MirrorOnTheWall
Iron
- Joined
- May 29, 2021
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The idea behind this stack is to approach the 5 main hormones/receptors that relates to gynecomastia (A.K.A. gyno); Estrogen, Progresterone, Prolactin, IGF-1, and Androgen. Additionally we want to use the drugs topically, so to react primarily in the lactiferous ducts, and maybe avoid potential side effects.
Estrogen creates the spread and growth of the ducts in breast tissue. Raloxifene is a selective estrogen receptor modulator (SERM) that's a common treatment for gynecomastia.
Prolactin induces lactogenesis, making the gyno larger. Raloxifene also has been shown to reduce Prolactin.
Progresterone increases alveolar cell differentiation & growth, and promotes ductal elongation. To address this, we need a selective progresterone receptor modulator (SPRM) such as Mifepristone or Telapristone acetate (TA).
Insulin-like growth factor 1 (IGF-1) virtually proliferates anything with insulin receptors. Tamoxifen (A.K.A. Nolvadex) is known to reduce IGF-1 in breast tissue.
So far we've only went on the defensive to prevent the gyno's mass from growing, now we need to go on the offense.
Androgens can shrink breasts' size, however, ones like testosterone aromatizes into estrogen which may comprise our goals (and overall cost). And nandrolone analogs are more anabolic than androgenic, which isn't that useful in our context. The best solution to the problem is to prehaps utilize DHT derivatives as they're bind to androgen receptors, fairly androgenic, also they don't aromatizes into estrogen.
Anavar could be a good fit. According to MPMD, it's one of the more hair safe of the DHT derivatives (although it's not as safe as not using it). Many body builders anecdotally claim that it's one of the more tolerable steroids. It also causes lipolysis in men, so the gyno might stand out even less.
Each one of these compounds are small enough to be applied topically (although Tamoxifen needs to be the parent compound without any additives like citrate, and TA seems too large but it's demonstrated to work topically IDKW tho) hence they might manifest localize effects, which should make your tits to bits without having fits.
Estrogen creates the spread and growth of the ducts in breast tissue. Raloxifene is a selective estrogen receptor modulator (SERM) that's a common treatment for gynecomastia.
Prolactin induces lactogenesis, making the gyno larger. Raloxifene also has been shown to reduce Prolactin.
Progresterone increases alveolar cell differentiation & growth, and promotes ductal elongation. To address this, we need a selective progresterone receptor modulator (SPRM) such as Mifepristone or Telapristone acetate (TA).
Insulin-like growth factor 1 (IGF-1) virtually proliferates anything with insulin receptors. Tamoxifen (A.K.A. Nolvadex) is known to reduce IGF-1 in breast tissue.
So far we've only went on the defensive to prevent the gyno's mass from growing, now we need to go on the offense.
Androgens can shrink breasts' size, however, ones like testosterone aromatizes into estrogen which may comprise our goals (and overall cost). And nandrolone analogs are more anabolic than androgenic, which isn't that useful in our context. The best solution to the problem is to prehaps utilize DHT derivatives as they're bind to androgen receptors, fairly androgenic, also they don't aromatizes into estrogen.
Anavar could be a good fit. According to MPMD, it's one of the more hair safe of the DHT derivatives (although it's not as safe as not using it). Many body builders anecdotally claim that it's one of the more tolerable steroids. It also causes lipolysis in men, so the gyno might stand out even less.
Each one of these compounds are small enough to be applied topically (although Tamoxifen needs to be the parent compound without any additives like citrate, and TA seems too large but it's demonstrated to work topically IDKW tho) hence they might manifest localize effects, which should make your tits to bits without having fits.
