For that are asking how R-Andro works for PFS

[TubZy]

Please see this study since people keep asking how R-Andro actually helps compared to using standard AAS. I would suggest reading through the entire thing, I just posted a short part taken out of it but def worth a read

Anticonvulsant Potencies of the Enantiomers of the Neurosteroids Androsterone and Etiocholanolone Exceed those of the Natural Forms

"Androsterone [(3α,5α)-3-hydroxyandrostan-17-one; 5α,3α-A] and its 5β-epimer etiocholanolone [(3α,5β)-3-hydroxyandrostan-17-one; 5β,3α-A)], the major excreted metabolites of testosterone, are neurosteroid positive modulators of GABAA receptors. Such neurosteroids typically show enantioselectivity in which the natural form is more potent than the corresponding unnatural enantiomer. For 5α,3α-A and 5β,3α-A, the unnatural enantiomers are more potent at GABAA receptors than the natural forms."

Certain endogenous steroid hormone metabolites are positive allosteric modulators of GABAA receptors at low concentrations and directly gate these receptors at higher concentrations (Lambert et al., 2009). As is the case for other agents that enhance inhibitory GABAergic function, such neurosteroids protect against seizures in diverse animal models, and there is emerging evidence that agents of this type are effective in the treatment of seizures and epilepsy in humans (Reddy and Rogawski, 2012; Bialer et al., 2013). The anticonvulsant potency of such steroids is closely correlated with their activity at GABAA receptors (Morrow et al., 1990; Kokate et al., 1994). Although the pregnanes allopregnanolone [(3α,5α)-3-hydroxypregnan-20-one)] and tetrahydrodeoxycorticosterone [(3α,5α)-3,21-dihydroxypregnan-20-one)] were the first endogenous GABAA receptor modulatory neurosteroids to be identified (Paul and Purdy, 1992), it is now recognized that a number of structurally related endogenous steroids have similar actions on GABAA receptors. In particular, the 17-ketosteroid androsterone (5α,3α-A; Fig. 1) potentiatates GABAA receptor responses albeit more weakly than allopregnanolone (Turner et al., 1989; Hawkinson et al., 1994; Anderson et al., 2000), and we demonstrated that it, as well as its 5β-epimer etiocholanolone (5β,3α-A), exhibit anticonvulsant activity in animal seizure models (Kaminski et al., 2005).