Anyone run MENT and tren together?

[Type-IIx]

While your information sounds good on paper, you still lack the personal experience of using it.

Good point. Personal experience with something is the only means to understanding it.

This MENT Profile [link] might actually be of some value if I had decided, after performing my own balancing of the known tolerability & efficacy factors in consideration of the the availability of other similarly situated AAS, to go ahead and use MENT despite its unfavorable risk/reward tradeoffs for myself.

Since I can really only learn from my mistakes, I should - instead of relying on facts from books, studies, dissertations, & reports from the boards and subreddits - seek to expand my knowledge by making as many archetypal bad life decisions as I can, so that NotHuman and other guys might say, yeah, this guy has practical knowledge, not just bullshit theories from books. Nubain, Cheque drops, snorting Tren base, injecting Progesterone, all forthcoming.

Ok stated another way. The shorter the ester, the higher the peak. So if you pin the shorter ester more often, which almost always goes hand in hand with a short vs longer ester, then the peaks will remain stable with the more frequent pins. The more frequent you pin, the steadier your blood levels will be. That's just the nature of half life. You get more bang for your buck with the shorter/more frequent pin combo.

Not true. You can try any permissible frequency (any more frequent and you'll become an actual pincushion) you'd like using SteroidPlotter to visualize how frequent administration of short esters does not cause any "smoothness" or stability, but rather results in more "spiking" meaning a greater # of "peaks" or Cmax # (Css # after 4 t1/2s) & therefore decreased Tmax (time to Cmax). A low Tmax is inherently related to side effects including erythrocytosis/polycythymia, and of course more frequent pinning is associated with greater swelling & pain at the injection site.

Here, I'll illustrate this for you:

Trenbolone enanthate, 350 mg q.w. (350 mg, once weekly)


Trenbolone acetate, 350 mg q.w. as 50 mg q.d. (50 mg daily = 350 mg weekly)

What I see is not in any sense a more stable delivery profile. Rather, given daily 50 mg trenbolone acetate administration, blood concentration oscillate between 60 & 40 mg (actual differences/degrees of change being fairly unimportant) at a considerably higher frequency of Cmax (# of peaks), resulting in reduced Tmax, which is the most important factor relating to the increase to hematocrit.

This frequent administration of a short ester certainly increases dose as fAUC * time, however. This, then, increases efficacy and AR activation (thereby eliciting greater increases in LBM, but also the classical negative side effects of androgens, androgenicity, etc.)

Right, to clarify by mental tolerability I'm not referring to positive effects, but the absence of negative effects. Obviously you do not need a study to come to the conclusion that most will tolerate MENT better than tren, but it is not comparable to tren, especially in a deficit. In the context of this post I would just add test/mast.

With Deca however I tend to see reports of paranoia despite a high dose of testosterone alongside it, so I'm not too sure on how it would just be estrogen related. Of course not everyone has these symptoms, but I do consider MENT to be at least somewhat more potent than Deca, so I don't see a reason to use it except for joint relief.

As far as gestagenic side effects, I never really understood what these are besides the suppression on the HPTA (unless we are to assume blood pressure and hypo symptoms are because of this). The underlying imbalance always seems to be estrogen.

Certainly I'm not trying to argue, you know a lot more than me, but if it was more popular maybe I could get it for cheaper

Article on distinguishing progestins, prolactin, and progestagenic androgens (e.g., Tren, MENT, Deca) & SERM vs. AI logic [by Type-IIx] is a writeup that I posted, written by request originally for but not contracted by ProM, to demystify the widespread confusion between gestagenicity (progestagenic effects), estrogenicity, prolactin vs. progesterone vs. progestagenic androgens, etc.

 

[rexy]

This frequent administration of a short ester certainly increases dose as fAUC * time, however. This, then, increases efficacy and AR activation (thereby eliciting greater increases in LBM, but also the classical negative side effects of androgens, androgenicity, etc.)

Can I just check my understanding of this point for my pea brain?

Is the reason the frequent use of a shorter ester increases efficacy and AR activation because it's trough in blood levels is infact higher than where you spend most time in the long ester scenario?

In other words, rather than levels oscillating between 55 and 20, with most time spent below 40 with the long ester weekly, the trough level of daily Ace shots is circa 40. So most of the time is spent above that vs. below it. Is that why it results in increases in efficacy and negative sides?

This is assuming same total dose used in both of course (as per your example).

 

[Type-IIx]

Can I just check my understanding of this point for my pea brain?

Is the reason the frequent use of a shorter ester increases efficacy and AR activation because it's trough in blood levels is infact higher than where you spend most time in the long ester scenario?

Greater area-under-the-curve of the free/bioactive fraction of administered AAS (fAUC).

It does follow that the nadir/trough is increased, but you can just look at that the area under the curve as a product of time as visualized to see there's more blue in the case of frequent acetate administration.

In other words, rather than levels oscillating between 55 and 20, with most time spent below 40 with the long ester weekly, the trough level of daily Ace shots is circa 40. So most of the time is spent above that vs. below it. Is that why it results in increases in efficacy and negative sides?

This is assuming same total dose used in both of course (as per your example).

 

[Type-IIx]

In other words, rather than levels oscillating between 55 and 20, with most time spent below 40 with the long ester weekly, the trough level of daily Ace shots is circa 40. So most of the time is spent above that vs. below it. Is that why it results in increases in efficacy and negative sides?

What you're focusing on with respect to the increase to average & trough levels is analogous to the observation that even though a car's traveling speed (distance/time) is an average value, we can confidently say that another car that overtook it on the road must have a higher mean & min speed than it to stay ahead of it... Because of course it does.

What I mean is, just simply compare the blue areas for the 50 mg acetate q.d. vs. 350 mg enanthate q.w. One is clearly larger (length × width; m²) than the other.

This is assuming same total dose used in both of course (as per your example).

So, this actually illustrates that dose (let's refer to it as biological dose) is greater in the case of 50 mg acetate q.d. vs. 350 mg q.w., because AAS dose is most accurately defined as time × fAUC (free area-under-the-curve; the free fraction representing 1 - 2% of total androgen blood concentrations), e.g., 168 h fAUC (nmol h/L), such that +Δ LBM can be described by a curvilinear function of bioavailable androgen in units of 168 h fAUC (nmol h/L). Since administering with a daily frequency increases the # of peaks (Cmax #) it necessarily increases the median & mean release mg, and (most importantly) decreases Tmax.

 

[rexy]

What you're focusing on with respect to the increase to average & trough levels is analogous to the observation that even though a car's traveling speed (distance/time) is an average value, we can confidently say that another car that overtook it on the road must have a higher mean & min speed than it to stay ahead of it... Because of course it does.

What I mean is, just simply compare the blue areas for the 50 mg acetate q.d. vs. 350 mg enanthate q.w. One is clearly larger (length × width; m²) than the other.


So, this actually illustrates that dose (let's refer to it as biological dose) is greater in the case of 50 mg acetate q.d. vs. 350 mg q.w., because AAS dose is most accurately defined as time × fAUC (free area-under-the-curve; the free fraction representing 1 - 2% of total androgen blood concentrations), e.g., 168 h fAUC (nmol h/L), such that +Δ LBM can be described by a curvilinear function of bioavailable androgen in units of 168 h fAUC (nmol h/L). Since administering with a daily frequency increases the # of peaks (Cmax #) it necessarily increases the median & mean release mg, and (most importantly) decreases Tmax.

Thank you - I really appreciate you following up the initial comment to help explain it further. It crossed my mind while reading whether that would suggest the dose is actually different between them (biological dose makes sense to me) but wasn't fully confident I'd understood correctly.

 

[trendbolwinstrol]

how about ment with tren masteron and test ... masteron can manage estrogen. how would 50mg per be to start? ment e

 

[ackmack78]

I ran ment for the first time a few months back at 25 a day. Blood pressure wasn’t as bad as I expected but my e2 was higher than it had ever been so I increased my ai dose and that took care of it. The overall sense of well being, strength gains, and muscle fullness were amazing. Would like to try it again at a lower mg, probably let 10 or 15 so I don’t have to take as much anaztrazole.

What does of test did you run with your ment and how long did you run it for?
Any other compounds?

 

[Pulpfiction]

What does of test did you run with your ment and how long did you run it for?
Any other compounds?

My test was just at trt level of 200. I ran it for 8 weeks. I had some s23 left over from a few years back that I used in the first 3 weeks to finish it off but other than that it was just the ment and test.