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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
 
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
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.
 
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.
Then why you even want to use it lol.
That's why one take it
 
Then why you even want to use it lol.
That's why one take it
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 DHT

The RU58841 seems effective with everything so could just rely on that - it’s quite similar to ADT used to treat prostate cancer, but in topical form so very limited systemic spillover. I doubt the systemic effects of topicals are significant with supraphysiologic androgens but they may be with natties.
 
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
I’ve seen studies showing 2-3x per week with similar efficacy of finasteride daily.

Not really sure why fina works as well as it does. I took it for 25 years and it stopped hair loss on my crown. Probably did cause minor loss of libido and more anxiety though. I stopped it at age 51.
 
Is high blood pressure a direct result of high hematocrit or red blood cells?
Last bloods on 9/12
Hematocrit 41.5%
Rbc 4.66
Will check bloods next couple weeks
 
Well DHT is the body’s apex androgen, excluding skeletal muscle, not testosterone. So reducing DHT will alleviate androgenic symptoms ie male pattern baldness, prostate enlargement, acne, etc. But higher local levels are important in the brain, breasts, and penis so it has potential side effects including anxiety, gyno, and ED.

Basically you want just enough to be fully functional. And it’s not replaceable but any ‘DHT derivates’ - basically they should be considered an attenuated testosterone (DHB possibly an exception there) that doesn’t 5α-reduce to DHT or aromatize to testosterone.

Testosterone is basically a prodrug for DHT and estradiol, and the anabolic endogenous androgen for skeletal muscle.
 
300mg 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?
The 300mg Trest and 1g Primo were run separately

Trest 300mg was solo, I think potentially 30mg Var in there?
I didn't run an AI, made really good progress and had no sides.

I'm Trestolone's #1 fan, got a decent bit of it tucked away...
Unfortunately, it's all 50mg/mL Trest A, and I hate short esters + low concentrations =(

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.
It takes quite a while to write up decent literature review posts, hopefully I can finish it soon.

The gist of it is that a series of other enzymatic reactions can theoretically produce E2 from Nandrolone in the liver

But this comes from a paper that looked at 17a-alkylated 19-Nortestosterone derivatives (two progestins) given orally. So I can't be sure that enough hepatic exposure would occur in IM/SC injection for it to be relevant.

"Can 19-nortestosterone derivatives be aromatized in the liver of adult humans?" (PDF attached)

Also, there is evidence that Nandrolone administration alters liver CYP enzyme activity:

1759229332527.webp

The 2nd most concrete evidence I've seen is a 2 year study on primates where Nandrolone administration produced E2 levels higher than untreated:


> "The data also suggest that nandrolone was converted to
estradiol, and this conversion also may play a role in the arterial and lipid effects observed."

White line below = natty monkeys. Both Nandrolone groups reached supraphysiological E2 levels.

1759231737565.webp
 

Attachments

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 :D

Everybody wins
 
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 :D

Everybody wins

Or he could do baseline labs with E1 included, run some EQ and recheck. I'm not so deep into biochemistry and maybe what he's reading is right but there's enough anecdotal reports telling that E1 increases with boldenone with some bloodwork included (like in the video i linked) and he seems to still be sceptical.
 
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.
are you sure it wasn't the 750 mg of Test that raised your e2? hmmmmm
 
Trestolone does not aromatize into, or increase levels of, E2

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.

Very possible that 193 was indeed all estradiol from testosterone, in which case total summed estrogen would be far higher, as that's a serious dose of trestolone. Either way, safe to assume very high DHT levels negated the estrogenic problems most men would have at a far lower E2 number.

I really need my E2 in a fairly tight 25-35 range to feel good physically/emotionally and be fully functional downstairs.

TRT clinics typically prescribe anastrozole with testosterone, focusing on lab values alone to keep it in range, or do not believe in using AIs practically ever with the philosophy that 'estrogen is natural and protects the body against androgens', 'estrogen is good', and attribute most of the estrogenic problems men get to something else. In reality both are probably correct, in different subpopulations; with sometimes 1000's of patients to keep track of, they aren't individualized enough to understand certain (likely most) men are very estrogen sensitive, while others are not - and DHT conversion is likely the differentiating factor.

@Calderon88 how is your hair? Higher DHT levels are typically associated with MPB, along with genetic predisposition. The link between high DHT and prostate hypertrophy/cancer is far more complex as estrogen and SHBG are at least as important. An example is that men who take 5a-reductase inhibitors for hair loss are less likely to develop BPH or low-grade prostate/favorable prognosis prostate cancer (Gleason 6), but more likely to develop high-grade/unfavorable diagnosis prostate cancer (Gleason 7-10). I took fina 0.5-1mg per day for over 20 years as a natty, but stopped about five years ago. I've been able to largely maintain my hair even on gear by using topicals only.
 
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.
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.
 
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.
Good luck with that.
 
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.
Nandrolone is for low aromatizers and Boldenone is for high aromatizers. In general terms. I've heard DHB is super toxic.
 
Nandrolone is for low aromatizers and Boldenone is for high aromatizers. In general terms. I've heard DHB is super toxic.
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.

The study showing increased liver weight was in rabbits… it also showed less muscle accumulation than test prop. So I don’t think rabbits are a good surrogate for humans. I do know some have gotten elevated GGT and/or hs-CRP with it, others do not. Some have developed ‘androgen flu’ while on it. I have not checked labs as it was going to be a brief run, but have felt fine with good appetite and no symptoms I can attribute to it.

I only foresee using it for short bursts ~ 4 wks. The extra strength I got from it came on surprisingly fast, and peaked by 2-3 weeks. Been in it four weeks now, took my last dose today. So only a few weeks at serum peak.
 
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