I wanted to mention this study by Patt et al. [1] that is making the rounds as evidence that Primo may pose a relative cardiac harm. Perhaps
@PeterBond will chime in if he's read this one, as he is the undisputed king of teasing out weaknesses and strengths of studies IMO.
This study showed that Promo may promote hypertension/cardiovascular disease via increased mineralocorticoid biosynthesis.
Primo increased mineralocorticoid production but decreased adrenal androgen production indicating CYP17A1 dysfunction via indirect inhibition (post-translation) and/or impaired protein synthesis. Was not supported by docking/modeling. In adrenocortical carcinoma H295R cells... seems highly speculative for authors to speculate hypertension/CVD in vivo?
"[Primo] exhibited the weakest CYP17A1 inhibition (among mesterolone, mestanolone and methenolone), with only a trend to increase progesterone production and no change in 17alpha-hydroxyprogesterone... total CYP17A1 activity was decreased in a compound-dependent manner... [Primo] the weakest." [1]
I thought its findings with regard to Adrol and Tbol were more relevant. Though, I cannot say I've ever heard of a single confirmed case of adrenal hyperplasia in a bodybuilder, nor have I looked. These findings were supported by docking.
Peter, do you suppose suppression of corticosteroid production coupled with increased DHEA and androgen synthesis in H295R could indicate an increase of aggression rather than "adrenal hyperplasia" in vivo?
References:
[1] Patt M, Beck KR, Di Marco T, Jäger MC, González-Ruiz V, Boccard J, Rudaz S, Hartmann RW, Salah M, van Koppen CJ, Grill M, Odermatt A. Profiling of anabolic androgenic steroids and selective androgen receptor modulators for interference with adrenal steroidogenesis. Biochem Pharmacol. 2020 Feb;172:113781. doi: 10.1016/j.bcp.2019.113781. Epub 2019 Dec 27. PMID: 31884045.