I'd say a blood test is a good idea. But if you want to know now, drop the Mast and use 250mcg of hCG followed by another, 4 days later.
It'll cause a short term spike in estrogen. So if low E was the culprit, then you'll know. When I've overdone AI's in the past, hCG has saved me.
Masteron is a DHT. DHT is an Estrogen antagonist. Not like an AI, but works by a different mechanism. Actually stops estrogen from doing it's thing.
Here's a study in which injected E2 was actually stopped from working by DHT:
Evaluation of androgen antagonism of estrogen effect by dihydrotestosterone.
Hung TT, Gibbons WE.
Abstract
The antagonism of estrogen effect on the immature rat uterus by dihydrotestosterone (DHT) was evaluated in vivo. One-hundred micrograms of DHT which has been shown by previous workers [4] to saturate the androgen receptor but not bind or translocate estrogen receptor was injected daily into immature rats with or without 5 micrograms of 17 beta estradiol (E2) for three consecutive days. The animals were sacrificed on the fourth day, the uteri were excised and the uterine wet weight, cytosol protein content, [3H]-leucine and [3H]-UTP incorporation into TCA-precipitable material, and cytosol and nuclear levels of estrogen and progesterone receptors were measured. When DHT was given in conjunction with estradiol, estrogen induced uterine growth as measured by increases in uterine weight, cytosol protein content, and [3H]-leucine incorporation was significantly reduced. However, cytosol and nuclear concentrations of estrogen receptors and cytosol progesterone receptor concentration were not significantly affected, whereas progesterone treatment significantly reduced estrogen and progesterone receptor concentrations in both the cytosol and the nucleus. DHT administration did not change the binding affinity of the estrogen receptor populations and the ratio between the higher (Kd = 10(-10) M) and lower (Kd = 10(-9) M) affinity components of estrogen receptor remained unchanged. DHT treatment was also shown to significantly reduce estrogen-induced [3H]-UTP incorporation. These findings suggest that the mechanism of DHT antagonism of estrogen effect in this organ systemdoes not involve inhibition of synthesis of estrogen receptor as has been shown for progesterone, but appears to occur by decreasing estrogen-induced RNA transcription at a point subsequent to estrogen receptor binding.