DHB (misnomer, it is 1-Testosterone) versus Tren: is it more like Primo or a "Tren lite"? [Author: Type-IIx]

Very good stack especially ment
It's going great. I'm only up to 8mg of ment a day. Almost 400 test and 200 Dhb. After a few weeks I intend to get test Dhb to 600/300.

I'm looking lean. Strength is fantastic. I've been running 2iu GH and bumping it to 4 for the next 10 weeks
 
It's going great. I'm only up to 8mg of ment a day. Almost 400 test and 200 Dhb. After a few weeks I intend to get test Dhb to 600/300.

I'm looking lean. Strength is fantastic. I've been running 2iu GH and bumping it to 4 for the next 10 weeks
Going too trial dhb at 300mg if it’s pip free I have too give it another try but can’t deal with pip so hopefully none
 
Definitely had some discomfort the first 2 weeks since then. I may be have a slight discomfort. One pin a week.

I pent daily by the way
 
I ran 100mg X 3 mixed with test and the pip does get to you after awhile so I tried daily @ 50mg sub-q and it did help a bit..
 
DHB (1-Testo) vs. Tren

Author: Type-IIx

On the matter of whether so-called "DHB" (this is not its accepted chemical identifier per the nomenclature; it is entirely unlike Boldenone [EQ] and not an EQ metabolite) is more like Primo or Tren, from a chemistry standpoint, it is completely unlike Tren and very similar to Primo.

1-Testosterone
17β-hydroxy-5alpha-androst-1-en-3-one; 17-hydroxyandrost-1-en-3-one; 1-Testo; alternatively, as errata, DHB or Dihydroboldenone
17β-hydroxy-5α-androst-1-en-3-one (A-7 in Vida)


non-aromatizable, non-5α-reducible.

View attachment 173129

An androst-1-ene-3-one (similar to Primobolan & Stenbolone [both are accepted as relatively attenuated androgens reduced in androgenicity and appropriate for cutting and for use in women]): double bond at C-1,2

Vida (A-7): 200:100 anabolic/androgenic ratio

Misconception that 1-Testo is the 5α-reductase product in man of boldenone



Metabolism of 1-Testo


Lacks the delta-4 double bond of testosterone, having a 1,2 double bond instead. This means that 1-Testo will not aromatise, and it will not 5α-reduce in androgen-sensitive tissues like testosterone can (since it's 5α-reduced already). However, due to its particular metabolism, its primary metabolite is DHT! Metabolism is limited, to a large extent, to reduction of the double bond and hydroxylation of the 3-ketone.

1-Testo produces as urine metabolites:

* 5α-dihydrotestosterone ("DHT")
* 5α-androst-1-ene-3α,17β-diol
* 5α-androst-1-ene-3,17-dione
* 5α-androst-1-ene-3α-ol-17-one
* 1-epitestosterone

It is noteworthy that 1-Testosterone's primary metabolite is 5α-DHT: as it is already 5α-reduced, one would infer that it is not a substrate for 5α-reductase, and therefore does not produce 5α-DHT.

There is currently no explanation for its yielding DHT as a metabolite aside from speculation that some enzyme, heretofore unidentified, is responsible for 1,2-dihydrogenation of this androst-1-ene-3-one (Peter Bond, personal communication). It is unlikely that 1-Test's acting as a prohormone to DHT results in increased skeletal muscle bioavailability as it will still be 3α-reduced by AKR1C1, AKR1C2, AKR1C3, & AKR1C4 (C3 being demonstrated to be expressed in human skeletal muscle).

Practical considerations (against the use of 1-Testosterone)

Anecdotally, blood test results demonstrate an increase in C-reactive protein (CRP) ["inflammation"] in common 1-Testo injectable preparations. It is difficult to keep in solution, so the product frequently "crashes" and it is known to cause unbearable "PIP" [post-injection pain].

Signs of hepatic strain in rats. The concentration/dosage used of 1 mg/kg bodyweight (rodent) for 12 days is roughly equivalent to 112 mg weekly for a 100 kg bodyweight man.

Guaiacol is a chemical irritant, a disinfectant, and cough expectorant. It is classified as a hazardous chemical.

From WHO, IARC:



Its use orally in humans acutely induces gastrointestinal, behavioral, tremor, and other changes.


From what I have seen, 1-Testo seems to always lead to elevated C-reactive protein (CRP), whether directly due to its inflammatory or immunogenic effects starting in muscle tissue, or due to guaiacol, or both. CRP is a liver-secreted marker of systemic inflammation that has some predictive power in cardiovascular/thrombotic risk, and is especially dangerous when elevated along with Lp(a) and LDL.

1-Testo would appear to exert its full spectrum of activity (i.e., is almost certainly subject to a sigmoidal S-curve dose/response) by AR agonism. Its optimal dose is likely that which stimulates maximal N retention. It lacks the unique features of Tren to be discussed in the following section (e.g., decreased PPARγ, decreased GR number, increased SC responsiveness to mIGF-I, etc.)


Trenbolone
α-Me-17α-OH-PR; 17β-hydroxy-4,9,11-estratrien-3-one; TBOH
17β-acetoxy-3-oxoestra-4,9,11-triene (Tren Ace)


View attachment 173128

Non-5α-reducible, non-estrogenic synthetic testosterone analogue. A triene (Δ4,9,11) steroid.
* The double bonds at C-4,5, C-9,10, & C-11,12 serve to flatten the steroid (so it can be visualized as slicing into the AR like a knife) but also broadens its homology (increases its affinity for GR, PR, ER, & likely MR).

Tren is insulin sensitizing via decreased PPARγ expression (anti-adipogenic, anti-hyperglycemic), increased muscular IGF-I activity (augments the satellite cell proliferative response to mIGF-I; increases the muscle isoform IGF-IEb mRNA expression, 3.6x) and decreased GR number (anti-catabolic). Relative cardiac harm derives from inhibition of cortisol oxidation and exerting MR action, aggravating atherosclerosis via MR activation and inflammatory processes in the vascular endothelium. Non-5α-reducible, non-estrogenic. Some considerations include reduced GH pulse amplitude and duration (resulting in decreased serum IGF-I).

Conclusion


These two androgens appear as opposite in potency and effects as could be. One is an androst-1-ene-3-one and the other a triene (Δ4,9,11) steroid. Neither provide for basal estrogen (e.g., important for bone metabolism, lipid metabolism, some increase in skeletal muscle size, etc.) One (1-Test) may act as a prohormone to DHT (but not selective in androgen-dependent tissues).

The bodybuilding community’s dosing (belying a sort of informal good enough dose/response relationship) readily belies the differences in potency between the compounds. For example, while 700+ mg of 1-Test is commonplace for modest cosmetic benefits, few would use Tren at this dosage (but rather, quite lower) and expect similar physique outcomes.

Whereas 1-Testo would appear to exert its full spectrum of activity (i.e., is almost certainly subject to a sigmoidal S-curve dose/response) by AR agonism and optimal dosing is likely that which stimulates maximal N retention, Tren is insulin sensitizing via decreased PPARγ expression (anti-adipogenic, anti-hyperglycemic), increasesmuscular IGF-I activity (augments the satellite cell proliferative response to mIGF-I; increases the muscle isoform IGF-IEb mRNA expression, 3.6x), and decreases GR number (anti-catabolic). Tren’s relative cardiac harm derives from inhibition of cortisol oxidation and exerting MR action, aggravating atherosclerosis via MR activation and inflammatory processes in the vascular endothelium. While Tren reduces systemic liver-secreted IGF-I, 1-Testo has no effect.

To illustrate Tren’s potency, consider that:

1. The 350 mg weekly Tren Ace first-time Tren cycle advice originates from Bill Roberts’ writings in the 1990s (he was a very intelligent man, but was excessive at times in his compound & dosage recommendations).

2. Trenbolone acetate’s human equivalent dose (HED):

HED(mg/kg) = (200mg/545kg) * (96/37) = 0.95 mg/kg (total)

Synovex Implant (Elanco) "Component® TE-200 with Tylan®" [Catalog #: 102-8495] contains 200mg TBA, 20mg E2; duration of activity 80 - 90 days

weekly HED(mg/kg) = 0.95 mg/kg * (7/85) ≈ 0.078 mg/kg weekly (or 7.8 mg for 100kg man)...

AR density in cattle



It follows that humans are actually more responsive (excluding differential effects of human metabolism, i.e., weakening of the parent steroid, that are substantial) to an equimolar dose of trenbolone acetate versus bovid with respect to AR-mediated muscle cell responsiveness.

While it does not follow that 10 mg of trenbolone acetate weekly is > a Synovex implant in inducing human skeletal muscle hypertrophy, it can certainly be stated confidently that 350 mg trenbolone acetate is an extremely high dose.

The same cannot at all be stated with respect to 1-Test.

References available upon request by private message (intended as an informal posting)
This is the most comprehensive post on these compounds together that Ive seen, thank you for all the information. DHB is the only injectable I have not yet ran, but looking at experimenting with it in the near future.
 
Is it worth the PIP tho, the fever, that's the question. BTW; did you lean out on DHB? I couldn't quite tell if DHB had a leaning effect. Tren obviously sucks you in due to GR and MR interaction, cortisol etc. Does DHB do anything similar? From what I gather in OP's post DHB seems kinda basic in it's method of action, straight AR agonism and some metabolism into DHT(which I suppose would help dry you out)

I wonder why people on the forums always talk about DBH as being some super rocket fuelled nutrient partioner and this amazing exotic compound, when on paper it appears to not be that way at all
I have dhb that’s 2% 20% holds at 75-100mg just fine and doesn’t hurt I love it at 300-400mg per week with some test and mast it’s much better than tren in my opinion …tren for last 6 weeks of prep that’s about it I feel like
 
Love primo and tren together but really been wanting to try dhb. Been staying away bc of horror stories I’ve heard with pip. I’m not SUPER pip prone but I do get it some
 
Question for @Type-IIx DHBs metabolism into DHT..is it quantifiable? For example does 10% of a certain dose of DHB metabolize into DHT?( the 10% is just an arbitrary number I’m using) is the metabolism into DHT so minuscule that you can’t really measure it like that? Thank you for any clarification
 
Question for @Type-IIx DHBs metabolism into DHT..is it quantifiable? For example does 10% of a certain dose of DHB metabolize into DHT?( the 10% is just an arbitrary number I’m using) is the metabolism into DHT so minuscule that you can’t really measure it like that? Thank you for any clarification
It's quantifiable but also miniscule. I could probably track down the quantity with some expenditure of effort, it's from a Chinese study that was part of a workshop in Cologne, Germany in 2004, but the interest doesn't seem compelling.

What is the reason that you ask? To compare it versus T's increase to DHT?
 
It's quantifiable but also miniscule. I could probably track down the quantity with some expenditure of effort, it's from a Chinese study that was part of a workshop in Cologne, Germany in 2004, but the interest doesn't seem compelling.

What is the reason that you ask? To compare it versus T's increase to DHT?
Yes, wanted to know if it was comparable to testosterone or if it metabolized enough to become problematic for acne, prostate..etc (barring individuals sensitivity to DHT) so I guess the simple answer would be…does it metabolize enough to even worry about…also thank you for answering
 
Yes, wanted to know if it was comparable to testosterone or if it metabolized enough to become problematic for acne, prostate..etc (barring individuals sensitivity to DHT) so I guess the simple answer would be…does it metabolize enough to even worry about…also thank you for answering
Just assess tolerability as usual, by how you actually tolerate it. Besides DHT, there are more pressing concerns that arise out of the use of 1-Test, such as the nigh universal: striking elevations to C-reactive protein (CRP), use of guaiacol as solvent, and the availability of better alternatives like Primo or Stenbolone.

To illustrate the theoretical ("on paper") rather than practical ("real world") aspect of quantifying DHT elevations by 1-Test dose, consider the following:

We know that testosterone =[5α-R]=> 5α-DHT, with a Km = 3.35 nm, following saturable Michaelis-Menten kinetics, such that 600 mg/w testosterone enanthate elevates DHT to ~ 25 ng/dL, 300 mg/w to ~ 15 ng/dL.

How does this knowledge inform your use of testosterone?
 
If 1-Test increases DHT by some unknown enzyme that 1,2-dihydrogenates it, this enzyme is probably not as richly expressed as 5α-R (or we'd have identified it by now) and not as selective in skin, prostate, etc. If 1-Test increases DHT by acting as a 17β-HSD1 inhibitor - a hypothesis I've been interested in that would result in increased DHT & decreased E2 - it's probably not potent or selective at this or it'd probably have been investigated by now as a candidate for therapeutic use in ER-positive breast cancer, especially where aromatase & sulfatase are not over-expressed.
 
Just assess tolerability as usual, by how you actually tolerate it. Besides DHT, there are more pressing concerns that arise out of the use of 1-Test, such as the nigh universal: striking elevations to C-reactive protein (CRP), use of guaiacol as solvent, and the availability of better alternatives like Primo or Stenbolone.

To illustrate the theoretical ("on paper") rather than practical ("real world") aspect of quantifying DHT elevations by 1-Test dose, consider the following:

We know that testosterone =[5α-R]=> 5α-DHT, with a Km = 3.35 nm, following saturable Michaelis-Menten kinetics, such that 600 mg/w testosterone enanthate elevates DHT to ~ 25 ng/dL, 300 mg/w to ~ 15 ng/dL.

How does this knowledge inform your use of testosterone?
I guess it doesn’t really inform my use for testosterone, more so I know what dosages of testosterone bring out certain “sides” for me that I attribute to DHT (bro science) and wasn’t sure if DHB was comparable dosage wise to testosterone to produce DHT…I appreciate the data/detailed answer
 
We know that testosterone =[5α-R]=> 5α-DHT, with a Km = 3.35 nm, following saturable Michaelis-Menten kinetics, such that 600 mg/w testosterone enanthate elevates DHT to ~ 25 ng/dL, 300 mg/w to ~ 15 ng/dL.

you mean that 600mg/w of TE elevates DHT by 25ng/dL not to 25ng/dL, right?
 
I'm currently experimenting with DHB and I have never used Tren. My initial impression is that DHB has a "fat burning" effect because I am leaning out very nicely and I feel it is happening since the addition of DHB. Other than that, so far it is pretty mild and I am not that impressed with it, but I just hit 4 weeks, so I obviously need more time. I feel good on it. Some minor pip occasionally, but I have tried products from three different sources and all of them are generally pip free, so far.

Maybe people are saying it is like tren because it absolutely leans you out.
 
I'm currently experimenting with DHB and I have never used Tren. My initial impression is that DHB has a "fat burning" effect because I am leaning out very nicely and I feel it is happening since the addition of DHB. Other than that, so far it is pretty mild and I am not that impressed with it, but I just hit 4 weeks, so I obviously need more time. I feel good on it. Some minor pip occasionally, but I have tried products from three different sources and all of them are generally pip free, so far.

Maybe people are saying it is like tren because it absolutely leans you out.
curious, how many mgs of dhb a week are you running and what other peds? Debating if I want to try it. You using GL's?
 
Top