I thought it was just OK with respect to the Anadrol portion. Not sure why he entertained MPMD's claim without analysis of any supporting literature. Sure, maybe (if even true that an Anadrol-only cycle increases serum estrogens; I'm willing to test this myself) oxymetholone decreases clearance and/or excretion of estrogens (by competitive glycolysation and/or conjugation?) but it's not particularly compelling, mostly because I doubt the claim that increased estrogens are attributable to oxymetholone to start.
Potential mAR binding: maybe, but that wouldn't result in pronounced anabolism, if anything mAR actions tend to attenuate rather than potentiate classical AR action (that's the prevailing hypothesis). These actions via mAR are transient, typified by GPCR nongenomic (rapid) action.
Very little discussion of metabolites and the Schanzer view that oxymetholone likely acts as a prohormone. My modeling data on 17α-methyl-5α-androstane-3α-17β-diol supports this. I posted this here:
https://www.professionalmuscle.com/forums/index.php?threads/can’t-use-nolva…-what-is-next-best.171373/post-3099138
He's clearly a fountain of knowledge but I feel he didn't do any homework on the Anadrol topic and was somewhat unprepared. I liked his discussion of protein requirements, protein leveraging, glucagon and appetite, J. Antonio, et al. I wished that he had explained the fact that T3 (Cytomel) increases net protein breakdown (particularly, type IIB atrophy, i.e., selective catabolism of hypertrophied muscle) at moderate - high doses. But everything he said was correct, he just did not present the converse possibility (the risks/tradeoffs) if doses go beyond optimal (bringing the individual to a euthyroid state).