Duta twice a week is the dosage used lately by many well renowned trichologist.
85+% reduction of DHT
Works like a charm, zero side effect
85+% reduction of DHT
Works like a charm, zero side effect
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Yeah that’s the problem, I don’t want an 85% reduction in DHT systemically, or 5α-reduced neurosteroids ie allopregnenolone. And the terminal half life is 4-5 weeks, so looking at months to reach steady state or effects to dissipate after cessation. Like EQ but much longer.Duta twice a week is the dosage used lately by many well renowned trichologist.
85+% reduction of DHT
Works like a charm, zero side effect
Then why you even want to use it lol.Yeah that’s the problem, I don’t want an 85% reduction in DHT systemically, or 5α-reduced neurosteroids ie allopregnenolone. And the terminal half life is 4-5 weeks, so looking at months to reach steady state or effects to dissipate after cessation. Like EQ but much longer.
Anyway that’s the rationale for the very infrequent dosing.
Would be nice if microdose capsules/tablets or a liquid solution were available, but have not found any.
Smaller reduction in DHT - trying to moderately reduce it not wipe it out. I need some, didn’t feel quite right when using MENT only. So I now use MENT + sub-TRT test to have some DHTThen why you even want to use it lol.
That's why one take it
I’ve seen studies showing 2-3x per week with similar efficacy of finasteride daily.Duta twice a week is the dosage used lately by many well renowned trichologist.
85+% reduction of DHT
Works like a charm, zero side effect
following, i would like to knowI don't understand what the advantage of reduced production of DHT would be, exactly.
The 300mg Trest and 1g Primo were run separately300mg Trestolone/MENT
1000mg Primo
How was that cycle? I've never taken Trest of Primo in high doses and that combo my curiosity. I'm guessing you still ran an AI?
It takes quite a while to write up decent literature review posts, hopefully I can finish it soon.please do
Have read it converts to ‘estrone’ in the liver. Have also read MENT (a nandrolone derivative) metabolizes to 7α-methylestradiol in the liver independent of aromatase.
But I’m not aware of any back door pathway for a male to synthesize any estrogen other than via aromatase of endogenous or exogenous androgens (unlike a woman with functioning ovaries). Changes to A-ring to make an estrogen are very, very specific to that enzyme… if there is another that can do it, I’m not aware of it being identified or described.


They have a C4-5 double bond... once that bond is 5⍺-reduced, it is permanent. I believe some fungi have an enzyme to restore it though.
This is why I can see Boldenone being more of a potential AI than DHB, and why I don't think primo is an AI. That's not to say primo cannot lower estradiol, it's just via some other mechanism like inhibition of 17β-HSD1 which will shift the overall estrogen distribution from estradiol > estrone (which is itself is weak agonist and essentially will act a competitive inhibitor to estradiol).
DHT and likely its derivatives are all inherently anti-estrogenic as well probably via down-regulation of the receptor and/or its transcription activity. This is why men with high DHT levels can tolerate higher estradiol levels, and conversely why men with normal estradiol levels can high high estrogen symptoms and body habitus from low DHT (i.e finasteride use).
I've read here and other places that EQ aromatizes to estrone, which is incorrect. It has a 17-OH hydroxyl group, not a keto group, so itself will leave the aromatase enzyme as estradiol. This is also confirmed in research papers, excluding body building anecdotals; the same applies to its major Bm1 metabolite.
Only steroidal molecules with a 17-keto group like androstenedione will be converted to estrone by aromatase. In post menopausal women, most of their estrogen is estrone because it is derived from DHEA > androstenedione > estrone.
What happens to that estradiol after being formed is another question. Estrone is both a metabolite of and precursor to estradiol so something affecting the 17⍺- and 17β HSD enzymes can certainly lower one and raise the other.
I'm not saying any of this is incorrect, and I actually quite appreciate the thoughtfulness of your posts in general, but if you'd cite sources for claims like these it'd improve the board's discussions as a whole.
If we can all get in the habit of saying: "ABC does XYZ [0]" with a citation link and (preferably) relevant quote/excerpt, then it becomes immediately easy to call out + dismiss unsubstantiated bullshit/broscience
Everybody wins
Trestolone does not aromatize into, or increase levels of, E2I was able to run 300mg of trest enanthate which raised my e2 to 193
are you sure it wasn't the 750 mg of Test that raised your e2? hmmmmmYoure right im a super high DHT converter. I was able to run 300mg of trest enanthate which raised my e2 to 193 with just 750mg Test Cyp. and was totaly fine until the end of the Cycle were progesterone became too high and made me act weird. Thats why i was thinking of increasing my trest dosage to 500 with my next cycle , however i will run 250 mgs of masteron with it to combat the progesterone. Im just worried about Blood pressure and heartrate going up too much.
That is true, one would need to consider estradiol (from test) + 7a-methylestradiol (from trestolone). Regarding bloodwork it depends on the test/lab- 7a-methylestradiol might detect on some ECLIA estrogen tests, but definitely not captured with LC/MS hs-Estradiol.Trestolone does not aromatize into, or increase levels of, E2
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7α-Methylestradiol - Wikipedia
en.wikipedia.org
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Trestolone - Wikipedia
en.wikipedia.org
Mast won't combat the progestogenic effects of 19-nors, you will want cabergoline for that. At lower doses SNS Inhibit-P (which contains p5p, vitex castus agnus, and mucana pruriens) may suffice. Trestolone and trenbolone both bind to then progesterone receptor with high affinity and likely are SPRMs, activating it in some tissues and blocking it (by preventing progesterone from binding) at others. One effect is an up-regulation or sensitization of PRLR, cabergoline is a band-aid that acts by crushing natural prolactin levels. It is uncommon for 19-nors to actually raise prolactin levels on blood work, but despite normal blood levels the symptoms are the same as prolactinemia. Just 0.25mg twice per week should be enough.Youre right im a super high DHT converter. I was able to run 300mg of trest enanthate which raised my e2 to 193 with just 750mg Test Cyp. and was totaly fine until the end of the Cycle were progesterone became too high and made me act weird. Thats why i was thinking of increasing my trest dosage to 500 with my next cycle , however i will run 250 mgs of masteron with it to combat the progesterone. Im just worried about Blood pressure and heartrate going up too much.
Good luck with that.My next blast will start will Nandrolone only, partially with the intent to prove that it does aromatize, albeit mildly. (Or more technically, has a metabolic by-product that is Estradiol).
Unrelated: I don't think it's aromatization happens via the aromatase enzyme. This is a long story, but I'll make a post explaining my reasoning with sources.
Nandrolone is for low aromatizers and Boldenone is for high aromatizers. In general terms. I've heard DHB is super toxic.Yeah that 20% figure is thrown around a lot as if it’s fact - believe it came from Llewelyn’s book so I get why, but if I remember the assays/studies he referenced were questionable at best.
Nandrolone probably aromatizes at more like 10%, if that, based on how much is needed to maintain adequate estrogen with it used solo. It does seem to upregulate aromatase and/or ER activity significantly when used with test - adding it to an established good test cycle is an easy path to gyno.
I’m trying EQ now hoping it acts as an AI… primobolan does not for me. Boldenone has an A-ring that shares features with steroidal AIs (exemestane, atamestane, formestane, etc) so it’s possible that it or a metabolite is one. Primobolan does not, and it cannot be metabolized into one because reduction of the c4-5 double bond all those steroidal AIs share is permanent in humans - there is no enzyme to restore it. It’s made me wonder if those using primo whi crash their estrogen got EQ - or a mix of primo/EQ, instead. Probably in some cases, in others that have had happen with tested/real primo it can reduce E2 via some other unclear mechanism.
DHB is nearly identical to primobolan - it’s just missing the C1 methyl group which makes it orally unavailable and much more potent - and have yet to hear any claim it has an AI effect. I’m familiar with the systemic inflammation and liver stress claims, but nothing has increased my strength like DHB even at just 105mg/wk! I’ll use it for short blasts ~ 4 wks to break gym plateaus.
I think the toxicity is overstated. Chemically it should not be toxic, being primobolan without the C1 methylation. It is far more potent than primobolan, so dosages shouldn’t be similar. I’ve seen YT videos suggesting 300-609mg/wk DHB, I would say 70mg/week on the low side and 210mg/wk on the high side is reasonable.Nandrolone is for low aromatizers and Boldenone is for high aromatizers. In general terms. I've heard DHB is super toxic.
Long half life. I do a half dose every 5 days but basically it's the sameDut every ten days? I cant' see that doing anything.
