BOOM! Article dropped! Thanks,
@Millard!
Oxandrolone at
20 mg daily decreased visceral adipose tissue (-20.9 +/- 12 cm(2); P < 0.001), abdominal sc adipose tissue (SAT) declined (-10.7 +/- 12.1 cm(2); P = 0.043), the ratio VAT/SAT declined from 0.57 +/- 0.23 to 0.49 +/- 0.19 (P = 0.002), and proximal and distal thigh SC fat declined [-8.3 +/- 6.7 cm(2) (P < 0.001) and -2.2 +/- 3.0 kg (P = 0.004), respectively].
Oxandrolone at
10 mg daily for 7 days increased fasting 3-hydroxybutyrate [a marker for hepatic ketogenesis] by 70% and 3-hydroxybutyrate AUC by 53% after oral fat loading.
We know that AR dose/response is logarithmic and according to Forbes, 1985, doses up to 1,000 mg/w are not S-shaped (sigmoidal function), but if an androgen's sole mechanism is AR agonism, then an inflection point should occur at some point > 1,000 mg/w [that has never been directly measured].
Since
this effect on fat mass is mediated by hepatic ketogenesis via oxandrolone effects on triaglycerol lipase, and the doses used are low, we can't infer or assume the shape of the dose/response curve without more data.
That is to say, that while 20 - 40 mg daily is a rough optimization of tolerability/efficacy trade-offs, considering muscle protein anabolism via the AR activity that is bounded by inherent hepatotoxicity of oxandrolone, we cannot say that hepatic ketogenesis does not continue unabated at higher doses.
But practically, since hepatic ketogenesis is directly related to HTGLA (the breakdown of lipoproteins from larger to smaller more atherosclerotic ones), we need to balance the benefit vs. the dyslipidemic cost.