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Tren and prostate (whether it causes BPH?)- the science

Type-IIx

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@OuchThatHurts this is for you.

When it was confidently asserted that Tren clearly causes BPH and prostate problems, I should have simply asked for a citation rather than accepting this as fact. However, after reading Peter Bond's latest Meso article and thinking back to some recent Tren research, I have some thoughts on the topic that should act as an effective correction/update to my prior comments on Tren and the prostate.

Hershberger Assay Results (TP “testosterone prop”; TB “trenbolone ace”, sc “subcutaneous”)
“In DHT-forming tissues, with 5α-reductase, such as seminal vesicle and VP [prostate] were much less affected compared to the effects of a similar dose of TP (only showing statistically significant increases at 200μg TB/day) while the levator ani, which exhibits a testosterone (T)-dependent response lacking this enzyme, is significantly increased in size at 50μg TB/day with a dose-response curve nearly identical to sc TP (Fig. 4). Hence TB, as compared to TP, differentially induced “anabolic” effects on androgen-dependent muscles, with lower “androgenic” potency on the sex accessory glands. This tissues elective response is likely based upon the ability of 5α-reductase to inactivate TB, while in contrast, testosterone is converted by the same enzyme to DHT, a more potent androgen. In the LABC, sc TB was equipotent with TP, while in the VP, SV, and GP, even 200μg/day fails to stimulate tissue growth to the same degree as 25μg TP/day.”
[1]

So in rats using the HA, tren has approx. 1/10 - 1/4 the potential to cause BPH as testosterone on a per-dose basis:

Tren-vs-Test-HA-Table.png
[1]


Tren-vs-Test-HA-Graph.png

Dotted lines: Tren Ace
Solid line: Test Prop
[1]

Looking at humans rather than rats (again considering the weaknesses of the HA), the assumption that tren (or AAS generally) causes BPH is far more equivocal, and there is evidence for the opposite (that tren may attenuate prostate growth [2]; that its metabolite 17α-TBOH may shrink the prostate [1 citing WHO]). Consider that in practice the dosage of tren used is far less than test typically. Given what we know about test's 5α-reduction and ubiquitious presence in AAS polypharmacy, it is probably safe to say that tren is not responsible for any significant occurrence of BPH versus high dose test.

The association between testosterone and prostate cancer is related to low (low hypogonadal!) T ranges versus zero T (castrate level), and an effective ceiling is reached in this risk in that hypogonadal range [3]. This squares with Bhasin et al. [4]'s 5α-reductase inhibitor (Dutasteride) + Test study where T supplanted the role of DHT in prostate function. Rather than demonstrating that testosterone (and AAS generally) can both exert androgenic effects in all androgen-sensitive tissues, and that their relative effects in any tissue depend upon their relative concentrations and potency, this data rather supports a model wherein testosterone's conversion to DHT is not obligatory, but amplifies the effects of testosterone in tissues with high 5α-reductase activity such as the prostate and skin, but not in tissues with low 5α-reductase activity such as skeletal muscle and bone [4]. The pertinent findings from Bhasin et al. were:
Prostate Volumes and PSA level

“Change in prostate volume and PSA level were not significantly related to either testosterone dose or concentration, and did not differ significantly between the placebo and dutasteride groups.”

See Figure:

Test-prostate-volume-Plot.png [4]

Conclusion: There is no evidence to suggest that long-term, supraphysiological dosages of AAS even cause BPH in humans!

[T]here are no clear indications, case reports, or systematic investigations demonstrating that AAS abuse causes benign prostatic hypertrophy (BPH)... As several AAS also have gestagenic activity in addition to androgenic effects, some AAS may prevent testosterone-dependent prostate growth when given in combination and this may explain the low incidence of BPH in AAS abusers.
[2]

Tren with its affinity for the PR, acting as a progestin, sure seems a good candidate.

_______________________________________
References:

[1] Vickie S. Wilson, Christy Lambright, Joe Ostby, L. E. Gray, Jr., In Vitro and in Vivo Effects of 17β-Trenbolone: A Feedlot Effluent Contaminant, Toxicological Sciences, Volume 70, Issue 2, December 2002, Pages 202–211, https://doi.org/~/70.2.202

[2] Nieschlag, E., & Vorona, E. (2015). MECHANISMS IN ENDOCRINOLOGY: Medical consequences of doping with anabolic androgenic steroids: effects on reproductive functions. European Journal of Endocrinology, 173(2), R47–R58. doi:10.1530/eje-15-0080

[3] Morgentaler, A., & Traish, A. M. (2009). Shifting the Paradigm of Testosterone and Prostate Cancer: The Saturation Model and the Limits of Androgen-Dependent Growth. European Urology, 55(2), 310–321. doi:10.1016/j.eururo.2008.09.024

[4] Bhasin S, Travison TG, Storer TW, Lakshman K, Kaushik M, Mazer NA, Ngyuen AH, Davda MN, Jara H, Aakil A, Anderson S, Knapp PE, Hanka S, Mohammed N, Daou P, Miciek R, Ulloor J, Zhang A, Brooks B, Orwoll K, Hede-Brierley L, Eder R, Elmi A, Bhasin G, Collins L, Singh R, Basaria S. Effect of testosterone supplementation with and without a dual 5α-reductase inhibitor on fat-free mass in men with suppressed testosterone production: a randomized controlled trial. JAMA. 2012 Mar 7;307(9):931-9. doi: 10.1001/jama.2012.227. PMID: 22396515; PMCID: PMC6035750.
 

OuchThatHurts

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Very interesting. It has never caused problems for me personally. I have never noticed prostate problems while using AAS (on or off), including trenbolone. I've always taken myself out of DHT discussions because genetically, I do not suffer from many of DHT's effects despite having naturally normal T levels, even now. In particular, effects where it's been suggested DHT is the cause; BPH and balding primarily. I believe much of that is genetic. If 5% of TT converts to DHT that would suggest a 20:1 ratio. Maybe there's something to be said for the T : DHT ratio (as I definitely believe this is true with E2). Of the isoenzymes of 5α-reductase, type 2 seems the most biologically active of types 1, 2 and 3.

This could mean several things. DHT is a intracellular androgen, binding inside the cell membrane (cytoplasm) and initiates a series of events leading to alteration in DNA expression at the nucleus (and these specific genes have been identified). It could mean that my reduction rate is normal and that my cells are simply not very dense with ARs (doubtful) or that my DHT levels are just naturally low in general, perhaps due to a greater production of types 1 and 3 5α-reductase. It would be hard to tell with so many variables. But there is certainly a genetic component in humans which can be observed even anecdotally.

It would be interesting to see this carried out with human subjects. It might be interesting to see if those males with a high level of DHT expression or high levels of DHT in general who exhibit balding and/or some prostatic hypertrophy, would experience an increase or attenuation in effects. To me, were it not for 3-hydroxysteroid dehydrogenase in muscle tissue, DHT might actually prove to be a potent anabolic. Masteron is very similar molecularly but far different in it's effects.

I remember my friend Don years ago, just in our 20's, he was already going bald and wow, it was not easy for him. He would say he shampooed his hair and had fistfuls of hair where he wanted to just cry. I'll be grey, but I'm not going to be bald. A little receding maybe but nothing on my crown. In fact, that's the thickest of all the hair on my head. This is one area where I know I'm an outlier. I've never had a single chest hair.

More on DHT:
 

b_cornelius

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In response to Ouch,
Aged thinning hair follicles overexpress the AR, thus also overexpressing TGF-Beta. If anyone wants to elaborate on DHT's particular androgen response elements, please do. I personally don't consider DHT to be particularly a huge factor over others.
 

Kaladryn

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@OuchThatHurts this is for you.

When it was confidently asserted that Tren clearly causes BPH and prostate problems, I should have simply asked for a citation rather than accepting this as fact. However, after reading Peter Bond's latest Meso article and thinking back to some recent Tren research, I have some thoughts on the topic that should act as an effective correction/update to my prior comments on Tren and the prostate.


[1]

So in rats using the HA, tren has approx. 1/10 - 1/4 the potential to cause BPH as testosterone on a per-dose basis:

View attachment 144610
[1]


View attachment 144609

Dotted lines: Tren Ace
Solid line: Test Prop
[1]

Looking at humans rather than rats (again considering the weaknesses of the HA), the assumption that tren (or AAS generally) causes BPH is far more equivocal, and there is evidence for the opposite (that tren may attenuate prostate growth [2]; that its metabolite 17α-TBOH may shrink the prostate [1 citing WHO]). Consider that in practice the dosage of tren used is far less than test typically. Given what we know about test's 5α-reduction and ubiquitious presence in AAS polypharmacy, it is probably safe to say that tren is not responsible for any significant occurrence of BPH versus high dose test.

The association between testosterone and prostate cancer is related to low (low hypogonadal!) T ranges versus zero T (castrate level), and an effective ceiling is reached in this risk in that hypogonadal range [3]. This squares with Bhasin et al. [4]'s 5α-reductase inhibitor (Dutasteride) + Test study where T supplanted the role of DHT in prostate function. Rather than demonstrating that testosterone (and AAS generally) can both exert androgenic effects in all androgen-sensitive tissues, and that their relative effects in any tissue depend upon their relative concentrations and potency, this data rather supports a model wherein testosterone's conversion to DHT is not obligatory, but amplifies the effects of testosterone in tissues with high 5α-reductase activity such as the prostate and skin, but not in tissues with low 5α-reductase activity such as skeletal muscle and bone [4]. The pertinent findings from Bhasin et al. were:


View attachment 144608[4]

Conclusion: There is no evidence to suggest that long-term, supraphysiological dosages of AAS even cause BPH in humans!


[2]

Tren with its affinity for the PR, acting as a progestin, sure seems a good candidate.

_______________________________________
References:

[1] Vickie S. Wilson, Christy Lambright, Joe Ostby, L. E. Gray, Jr., In Vitro and in Vivo Effects of 17β-Trenbolone: A Feedlot Effluent Contaminant, Toxicological Sciences, Volume 70, Issue 2, December 2002, Pages 202–211, https://doi.org/~/70.2.202

[2] Nieschlag, E., & Vorona, E. (2015). MECHANISMS IN ENDOCRINOLOGY: Medical consequences of doping with anabolic androgenic steroids: effects on reproductive functions. European Journal of Endocrinology, 173(2), R47–R58. doi:10.1530/eje-15-0080

[3] Morgentaler, A., & Traish, A. M. (2009). Shifting the Paradigm of Testosterone and Prostate Cancer: The Saturation Model and the Limits of Androgen-Dependent Growth. European Urology, 55(2), 310–321. doi:10.1016/j.eururo.2008.09.024

[4] Bhasin S, Travison TG, Storer TW, Lakshman K, Kaushik M, Mazer NA, Ngyuen AH, Davda MN, Jara H, Aakil A, Anderson S, Knapp PE, Hanka S, Mohammed N, Daou P, Miciek R, Ulloor J, Zhang A, Brooks B, Orwoll K, Hede-Brierley L, Eder R, Elmi A, Bhasin G, Collins L, Singh R, Basaria S. Effect of testosterone supplementation with and without a dual 5α-reductase inhibitor on fat-free mass in men with suppressed testosterone production: a randomized controlled trial. JAMA. 2012 Mar 7;307(9):931-9. doi: 10.1001/jama.2012.227. PMID: 22396515; PMCID: PMC6035750.
Let me ask you this, how many tren cycles have you done, and up to what dosage? Also, how many people (friends, clients, workout partners) do you know personally who have used tren and have discussed their prostate issues, or lack thereof?

Also, another interesting question along these lines would be, how are we defining prostate issues? Urination frequency? Urination volume? Medically diagnosed BHP? Self-diagnosed BHP?
 

Kaladryn

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This could mean several things. DHT is a intracellular androgen, binding inside the cell membrane (cytoplasm) and initiates a series of events leading to alteration in DNA expression at the nucleus (and these specific genes have been identified). It could mean that my reduction rate is normal and that my cells are simply not very dense with ARs (doubtful) or that my DHT levels are just naturally low in general, perhaps due to a greater production of types 1 and 3 5α-reductase. It would be hard to tell with so many variables. But there is certainly a genetic component in humans which can be observed even anecdotally.

It would be interesting to see this carried out with human subjects. It might be interesting to see if those males with a high level of DHT expression or high levels of DHT in general who exhibit balding and/or some prostatic hypertrophy, would experience an increase or attenuation in effects. To me, were it not for 3-hydroxysteroid dehydrogenase in muscle tissue, DHT might actually prove to be a potent anabolic. Masteron is very similar molecularly but far different in it's effects.

I remember my friend Don years ago, just in our 20's, he was already going bald and wow, it was not easy for him. He would say he shampooed his hair and had fistfuls of hair where he wanted to just cry. I'll be grey, but I'm not going to be bald. A little receding maybe but nothing on my crown. In fact, that's the thickest of all the hair on my head. This is one area where I know I'm an outlier. I've never had a single chest hair.
Receptor density isn't generally a huge factor in DHT-related issues, neither are plasma DHT levels, these tend to be fairly uniform. Loads of in-depth info on DHT and hairloss as this has been studied extensively. I've spent some time on hair loss forums, it's amazing how deep the knowledge is on this subject. I personally don't deal with hair loss so it's never been that much interest to me, although I do use 5ARIs on heavier cycles.
 

OuchThatHurts

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As I said above, this is why I drop out of the DHT discussions. It's never been an issue for me personally and it's been studied extensively. I'm certainly not about to debate the topic. I'm not even certain what prompted the OP to start a thread on it. I have a steady stream and a dark pelt on my head. It's interesting though and may be helpful to some guys here.
 

Type-IIx

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Let me ask you this, how many tren cycles have you done, and up to what dosage? Also, how many people (friends, clients, workout partners) do you know personally who have used tren and have discussed their prostate issues, or lack thereof?

Also, another interesting question along these lines would be, how are we defining prostate issues? Urination frequency? Urination volume? Medically diagnosed BHP? Self-diagnosed BHP?
I'm not sure, 6 maybe? Up to 450mg. Been a long while though. Several people I know have also, but nobody has ever mentioned anything about prostate stuff or mentioned it IME. My post was directed at BPH and the actual issue of T (endogenous) and prostate cancer risk. That's all man. I honestly thought BPH was a common AAS risk, but apparently it's a misconception. Hopefully that makes people happy bro.
 

Type-IIx

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As I said above, this is why I drop out of the DHT discussions. It's never been an issue for me personally and it's been studied extensively. I'm certainly not about to debate the topic. I'm not even certain what prompted the OP to start a thread on it. I have a steady stream and a dark pelt on my head. It's interesting though and may be helpful to some guys here.
Continuation of the topic of tren and clarifying the disincentives a bit. I always appreciate people sharing shit they learn, and you seemed like someone that has a mind for this stuff.
 

b_cornelius

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Are we truly talking BPHypertrophy of existing cells or BPHyperplasia of proliferating cells?
Got two words about Hyperplasia: Contact Inhibition, Confluence

I'm gonna start selling words like Sonic Hedgehog/Smoothened, Hippo/YAP. Yah, the advanced stuff sounds like a joke.
 

Type-IIx

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Are we truly talking BPHypertrophy of existing cells or BPHyperplasia of proliferating cells?
Got two words about Hyperplasia: Contact Inhibition, Confluence

I'm gonna start selling words like Sonic Hedgehog/Smoothened, Hippo/YAP. Yah, the advanced stuff sounds like a joke.
Correspondence: [email protected]

Perhaps he can tell you about normal prostate growth in a way that won't make you react the way I seem to.
 

KillerStack

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Tren does "irritate" my prostate. More pissing problems when I'm on it. For sure.
 

mexbeast

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I used tren for about 10 years straight, starting low but increasing to 600mgs within weeks and at 600 i could see and feel what everyone talked about, i stayed at that dose for a year or two then increased to 800 for another year or two and for the rest of my cycling years i used 800 to 1000mgs a week that was up to my 38 years old or so, in all those years i never felt anything related to prostate issues. The only time i felt a wired feeling was when i used 400mgs of masteron which was bad enough that i discontinued it after a couple months.
Right about 5 to 7 years after quitting cycling i requested my doctor to do a psa test to have as a base and to see where it was and i was happy that it was low, can't remember the numbers but low, hope that helps
 

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