Type-IIx
Well-known Member
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.
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)
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)
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.
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)
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)
