Sore Nipples (pre existing gyno) when taking orals

hawkberry04

New Member
I have a little pre-existing gyno that often feels “sore” when I take orals. For example, yesterday I started Tbol and I have subtle soreness behind my nipples but the gyno isn’t necessarily growing. I’ve experienced the same with pharma Anavar. Anyone else experienced something similar to this?
 
Higher free t causing higher e2? You could take raloxifene to block the receptors there and see if it goes away. Or aromasin to lower e2 but I would get an ultrasensitive e2 test before going that route

I'm just guessing

Post in thread 'Opinions about my Blast & Cruise protocol?' Opinions about my Blast & Cruise protocol?
 
Last edited:
I have a little pre-existing gyno that often feels “sore” when I take orals. For example, yesterday I started Tbol and I have subtle soreness behind my nipples but the gyno isn’t necessarily growing. I’ve experienced the same with pharma Anavar. Anyone else experienced something similar to this?

Higher free t causing higher e2? You could take raloxifene to block the receptors there and see if it goes away. Or aromasin to lower e2 but I would get an ultrasensitive e2 test before going that route

I'm just guessing

Post in thread 'Opinions about my Blast & Cruise protocol?' Opinions about my Blast & Cruise protocol?
Raloxifen will be your best bet if your looking to target the actual receptors at the breast tissue. Keep in mind that it still mitigates estrogen at the tissue level elsewhere. While it is a better option than tamoxifen both taken long term can start to have some negatives.

You could also try implementing an injectable DHT derivative. Mast is a great example and acts as an antagonist for gyno.

This will probably leave you questioning why Anavar aggravated while mast can help with both being DHT derivatives.

Anavar has weak AR binding, weak androgenic signal. On the other hand mast is a potent AR binder and highly androgenic.

Masteron behaves like a functional antiestrogen in breast tissue.
Strong AR binding, Mast has very high androgen receptor affinity in breast tissue, AR activation directly opposes ER signaling. Think like this it... “crowds out” estrogen’s ability to signal. Androgen dominance locally suppresses estrogenic transcription. Mast strongly lowers SHBG giving more free androgens relative to estrogen so it improves androgen/estrogen signaling ratio. Drostanolone was originally designed for breast cancer. Even if E2 stays the same, estrogen becomes less effective where gyno forms.

Anavar does not meaningfully dominate ARs in breast tissue, estrogen signaling remains unchecked and increases total androgen load, more aromatization elsewhere. Anavar itself doesn’t aromatize
But it allows higher testosterone dosing tolerance....more test →moreE2→breast tissue still sensitive. SHBG suppression without ER antagonism so anavar lowers SHBGin turn that can raise free estrogen AND free testosterone. If AR signaling is weak estrogen wins. It can enhance estrogen sensitivity, some DHT derivatives (especially weaker ones) upregulate ER expression, this makes existing estrogen more effective.

Hope that helps.
 

Sponsors

Back
Top