ancora dubbi sul 6-oxo
 

salve ....quale è l'effettivo dosaggio del 6-oxo della SNS (serious nutririon solution) ?
Vi do il contenuto del prodotto perchè forse non è proprio 6-oxo...
il serving size della ditta è 3 capsule al giorno ,e sull'etichetta leggo:1-4-6 androstatriene -3,17-dione (3,17 keto etiochol-triene) 25mg x capsula ...
quindi consigliano 75 mg al dì ....però leggevo di alcuni test fatti ,dove consigliavano 300 mg al dì per il 6-oxo generico .....
potete chiarirmi le idee ?
thanks....

non si può parlare di dosaggi di integratori illegali in italia

allora riformulo la domanda ,l'inhibit-E della SNS :1-4-6 androstatriene -3,17-dione (3,17 keto etiochol-triene) 25mg x capsula .
è uguale al 6-oxo generico ?

no!

quello è puro ATD, gli estrogeni te li azzera totalmente, se fai una ricerca qui trovi quello che si è già detto su questi 2 integratori

thanks...
PS:non trovo la discussione...me la potresti linkare ..?

cmq nn li azzera totalmente...

in che percentuale li azzera ?
può funzionare anche come anti aromatase in associazione ad AAS ?

un buon 80%

salve ho trovato quest'altro studio che mi mette altri dubbi ...possibile che ATD blocca anche i recettori degli androgeni o addirittura li danneggia ?

Effects of ATD on male sexual behavior and androgen receptor binding: a reexamination of the aromatization hypothesis.
Kaplan ME, McGinnis MY.

Department of Anatomy, Mount Sinai School of Medicine, CUNY, New York 10029.

The aromatization hypothesis asserts that testosterone (T) must be aromatized to estradiol (E2) to activate copulatory behavior in the male rat. In support of this hypothesis, the aromatization inhibitor, ATD, has been found to suppress male sexual behavior in T-treated rats. In our experiment, we first replicated this finding by peripherally injecting ATD (15 mg/day) or propylene glycol into T-treated (two 10-mm Silastic capsules) or control castrated male rats. In a second experiment, we bilaterally implanted either ATD-filled or blank cannulae into the medial preoptic area (MPOA) of either T-treated or control castrated male rats. With this more local distribution of ATD, a lesser decline in sexual behavior was found, suggesting that other brain areas are involved in the neurohormonal activation of copulatory behavior in the male rat. To determine whether in vivo ATD interacts with androgen or estrogen receptors, we conducted cell nuclear androgen and estrogen receptor binding assays of hypothalamus, preoptic area, amygdala, and septum following treatment with the combinations of systemic T alone. ATD plus T, ATD alone, and blank control. In all four brain areas binding of T to androgen receptors was significantly decreased in the presence of ATD, suggesting that ATD may act both as an androgen receptor blocker and as an aromatization inhibitor. Competitive binding studies indicated that ATD competes in vitro for cytosol androgen receptors, thus substantiating the in vivo antiandrogenic effects of ATD. Cell nuclear estrogen receptor binding was not significantly increased by exposure to T in the physiological range. No agonistic properties of ATD were observed either behaviorally or biochemically. Thus, an alternative explanation for the inhibitory effects of ATD on male sexual behavior is that ATD prevents T from binding to androgen receptors.

PMID: 2925181 [PubMed - indexed for MEDLINE]

Effects of ATD on male sexual behavior and androge...[Horm Behav. 1989] - PubMed Result