Anyone run MENT and tren together?

[Type-IIx]

Where does MENT make sense to me? MENT can be used to replaced testosterone with some anecdotal reports that 20 mg/d sufficiently supports sexual function (speculatively), but not at or above moderately-high doses of MENT & Tren, because of their potent combinatory gestagenic effects and the interactions of the potent 7a-ME aromatic product of MENT with progestins, increasing estrogen sensitivity. MENT & Tren, sans testosterone, will not adequately replete the functions of 5α-reductase to support sexual function in peripheral (e.g., gonadal) & CNS tissues. Since MENT is a weaker androgen (reduced AR nuclear retention vs. trenbolone) than Tren it can be viewed as taking up more room in the syringe than Tren for less benefit; and since it is a more potent estrogenic agent (as a result of its aromatization to 7a-ME) than Test with reduced androgenicity, its use is spurious where Test & Tren already maximally synergize (combine greater than additively).

Basically, MENT makes sense in very limited circumstances, most clearly as a male contraceptive and HRT alternative for men.

 

[Type-IIx]

That doesn't surprise me at all, I'd imagine because it's peak, and subsequent clearance times as so short it's not enough time for any meaningful aromatization or other retention mechanisms to take place?

That's my thinking also, because it is, so it must be, basically.

I have kept this data (TNE; testosterone base, oil vehicle) to show that it is not as potently estrogenic at 2.5 - 3 h as one might assume (50 mg TNE) following single dose pharmacodynamics. Testosterone No Ester (TNE) PART 2...
* At 2.5 - 3 h post-injection (50 mg testosterone base, oil vehicle; TNE):
* Noteworthy Results: insignificant rise in estradiol (E2: 22.6 vs. 20.1 [base-line] pg/mL; no significant increase to HCT, Hb; LH & FSH remained normal).
* Private medical advisor consultation, informed that:
- Erythropoiesis: Erythrocyte (RBC; red blood cell) formation takes 7 days to fully form, such that injecting a rapid source of testosterone would not cause the body to create as many RBCs as a longer ester testosterone formulation, and that the body would clear the single dose (TNE; 50 mg) before a full account of the production of RBC would occur, thereby maintaining normal RBC # on short time-frames & wide injection frequencies.
- Although the body does compensate for the increased level of testosterone, it's a longer process then the peak of the half life testosterone itself, and the rise in estrogen is more of an after-effect than something that will perfectly coupled to by testosterone dose. Daily injections of TNE will superimpose estradiol elevations dose- & time- dependently; indeed, injecting as frequently as q9d (every nine days) may lead to superimposition (from the Tlast PK data for aqueous testosterone suspension).

I also posted some additional data on testosterone suspension (aqueous) pharmacokinetics, etc. in that same thread: Testosterone No Ester (TNE) PART 2...

 

[NotHuman]

That's my thinking also, because it is, so it must be, basically.

I have kept this data (TNE; testosterone base, oil vehicle) to show that it is not as potently estrogenic at 2.5 - 3 h as one might assume (50 mg TNE) following single dose pharmacodynamics. Testosterone No Ester (TNE) PART 2...
* At 2.5 - 3 h post-injection (50 mg testosterone base, oil vehicle; TNE):
* Noteworthy Results: insignificant rise in estradiol (E2: 22.6 vs. 20.1 [base-line] pg/mL; no significant increase to HCT, Hb; LH & FSH remained normal).
* Private medical advisor consultation, informed that:
- Erythropoiesis: Erythrocyte (RBC; red blood cell) formation takes 7 days to fully form, such that injecting a rapid source of testosterone would not cause the body to create as many RBCs as a longer ester testosterone formulation, and that the body would clear the single dose (TNE; 50 mg) before a full account of the production of RBC would occur, thereby maintaining normal RBC # on short time-frames & wide injection frequencies.
- Although the body does compensate for the increased level of testosterone, it's a longer process then the peak of the half life testosterone itself, and the rise in estrogen is more of an after-effect than something that will perfectly coupled to by testosterone dose. Daily injections of TNE will superimpose estradiol elevations dose- & time- dependently; indeed, injecting as frequently as q9d (every nine days) may lead to superimposition (from the Tlast PK data for aqueous testosterone suspension).

I also posted some additional data on testosterone suspension (aqueous) pharmacokinetics, etc. in that same thread: Testosterone No Ester (TNE) PART 2...

Interestingly, I watched a video on youtube yesterday where a doctor said he saw patients have a lower hematocrit elevation on test prop for trt vs test cyp

 

[Type-IIx]

Interestingly, I watched a video on youtube yesterday where a doctor said he saw patients have a lower hematocrit elevation on test prop for trt vs test cyp

Goes to the heart of the weakness of observational (epidemiological) data & drawing informal conclusions, how even MDs are prone. There is a TRT doc here on Meso who was convinced AAS dose-dependently increased basal metabolic rate because of, what can only be, random noise in some data he collected from his patients; and reflects more his own desires & assumptions than anything factual.

The data I have seen a lot of shows pretty convincingly that propionate > everything else in potency to increase HCT/Hb... Except probably acetate; a form of testosterone I haven't seen anyone use in a long time until you mentioned it. And this makes sense, given that rapidity of action (low Tmax; and high Cmax #, or number of "peaks") is shown to be directly related to stimulating erythropoiesis/suppressing hepcidin.

 

[Type-IIx]

Interestingly, I watched a video on youtube yesterday where a doctor said he saw patients have a lower hematocrit elevation on test prop for trt vs test cyp

An interesting counterpoint though that could be raised to what I said above is seen with daily subcutaneous administration. With daily, small injections into adipose tissue, this effect is reversed.

This is probably related to low absorption into the blood from the adipose depot though.

So, really, despite seeming to support an increased admin. frequency & reduced erythropoiesis, this just reflects the same underlying phenomenon as above, where Tmax as appearance into blood ends up delayed even with frequent administration of any logP/ester length, because absorption for the subcutaneous route is slowed due to a low surface area. Probably some effects on lag time also.

 

[barbell001]

I still don't know what to think of MENT - I keep trying different labs but all I end up with is stonking high BP which meds don't seem to bring down much. I haven't seen any of these big strength gains either.

 

[NotHuman]

Goes to the heart of the weakness of observational (epidemiological) data & drawing informal conclusions, how even MDs are prone. There is a TRT doc here on Meso who was convinced AAS dose-dependently increased basal metabolic rate because of, what can only be, random noise in some data he collected from his patients; and reflects more his own desires & assumptions than anything factual.

The data I have seen a lot of shows pretty convincingly that propionate > everything else in potency to increase HCT/Hb... Except probably acetate; a form of testosterone I haven't seen anyone use in a long time until you mentioned it. And this makes sense, given that rapidity of action (low Tmax; and high Cmax #, or number of "peaks") is shown to be directly related to stimulating erythropoiesis/suppressing hepcidin.

So to rank the different testosterone esters in order of highest HCT elevation to lowest, we have
1. prop
2. cyp/enanthate
3. acetate
4. TNE
?

 

[NotHuman]

I still don't know what to think of MENT - I keep trying different labs but all I end up with is stonking high BP which meds don't seem to bring down much. I haven't seen any of these big strength gains either.

For me, the strength gains are the most prominent when I use MENT

 

[barbell001]

For me, the strength gains are the most prominent when I use MENT

Are you allowed to say which lab you use on this forum?

 

[Type-IIx]

So to rank the different testosterone esters in order of highest HCT elevation to lowest, we have
1. prop
2. cyp/enanthate
3. acetate
4. TNE
?

Well we know that Prop > Cyp > Ena in stimulating erythropoiesis.

Base (suspension; TNE), as used in practice (i.e., short-term, 1 - 2 weeks, because nobody wants to pin that frequently and/or pre-workout for a couple sessions weekly) tends to actually fall on the very low side of the continuum, for the reasons explained here: [link], that because red blood cells are formed over 7 days & the elimination of testosterone base is very rapid, there is not the same superimposition of peak T to stimulate erythropoiesis as with esterified testosterone.

Acetate, since it is not used like testosterone base (e.g., TNE), but instead medium- to long- term (in terms of months) & daily (q.d.) or every other day (q.o.d.), its rapidity of action being associated with low Tmax & a high Cmax # (frequent "peaks"), falls on the very high end of the continuum.

So, in practice:
1. Acetate
2. Propionate
3. Cypionate
4. Enanthate
5. Base

If, however, the assumption of use regarding testosterone base were to break down because the user doesn't mind feeling like a pincushion or prefers aqueous suspension & pinning once or twice daily for months on end, then we would pop 5. off this stack and push it into the 1. slot, everything else shifting down by one space.

 

[NotHuman]

Well we know that Prop > Cyp > Ena in stimulating erythropoiesis.

Base (suspension; TNE), as used in practice (i.e., short-term, 1 - 2 weeks, because nobody wants to pin that frequently and/or pre-workout for a couple sessions weekly) tends to actually fall on the very low side of the continuum, for the reasons explained here: [link], that because red blood cells are formed over 7 days & the elimination of testosterone base is very rapid, there is not the same superimposition of peak T to stimulate erythropoiesis as with esterified testosterone.

Acetate, since it is not used like testosterone base (e.g., TNE), but instead medium- to long- term (in terms of months) & daily (q.d.) or every other day (q.o.d.), its rapidity of action being associated with low Tmax & a high Cmax # (frequent "peaks"), falls on the very high end of the continuum.

So, in practice:
1. Acetate
2. Propionate
3. Cypionate
4. Enanthate
5. Base

If, however, the assumption of use regarding testosterone base were to break down because the user doesn't mind feeling like a pincushion or prefers aqueous suspension & pinning once or twice daily for months on end, then we would pop 5. off this stack and push it into the 1. slot, everything else shifting down by one space.

Great information

 

[Imaghost]

I’ve been very curious about using Ment over the last few months bf have tracked down about a half dozen options to purchase MENT but would really like to hear what brand anyone would recommend for the MENT given it’s high price point and it being notoriously faked. If this is against the rules I apologize and will delete it immediately but really curious to hear what brand everyone finds to be the most reliable for MENT. Thank you

 

[Juggy3838]

Well we know that Prop > Cyp > Ena in stimulating erythropoiesis.

Base (suspension; TNE), as used in practice (i.e., short-term, 1 - 2 weeks, because nobody wants to pin that frequently and/or pre-workout for a couple sessions weekly) tends to actually fall on the very low side of the continuum, for the reasons explained here: [link], that because red blood cells are formed over 7 days & the elimination of testosterone base is very rapid, there is not the same superimposition of peak T to stimulate erythropoiesis as with esterified testosterone.

Acetate, since it is not used like testosterone base (e.g., TNE), but instead medium- to long- term (in terms of months) & daily (q.d.) or every other day (q.o.d.), its rapidity of action being associated with low Tmax & a high Cmax # (frequent "peaks"), falls on the very high end of the continuum.

So, in practice:
1. Acetate
2. Propionate
3. Cypionate
4. Enanthate
5. Base

If, however, the assumption of use regarding testosterone base were to break down because the user doesn't mind feeling like a pincushion or prefers aqueous suspension & pinning once or twice daily for months on end, then we would pop 5. off this stack and push it into the 1. slot, everything else shifting down by one space.

So hypothetically someone who struggles with E2 or HCT, they could lower their weekly test E/C dose, and supplement with test base pre workout (say 4x a week) and get the immediate ergogenic effects, and maybe have a better HCT/E2 profile than a higher dose of longer esters?

Have you ran across any literature on the ester affecting MPB and nitrogen retention? Is nitrogen retention/MPS increased when AUC of testosterone is in play or is it more of a cascade effect thst lasts longer? I probably didn’t use the correct terms, but is flipping the light switch “ON” with test base just as good as “leaving the light on longer” with an estered testosterone? I guess it’s splitting hairs if someone trains multiple days a week.

 

[Type-IIx]

So hypothetically someone who struggles with E2 or HCT, they could lower their weekly test E/C dose, and supplement with test base pre workout (say 4x a week) and get the immediate ergogenic effects, and maybe have a better HCT/E2 profile than a higher dose of longer esters?

Have you ran across any literature on the ester affecting MPB and nitrogen retention? Is nitrogen retention/MPS increased when AUC of testosterone is in play or is it more of a cascade effect thst lasts longer? I probably didn’t use the correct terms, but is flipping the light switch “ON” with test base just as good as “leaving the light on longer” with an estered testosterone? I guess it’s splitting hairs if someone trains multiple days a week.

Since testosterone suspension actually provides adequate T replacement at 20 mg for 4 - 7 days in frank hypogonadism, I think that after the first week or so, 4X weekly application of testosterone base might just as well stimulate erythropoiesis & E2 as acetate, unfortunately. Note its biphasic (two distinct) release profile, with an early peak, and then a more gradual release as the crystals dissolve basically. We end up with a 9 day Tlast max, meaning that in some individuals there's actually still some testosterone being released 9 days after a single dose (aqueous testosterone suspension).

What directly determines +Δ LBM is dose as time × fAUC (free androgen area-under-the-curve), i.e., in units 168 h fAUC (nmol h/L).

The frequent administration schedules that bodybuilders often follow in practice (e.g., every t1/2) results in higher fAUC, and in shorter Tmax & more frequent Cmax (# of "peaks"), that probably enhance strength through nongenomic mechanisms (rapid effects; e.g., membrane-bound AR) such as increased neural drive. There is a tradeoff consideration for this enhanced efficacy, however, in terms of tolerability (pain, swelling at the injection site; erythrocytosis/polycythymia).

 

[Vanargandar]

Every time I see @Type-IIx post something I feel 1) privileged to have someone on this board with such a wealth of knowledge 2) absolutely retarded.

 

[Juggy3838]

Since testosterone suspension actually provides adequate T replacement at 20 mg for 4 - 7 days in frank hypogonadism, I think that after the first week or so, 4X weekly application of testosterone base might just as well stimulate erythropoiesis & E2 as acetate, unfortunately. Note its biphasic (two distinct) release profile, with an early peak, and then a more gradual release as the crystals dissolve basically. We end up with a 9 day Tlast max, meaning that in some individuals there's actually still some testosterone being released 9 days after a single dose (aqueous testosterone suspension).

What directly determines +Δ LBM is dose as time × fAUC (free androgen area-under-the-curve), i.e., in units 168 h fAUC (nmol h/L).

The frequent administration schedules that bodybuilders often follow in practice (e.g., every t1/2) results in higher fAUC, and in shorter Tmax & more frequent Cmax (# of "peaks"), that probably enhance strength through nongenomic mechanisms (rapid effects; e.g., membrane-bound AR) such as increased neural drive. There is a tradeoff consideration for this enhanced efficacy, however, in terms of tolerability (pain, swelling at the injection site; erythrocytosis/polycythymia).

Ahh makes sense. I was not aware of the biphasic release!

It is quite neat to me, that daily pins of an an estered testosterone, and trying to have no peaks keeps E2 better controlled than a 1-2x large weekly bolus (cyp/eth) , but also, an extremely rapid peak isn’t the boogeyman either.


So what your saying is….on deadlift max effort days, add 50mg suspension injection with my morning coffee? Lol I’m kidding, kinda.

Thanks for these compound write ups brother. I love the nuances of pharmacology.

 

[Type-IIx]

Every time I see @Type-IIx post something I feel 1) privileged to have someone on this board with such a wealth of knowledge 2) absolutely retarded.

Thanks for the kind words bro. I regard your posts as informative and valuable. Everyone has different strengths, interests, etc. So long as you make valuable contributions, you are a wealth of knowledge and absolutely not retarded.

 

[AlwaysHungry]

So if you switch from regular trt cyp/enan to test prop or TNE you’re gonna see lower hematocrit and e2?

 

[Country Club Hero]

MENT is the only drug I have used in recent years whenever I blast and it works extremely well. I just usually use a very low dose and this time around, I want to kick it up a bit, but don’t want to use enough where I start to develop estrogen sides.

I used to use tren in my earlier days and high doses of it but it’s been a while, so I was thinking I can use a lower dose. I just worry a bit about insomnia.

I am hesitant to use a high dose of test because I don’t want too much water retention and worry about it possibly spiking hematocrit too much.

Nebivolol (40mg) and Telmisartan (5mg) I am on permanently and have been for years. I even have a legitimate prescription for them.

I really don’t want to use an AI. I have Raloxifene if I need it but don’t expect to use it.

Type 2 hates Ment for some reason. Maybe like I think primo is trash. But i almost added a little Ment to my regular test/tren/mast run recently because I’m dating a new gal and NOTHING boosts my sex drive like tren and ment.

Type 2 can’t comprehend that some people react differently to different drugs. If it’s not been researched by 200 lab coat wearing nerds and they all agree, then it jus won’t work.

I say do it and it will probably be awesome and your new favorite combo. But what do I know? Just been doing this a long time without a lab coat and am as healthy as a mule deer.

 

[RzSco]

Me. Nothing much happened. I was a bit angry sometimes.

I am beginning to suspect I have no androgen receptors.