MESO-Rx
Anabolic Steroids
Ment / test cycle and how much AI?
- Thread starter DrSauce
- Start date
I agree. I don't get these guys saying they are running hundreds of mgs of MENT per week, like it is the same as test. Maybe their product is just bunk? That's my only explanation as to how they aren't having the worst E2 issues of their life. At 5mg per day MENT has a noticeable impact on me. 10mg has me looking super swoll and pumped 24/7 and my strength goes up quite a lot. Also I am so horny I wake up with erections that could cut granite every night lmao
bigtdawgwassupbro
Member
pics or gtfo
what are you running along side it? I am doing 50mg test P, 25mg ment EOD, about 9 days in so far. I got sick so havent been able to work out yet. Ive been tinkering with tiny doses of .25mg adex but seems to crash my E2 each time. Any directive would be great! How much test/AI your running etc?
what are you running along side it? I am doing 50mg test P, 25mg ment EOD, about 9 days in so far. I got sick so havent been able to work out yet. Ive been tinkering with tiny doses of .25mg adex but seems to crash my E2 each time. Any directive would be great! How much test/AI your running etc? Thanks abunch
I run MENT with Mast P and a little TRT test C (but am experimenting with removing that). 10 mg/day (max, normally just 5) and 50 MG per day, and 50 mg 2x per week, respectively. Normally dose of test c is 180/ week, lowered to 100 to combat e2 from MENT. Really really feel great, libido and dick gainz are insane. Look pumped and shredded literally within a week. It's pretty crazy. This is my new go to cycle I think, but will pay with the dosages.
I still have so much NPP and test e around that I feel obligated to run a cycle of that sometime soon ish
wait can you clarify exactly what you’re running again? Is it 10mg mast P daily? Then 50mg ment daily and 50mg test c 2x a week is that right? Any AI needed?
how come not double the dosage every other day on ment and mast p? Don’t you get inflammation from
Daily pinning? I can’t do it for an extended period of time.
Any other details appreciated!
Type-IIx
Well-known Member
Practically speaking, the difficulty in even approximating AI dose for mitigating 7alpha-ME's effects derives largely from the poor efficacy of AIs in reducing even E2, as well as the (at least known) unknowns: 7alpha-ME's metabolites, rate of breakdown, and the very basic fact that it almost certainly doesn't even appear on any routine bloodwork. It's a tremendous known unknown.
I think I prefer MUCH LOWER doses than I'm seeing of MENT as well as Aromasin generally on cycle, if running a sane MENT dose. It acts as an estrogen agonist in some tissues, antagonist in others, has some procollagenous features and may augment bone density, if one is optimistic rather than parsimonious in interpreting the literature, exemestane/Asin may have advantages over its counterparts for augmenting joints/tendon that AIs tend to "crush," while perhaps not exerting as negative an influence on lipids, cardiovascular risk (hopefully is more similar to tamoxifen in that regard... but I am straying from the topic).
Better to minimize the substrate for 7alpha-ME (i.e., reduce MENT dose) than attempt to ascertain whether and to what extent we can control it.
Bear in mind with AIs: they're just damn ineffective in lowering E2 for young men compared to women (i.e., ~50% vs. 90+% efficacy)... true, they are decently efficacious in reducing E2 with the use of exogenous Test (see J. S. Finkelstein, H. Lee, S.-A. M. Burnett-Bowie, J. C. Pallais, E. W. Yu, L. F. Borges, B. F. Jones, C. V. Barry, K. E. Wulczyn, B. J. Thomas, et al. Gonadal steroids and body composition, strength, and sexual function in men. New England Journal of Medicine, 369(11):1011–1022, 2013), but whether and to what extent this is the case with MENT and its aromatic product is yet another unknown.
In principle, suppressing the aromatase enzyme will suppress some 7alpha-methylestradiol... to what extent is... unknown.
Remember that MENT is highly potent both as an AR agonist, but also in its ER and PR activity. It is non-17alpha-alkylated mibolerone (cheque drops). It is highly suppressive of the HPG axis (clinical use obtains of this feature).
Reddit has proven, IMO, a dangerous source rife with confident misunderstanding or real misrepresentations of AAS. There are no Peter Bonds, there is a MENT cheerleader that administers the reddit and maintains a highly erroneous wiki, and a cadre of sycophants parading the same nonsense.
They think high E2/estrogens is a net positive. It's more nuanced than that. While in situ aromatization offers benefits, braggadocio over who "feels good" with the highest E2 is telling over the level of knowledge over there. I believe MENT's popularity is largely driven by that subreddit.
MENT is complex, and it's best run at low doses and with a firm commitment that you'll likely be plugged into the black market or your TRT doc's whims for a long time/forever once you blast with it.
I think I prefer MUCH LOWER doses than I'm seeing of MENT as well as Aromasin generally on cycle, if running a sane MENT dose. It acts as an estrogen agonist in some tissues, antagonist in others, has some procollagenous features and may augment bone density, if one is optimistic rather than parsimonious in interpreting the literature, exemestane/Asin may have advantages over its counterparts for augmenting joints/tendon that AIs tend to "crush," while perhaps not exerting as negative an influence on lipids, cardiovascular risk (hopefully is more similar to tamoxifen in that regard... but I am straying from the topic).
Better to minimize the substrate for 7alpha-ME (i.e., reduce MENT dose) than attempt to ascertain whether and to what extent we can control it.
Bear in mind with AIs: they're just damn ineffective in lowering E2 for young men compared to women (i.e., ~50% vs. 90+% efficacy)... true, they are decently efficacious in reducing E2 with the use of exogenous Test (see J. S. Finkelstein, H. Lee, S.-A. M. Burnett-Bowie, J. C. Pallais, E. W. Yu, L. F. Borges, B. F. Jones, C. V. Barry, K. E. Wulczyn, B. J. Thomas, et al. Gonadal steroids and body composition, strength, and sexual function in men. New England Journal of Medicine, 369(11):1011–1022, 2013), but whether and to what extent this is the case with MENT and its aromatic product is yet another unknown.
In principle, suppressing the aromatase enzyme will suppress some 7alpha-methylestradiol... to what extent is... unknown.
Remember that MENT is highly potent both as an AR agonist, but also in its ER and PR activity. It is non-17alpha-alkylated mibolerone (cheque drops). It is highly suppressive of the HPG axis (clinical use obtains of this feature).
Reddit has proven, IMO, a dangerous source rife with confident misunderstanding or real misrepresentations of AAS. There are no Peter Bonds, there is a MENT cheerleader that administers the reddit and maintains a highly erroneous wiki, and a cadre of sycophants parading the same nonsense.
They think high E2/estrogens is a net positive. It's more nuanced than that. While in situ aromatization offers benefits, braggadocio over who "feels good" with the highest E2 is telling over the level of knowledge over there. I believe MENT's popularity is largely driven by that subreddit.
MENT is complex, and it's best run at low doses and with a firm commitment that you'll likely be plugged into the black market or your TRT doc's whims for a long time/forever once you blast with it.
Last edited:
MulberryTrees
New Member
Can you speak a bit about what you consider low dosages?
Regarding aromasin, my limited understanding is that a suicidal AI disables the aromatase enzyme by permanently binding to it's active site. Would this not knock out the same potential for aromatization regardless of the substrate? Can you go into why MENT would be different?
Thanks for your contribution through your original post that I cited. Admittedly much of my understanding of MENT comes from Reddit. I'm trying to verify claims as best as I can through the primary sources cited there, but my knowledge of pharmacology and biology is extremely limited.
Type-IIx
Well-known Member
Your description and analogy in this thread was correct and very good. Without directly quoting you since I just skimmed through the thread and lost the exact page/post, it's also additional data in favor of aromasin. MENT is only unique within the context of aromatization only because its aromatic product, 7alpha-ME, is so potent and unresearched, there's no data on efficacy of any SERMS nor AIs and combating its effects.
Liver metabolism of 7alpha-ME is largely irrelevant I would say, since the aromatase enzyme is present throughout the body, chiefly in testes, brain, and adipose tissue.
While SERMs function as an ER antagonist at the hypothalamus/pituitary, increasing LH and T secretion, AIs block aromatase action (T ⇒ E₂), thus reducing the absolute concentration of E₂ (effectively reducing its inhibitory action at the pituitary, increasing LH and T secretion).
AIs greatly reduce E2 while on exogenous testosterone but not otherwise. Peter Bond speculates that full suppression of E2 would require incredibly high AI dosages due to E2 production in the testes where testosterone concentrations are so high. By extrapolation, it's probably safe to say that given 7alpha-ME's potency and rate of aromatization, the same or worse is true in its case/MENT's, trying to battle aromatization with AIs.
With respect to dosages, consider the low therapeutic doses used, the very high anabolic ratio (given that it's not even close to directly applicable in humans given the HA weaknesses), and the unknown quantities surrounding this potent methylestrogen. But especially consider the fact that MENT binds quite strongly to PR, ER, and is just a bit of a "messy compound." I'd say, just use it at perhaps 4-5x its therapeutic dose to start, considering it is apparently so anabolic, and just adjust upwards gradually over multiple trials. Though to be truthful (my opinion), I just think it makes sense as a male contraceptive/T replacement more than as a useful AAS for most, considering the better options available.
I'm not categorically anti-MENT, I'm anti-crazy dosages of it as it seems like people are unaware of its potency and sides; and I'm anti-misrepresentation of its aromatization.
Last edited:
MulberryTrees
New Member
Thanks for going into such detail, I think I understand a bit better now.
For me, a lot of MENT's allure came from the fact that it was trialed for hormone replacement monotherapy; that it is incredibly potent, allowing for low injection volumes; that (supposedly) it is minimally androgenic; that (supposedly) it has low impact on health markers; and that (supposedly) its aromatization is unproblematic for lower blast dosages. But it sounds like there's a lot of disgreement about those last few statements.
I really want MENT to be a miracle steroid, because I decided early I'd stick to "safer" compounds--test, primo, anavar, hGH, hCG, and ancillaries like aromasin, raloxifene, telmisartan, and metformin. MENT would be perfect for rounding that out, though admittedly out of everything it's the compound with the least data behind it.
This may be even more of a known unknown, but can you speak to managing the estrogenicty of MENT with primo? TRT test, blast dosages of MENT, and enough primo to counteract aromatization--that's kind of my long term goal for blasts.
Type-IIx
Well-known Member
Sure. Just please try to remove all preconceptions despite the voluminous anecdotes of confident claims that primo reduces E2. I know they are convincing.
I can only say that from the disparate sample of primo+test only bloodwork I have collated, it does not seem to reduce E2.
Either A) nobody has true primo, or B) primo does not lower E2. Primo can increase the androgen-estrogen ratio and reduce symptoms, but I am as yet unconvinced many people really do bloodwork on primo or primo/test. And those that do are constantly told "looks like you got Test!"
I suspect it simply lacks a mechanism for reducing E2.
Now, it may reduce E2 uptake into breast cells, and likely other tissue, exerting a tissue-dependent anti-E effect (as Masteron is demonstrated to do), but I do not believe I see the evidence that Primo lowers serum E2.
Last edited:
MulberryTrees
New Member
I don't know that you'd find this particular source compelling, but here's MPMD talking about Vigorous Steve adding 200mg primo on top of his 250mg test, DHEA and pregnenolone. His E2 was 73pg/mL, and after primo it dropped to 38pg/mL. This seems pretty significant, if you believe the bloodwork.
There are some other variables though--he also added 200mg DIM and 1000mg calcium d-glucarate to help control E2. I don't know how effective these are though at E2 control, I haven't done any reading on them.
But yeah, I guess as with all compounds, I guess it comes down to doing the bloodwork and seeing for yourself.
Type-IIx
Well-known Member
Yeah, too many variables. I consider MPMD and Vigorous Steve entertainers. I read Steve's book and found it relevant for current insulin practices, but regard it as educational of current practices, NOT best practices or even safe practices. It's mixed bro-science (some good, most bad). I'm personally steering clear of the gurus on these matters, as they always brand themselves under some particular contentious point or belief. You have MPMD shilling, Victor Black on boldenone and kidneys, it's all to drive sales.
Based on my experience I’d have to disagree with you, take a look at my most recent bloodwork:
Circled in red is me running 300mg Test E per week and 180mg Primo E per week, bloods drawn 84 hours after last injection. I pin E3.5D so I pin 150mg test 90mg primo each time, no AI. I had just pinned my Saturday dose and went right to get the bloodwork so this would be the trough.
Circled in blue is 200mg Test C per week, no AI. 100mg E3.5D, bloods drawn 30 hours after last pin, so this would be the peak.
Interesting to note that my total T on 300mg/week at the trough is nearly identical to 200mg/week at the peak. But you’ll notice my E2 is less than half with the recent bloodwork. I can only attribute this to the primobolan. Why else would my E2 be so much lower on 300mg than it is on 200mg? Even having taken it during the trough cannot be enough to account for this because it is a significantly higher dose.
Type-IIx
Well-known Member
Bro THANK YOU, this is exactly what I have been hoping to see. High-quality data from bloodwork results to show E2 lowering attributable to Primo.
Yours is now the first piece of high quality evidence that I have seen!
You’re welcome, and it’s also interesting to note that the primobolan dose is just about half of the test dose (300mg/180mg), and yet the E2-lowering effect is still very significant for me. This is important because it is taken as common bro-knowledge across the internet that you run test-primo at a 1:1 ratio, with many even suggesting to run primo HIGHER than test. If I took this advice and did it myself, I would most certainly crash my E2.
GuerillaPete
Well-known Member
Vigorous Steve has a video on youtube with bloodwork and proof of primo lowering e2 posted like two years ago.
He was the first person with this information on the web.
Type-IIx
Well-known Member
Yeah, but he was on other compounds that could cause this, and most importantly, he has a vested interest in churning out interesting/surprising factoids. Jfire132 on Meso has no conflicts in reporting this, and it's a snapshot of actual blood work results.
