FORMADROL OR 6 OXO

samva777

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Ok I had an idea and wanted to run it past you fellow lifters , relise I am an old man 45 so you younguns have some patience.

The Idea is run a moderate havoc cycle and use Formodrol or 6 oxo as pct , also instead of stopping the havoc cycle at its highest intake taper it down to 1 cap for a week since it acts like a SERM and then switch to Formadrol or 6 oxo.

So 2 questions 1. Is this a good plan an2. which is better FORMADROL or 6 OXO
 
bla55

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If you're gonna go for OTC PCT my personal suggestion is to just pulse it instead of phasing down, which I'm unsure of how effective it is.

As far as what to use I'm a big fan of ATD + Stocked!, but I'd guess 6-Oxo + Stocked would work too.
 
rms80

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Ok I had an idea and wanted to run it past you fellow lifters , relise I am an old man 45 so you younguns have some patience.

The Idea is run a moderate havoc cycle and use Formodrol or 6 oxo as pct , also instead of stopping the havoc cycle at its highest intake taper it down to 1 cap for a week since it acts like a SERM and then switch to Formadrol or 6 oxo.

So 2 questions 1. Is this a good plan an2. which is better FORMADROL or 6 OXO


As far as pct- the higher you go with formestane, the more of a chance it can convert to an active non-aromatizing androgen....form is structurally altered @ C4 w/ a hydroxyl- and has a 4-en to protect the A ring, along with a 3,17 dione. The significance? Reduce the ketone on 17 to a diol, and you have 4-hydroxytestosterone- and the ketone @ 17 is not well protected- go too high on the dose, and it can convert to a fairly decent non-aromatizing androgen :)



6-oxo is the better choice- the oxygenation of C6 makes the molecule a strong binder of aromatase (any alteration on C6 will influence this aspect)- and even if it does convert to 17-ol- any compound with a C6 structural alteration will bind the AR poorly.....
 
mooch2321

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rms...i was just looking at a study that showed 52 percent increase in estrone after eight weeks of six oxo usage....now im not real familiar with estrone and estrogen but estrone is the type of estrogen found in menopausal women right? so wouldnt this be the exact opposite of what we are looking for in a pct? ive been looking into six oxo all day tday after i was kinda stumped on a thread yesterday and what im finding has me very confused....mabye you could shed some light...heres the study
http://www.jissn.com/content/4/1/13
 
rms80

rms80

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rms...i was just looking at a study that showed 52 percent increase in estrone after eight weeks of six oxo usage....now im not real familiar with estrone and estrogen but estrone is the type of estrogen found in menopausal women right? so wouldnt this be the exact opposite of what we are looking for in a pct? ive been looking into six oxo all day tday after i was kinda stumped on a thread yesterday and what im finding has me very confused....mabye you could shed some light...heres the study
http://www.jissn.com/content/4/1/13
It seems logical that DHT concentration would increase concomitantly with elevations in TST because DHT is a TST metabolite. Relative to the change in FT and the significant increases in DHT over the eight-week period, the present data suggest a role for 6-OXO in up-regulating the activity of the 5α-reductase enzyme. Unlike TST, DHT is a non-aromatizable androgen [13]. Because 6-OXO is a type I steroidal aromatase inhibitor, it is assumed that this supplement would completely inhibit aromatase activity, thereby leading to elevations in endogenous TST. However, our results suggest the contrary; 6-OXO does elevate TST and DHT levels without the complete inhibition of serum aromatase activity. As a result, it is conceivable that the apparent TST aromatization occurring was in part responsible for the observed elevations in estradiol and estrone. Aromatase catalyzes the conversion of TST to estradiol, of androstenedione to estrone, and of 16α-hydroxylated dehydroepiandrosterone to estriol [25]. The purported mechanism for an increase in TST with aromatase inhibition has been reported as a decrease in estradiol levels that leads to feedback to the hypothalamus to stimulate TST-induced increases in estradiol [26,27]. This would infer that in order for an increase in TST to occur, a decrease in estradiol would have to be seen, and this is not what happened in this study.

Pretty interesting- you can look at something on paper, but it doesn't always pan out in the real world- if I had to throw out a guess- there could be some sort of 17 alpha reduction going on- which would turn convert the molecule into a 3,6-dione 17b-ol- which would be similar in structure to testosterone- but still would not aromatize

part I don't get- the study stated that DHT levels and TST levels increased, so 5-AR of TST to DHT is occurring, and aromatization of TST to estradiol is also occurring. Weird, b/c the way the C6 is configured, no aromatization should occur- strip the C6 configuration, and you are left with androstenedione- which is aromatizable (and easily so)....can't really speculate past that......doesn't really make sense
 
mooch2321

mooch2321

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yeah as i said...the more i look into this product the more confused i get....
 

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