is better. Think of it this way; if letro is preventing the conversion of androgens to estrogen than there is no estrogen, what would the purpose of a SERM be when there is no estrogen to bind to the receptors? Nolva will only take away from the effectiveness of letro.
This brings me to my next point. Do not listen to anyone who tells you to bump up your nolvadex to 60+mg ED if you get gyno. I have no idea where this idea started but I have seen it suggest far too many times recently.
Nolvadex will do nothing to reverse your gyno, let me make that clear IT WILL DO NOTHING FOR GYNO. If you are running nolva as your anti-e and start to develop gyno than sure you can bump the dosage a small amount to try to prevent it from progressing further, but letrozole must begin ASAP.
It is very important that you begin taking letrozole immediately, the longer your wait the more risk you take in not being able to reverse it.
How do I know if I have gyno?
If you have developed gyno you will have a lump behind your nipple. It will be fairly hard, and it will be tender to touch.
Running letro to reverse gyno:
I am going to go over the three different scenarios which people could fit into. Remember regardless of what scenario you are in it is important that you begin taking the letro ASAP.
Already using an anti-e aside from letro.
Already using letro @ a dose of .25mg or .50mg ED.
Not running any estrogen protection.
Day 1: .25mg Letro + anti-e*
Day 2: .50mg Letro
Day 3: 1.0mg Letro
Day 4: 1.5mg Letro
Day 5: 2.0mg Letro
Day 6: 2.5mg Letro **
Day 1: .50mg Letro
Day 2: 1.0mg Letro
Day 3: 1.5mg Letro
Day 4: 2.0mg Letro
Day 5: 2.5mg Letro **
Day 1: .50mg Letro
Day 2: 1.0mg Letro
Day 3: 1.5mg Letro
Day 4: 2.0mg Letro
Day 5: 2.5mg Letro **
*Regardless of the anti-e you are using it is important to still use it for the first day you begin letro as the letro will not have taken any effect and you by no means want your body to be without any protection when gyno is already prevalent.
** You will remain at this dose until gyno symptoms subside. Once you believe your gyno is gone it is important to stay at this dose for another 4-7 days to ensure all traces are gone. It’s recommended that people with a bf% over 15 stay on for a week as it may be harder to judge completely whether the lump is completely gone.
Once this period is over it will be important to taper letro down slowly rather than coming off it completely. Regardless of which manner you tapered up your dose you will all taper down in the same fashion.
Day 1: 2.0mg
Day 2: 1.5mg
Day 3: 1.0mg
Day 4: .50mg***
Day 5: .25mg
***You can remain at this dose or go down further to .125mg. It is really up to you at this point. They are both very common maintenance doses as an anti-e while on cycle. Personally, most have stayed with .25mg and never had a problem.
Letro and the estrogen rebound:
With your estrogen being completely inhibited there is a definite estrogen rebound as your body tries to re-stabilize the testosterone:estrogen balance. We can prevent this rebound effect by supplementing further with another AI or SERM.
So, it’s suggested that when you are coming to the end of your cycle you will more than likely be using Nolva in your PCT so just make sure that you begin taking nolva the last day you are going to take your letro and then continue on as you would with regular PCT.
This now leads us into the question of reversing gyno while not on cycle. There are a few things to remember here. You have already waited longer than you should have, and your sex drive will be shot.
You can use tribulus or another natural test booster to help you in this scenario but I can’t guarantee the effectiveness. Just follow gyno reversal protocols 2 or 3. When coming off again you must taper and begin using nolvadex to prevent any rebound effect that may occur.
How much nolvadex should you use if you are not going into PCT and running this off cycle? I suggest starting at 20mg ED for a week and then lowering it to 10mg for another week and then coming off completely.