In a lot of anecdotal cases, we have heard how dihydrotestosterone (DHT) derivatives “mask” high estradiol (E2) side effects mainly pertaining to gynecomastia.

The most common DHT derivatives that are used by the community include, but are not limited to, 1-testosterone (DHB—dihydroboldenone), drostanolone (Masteron), mesterolone (Proviron), and metenolone (Primobolan).

I have mentioned multiple times throughout the AA threads that taking these DHT derivatives can prevent high E2 sides based on the ratio of DHT:E2 in the body being more in favor of DHT. While this is great broscience and has worked for many people throughout our community, it is crucial that we understand what the specific mechanism is that causes this suppression of E2 side effects.

Anecdotally, my total testosterone level measured at ~1600ng/dL with E2 at ~118pg/mL during my last blast (500mg test e weekly, 40mg Tbol ED for 50 days, 50mg Proviron ED) with no E2 side effects. Shortly after dropping all compounds and moving to my cruise dosage of 150mg test weekly, I experienced high E2 side effects (inadequate erections/libido and gyno lump) with bloodwork showing 657 test with 72 E2. Obviously, I’m a shitty responder to test and a heavy aromatizer, but on cycle with my test being barely above natural levels and E2 being 3x the upper natural limit, I had no problem whatsoever with gyno, blood pressure, mood, erections, or libido. I did have bloat, but I contribute that to a shitty diet.

While these compounds do not decrease circulating E2 levels, they do act as an indirect antagonist (a compound that acts against or blocks typical ligand-receptor action). What this means is that they do not block E2 receptors like SERMs do in the breast tissue, but somehow still prevent binding in a different way.

I did some poking around on the internet and found some studies that have looked at this phenomenon. See below:

Antiestrogenic Action of Dihydrotestosterone in Mouse Breast. Competition With Estradiol for Binding to the Estrogen Receptor

Dihydrotestosterone does not compete for binding to the progesterone receptor, but it does inhibit estrogen-mediated increases of progesterone receptor content of breast tissue cytosol...

This suggests that DHT blocks elevated E2 from increasing progesterone receptors in breast tissue which can lead to milk production.

Since [mice with X-linked testicular feminization] lack a functional androgen receptor, we conclude that this antiestrogenic action of androgen is not mediated by the androgen receptor.

Even mice that had no androgen receptors still saw a decrease in E2 expression meaning that DHT has a somewhat direct impact on blocking of female hormones.

Dihydrotestosterone competes with estradiol for binding to the cytosolic estrogen receptor of mouse breast

This suggests that DHT does compete with E2 in breast tissue meaning higher levels of DHT will lead to less breast growth.

Dihydrotestosterone also promotes the translocation of estrogen receptor from cytoplasm to nucleus; the ratio of cytoplasmic-to-nuclear receptor changes from 3:1 in the castrate to 1:2 in dihydrotestosterone-treated mice. Thus, the antiestrogenic effect of androgen in mouse breast may be the result of effects of dihydrotestosterone on the estrogen receptor.

Interestingly, high levels of DHT causes the E2 receptors to move from the cytosol, where they can be actively bound to, to the nucleus, which more or less inhibits the mechanism.

https://pubmed.ncbi.nlm.nih.gov/6542571/

Here’s another:

Evaluation of Androgen Antagonism of Estrogen Effect by Dihydrotestosterone

“These findings suggest that the mechanism of DHT antagonism of estrogen effect...does not involve inhibition of synthesis of estrogen receptor...but appears to occur by decreasing estrogen-induced RNA transcription at a point subsequent to estrogen receptor binding.”

In layman’s terms, DHT was shown to decrease the effects of estrogen by decreasing the body’s ability to “write instructions for use of the E2” after the E2 had already been bound to the receptor.

So, the E2 still binds, but the DHT makes the body uncertain of what to do once the E2 is there, and this leads to inaction by the body, i.e., no gynecomastia.

This is similar to what we saw in the first study where “moving” the receptor essentially changes the body’s ability to recognize that it needs to act upon elevated E2 levels.

https://pubmed.ncbi.nlm.nih.gov/6645492/

In conclusion, it seems that running a DHT derivative alongside a cycle that has potential estrogenic concerns (looking at you, Dbol) can heavily mitigate the potential side effects caused by elevated E2 with the primary concern for most individuals being gyno.

Some individuals have shared concerns about running these compounds due to increased androgenic activity that can have sides such as benign prostatic hyperplasia, increased body hair growth, scalp alopecia, etc. This is something that needs to be considered by the individual and weighed against the potential issues from elevated E2.

For my personal recommendation, taking Proviron at 50mg ED for the duration of the cycle is a good, safe bet and can provide the protection against E2 described above with very low risk of androgenic side effects.

I am definitely interested in hearing suggestions as far as effective dosages for others regarding Mast, Primo, Proviron, etc.