Stack for Height and Dimo - GTFIH

[Trenscension]

Test Base - 5 mg ed
Primo - 20 mg ed

 

[Zagro]

Yo seem like you know what you are doing instead of blasting everything inside of your body to hope that it works could you explain further, I saw you post about letrozole being to much what were the side-effects you experienced (thinking about taking 2.5mgED)?

Tearing up daily, insanely depressed, zero motivation, fatigue and having to distract myself in every way possible to keep on going

If you already are in a bad place mentally, lack motivation or have body dysmorphia like 99% of users here do not take it without an SSRI or even ERb agonists

You will become miserable on it

 

[Zagro]

Infinite evidence

Send one

 

[AtrophicPyra]

Send one

Am too lazy and busy rn in all seriousness but look at this thread I made I made more on other forums too

https://looksmax.org/threads/height-cycle-first-real-cycle.2148853/#post-29648310
This was the thread btw, very cancerous @AtrophicPyra

Oh shit it was you https://looksmax.org/threads/trenbo...-the-main-driver-take-a-look-at-this.2152733/

click on the second thread scroll in the study,
You will see tren+excerise was taller but it’s solely because rats get bigger under tension more than humans but if we remove that variable u can see their femurs r actually smaller than the control group

 

[Zagro]

Am too lazy and busy rn in all seriousness but look at this thread I made I made more on other forums too

click on the second thread scroll in the study,
You will see tren+excerise was taller but it’s solely because rats get bigger under tension more than humans but if we remove that variable u can see their femurs r actually smaller than the control group

Without nuking E2 it surely will rape any existing growth and just from looking at the results none are statistically significant as the paper states itself, as ive said not nuking E2 (thereby progesterone being net-negative) or controlling other things such as prolactin could be negative i guess.

The rats had a weight of 61.80 grams and with a dosage of 500mcg once a week even less considering the enanthate ester so 70% active trenbolone 350mcg once a week in their weaning phase (28 days old) when they're still pups/baby rats, hard to extrapolate from here honestly.

The p-values are not supporting anything aswell as there is a 35.5% probability of the results being a coincidence and the f-value proves further that there isn't anything that statistically significant among all groups.

The reason for the slightly reduced length can be caused by a plethora of causes, not controlled estrogen + high progesterone from trenbolone is very likely to "rape" any existing growth adding on the prolactin problems aswell. The effects aren't as pronounced because of the low dosages used probably, and possible would cause centimetres of height loss in pre-adolescent children but you have to consider the fact that you still gain positive effects on primarily on IGF-1, glucocorticoids, androgens and etc so it wont be as dramatic maybe.

Now that ive read it again this may be all bullshit because tren would suppress the endogenous testosterone production thereby lowering systemic estrogen levels but still amplifying the effect of the remaining local estrogen so the body would still compensate greatly with sensitivity etc. This is if the dose was enough to suppress it adequately.

Just wrote a lot of shit here for you to explain how many theories there could be and that this isn't enough information, not even close by miles, to make a consensus on anything

 

[infrainfra]

Without nuking E2 it surely will rape any existing growth and just from looking at the results none are statistically significant as the paper states itself, as ive said not nuking E2 (thereby progesterone being net-negative) or controlling other things such as prolactin could be negative i guess.

The rats had a weight of 61.80 grams and with a dosage of 500mcg once a week even less considering the enanthate ester so 70% active trenbolone 350mcg once a week in their weaning phase (28 days old) when they're still pups/baby rats, hard to extrapolate from here honestly.

The p-values are not supporting anything aswell as there is a 35.5% probability of the results being a coincidence and the f-value proves further that there isn't anything that statistically significant among all groups.

The reason for the slightly reduced length can be caused by a plethora of causes, not controlled estrogen + high progesterone from trenbolone is very likely to "rape" any existing growth adding on the prolactin problems aswell. The effects aren't as pronounced because of the low dosages used probably, and possible would cause centimetres of height loss in pre-adolescent children but you have to consider the fact that you still gain positive effects on primarily on IGF-1, glucocorticoids, androgens and etc so it wont be as dramatic maybe.

Now that ive read it again this may be all bullshit because tren would suppress the endogenous testosterone production thereby lowering systemic estrogen levels but still amplifying the effect of the remaining local estrogen so the body would still compensate greatly with sensitivity etc. This is if the dose was enough to suppress it adequately.

Just wrote a lot of shit here for you to explain how many theories there could be and that this isn't enough information, not even close by miles, to make a consensus on anythin

my opinion is that androgens ALONE arent good for longitudinal growth. look at androgens effects on mineralization and then look at how negligible the results of non aromatizable androgens are on longitudinal bone growth or even isolated lab setting growth plate cartilage. tho tren upregulating igf-1 (not proven in bone cells) may be controversial after reading this study

 

[Paul.jnxy]

Yeah so people lowk never even cycle erda or you just run it for like 3 months and then wait a month

Hmmm.

 

[Paul.jnxy]

Yo prove me wrong? View attachment 5242933

Nigha it gen says health adults. In puberty some poeple reach 9 ius.

 

[fraudster#1]

@peterk1287

 

[Paul.jnxy]

you can go up to 80mg test a week and up tren
choose 1 ai(letro is for rtds)
go up 5mg ed erda and dnr sides
i do not reccomend serm,
halo is will give linear height/spurt), but it will accelerate bone age and will lowere fah
t4, t3 ancillaries jfl

No point in really upping by 10 mgs. Care to explain and give an argument? No sir I won't be DNRing CATSHL syndrome. Why not SERMs are peak. t3 and t4 only on standby.

 

[fraudster#1]

absloutely, test, tren, all anabolics have been proven to stunt growth no matter how much they dont aromatize

anavar does this too in higher doses except its so mild that u can actually use it in specific doses for a specific time frame to increase height velocity and fph, this is bec it sensitizies the locks in the igf1r and is paired with gh for height growth

how so? care to explain?

 

[Paul.jnxy]

Without nuking E2 it surely will rape any existing growth and just from looking at the results none are statistically significant as the paper states itself, as ive said not nuking E2 (thereby progesterone being net-negative) or controlling other things such as prolactin could be negative i guess.

The rats had a weight of 61.80 grams and with a dosage of 500mcg once a week even less considering the enanthate ester so 70% active trenbolone 350mcg once a week in their weaning phase (28 days old) when they're still pups/baby rats, hard to extrapolate from here honestly.

The p-values are not supporting anything aswell as there is a 35.5% probability of the results being a coincidence and the f-value proves further that there isn't anything that statistically significant among all groups.

The reason for the slightly reduced length can be caused by a plethora of causes, not controlled estrogen + high progesterone from trenbolone is very likely to "rape" any existing growth adding on the prolactin problems aswell. The effects aren't as pronounced because of the low dosages used probably, and possible would cause centimetres of height loss in pre-adolescent children but you have to consider the fact that you still gain positive effects on primarily on IGF-1, glucocorticoids, androgens and etc so it wont be as dramatic maybe.

Now that ive read it again this may be all bullshit because tren would suppress the endogenous testosterone production thereby lowering systemic estrogen levels but still amplifying the effect of the remaining local estrogen so the body would still compensate greatly with sensitivity etc. This is if the dose was enough to suppress it adequately.

Just wrote a lot of shit here for you to explain how many theories there could be and that this isn't enough information, not even close by miles, to make a consensus on anything

I'm curious what's the basis for your understanding of this and how do you like kind of draw the line btw actual facts and speculation or conjecture as I have always struggled with ts

 

[ayingsdud]

IGF-1/GH Axis:
rHGH - 16 ius ed

Androgens:
Test Base - 5 mg ed
Primo - 20 mg ed
Oxandrolone - 10 mg (morning/pre)
Fluoxymesterone - 2.5 mg ed (21 days on 7 off)
Tren - 30 mg pw microdose

E2:
Exemestane - 25 mg eod
Letrozole - 1.25 mg eod
Tamoxifen/Nolvadex - 20 mg ed

FGFR Axis:
Balversa - 3 mg ed (14 days on 7 off)

Skin and Hair:
RU58841 - 20-50 mg per day (5% solution)
Minox - 2.5 mg ed
Isotret - 20mg ed (incase of acne outbreak)
Asthaxanthin - 8 mg ed
GHK-cu - 2 mg ed

Ancillaries:
Empagliflozin
T3
T4
Sevelamer Carbonate
High EPA/DHA Fish Oil
Melatonin
Telmi
Cabergoline
P5P
Aspirin
NAC
TUDCA
Taurine
Lutein
Zeaxanthin
Plus Tons of other shit I will not mention

This will be my second blast as my current first cycle is a lot milder. Any advice is appreciated.

what side effects are there of Exemestane just curious if i should get me some

 

[AtrophicPyra]

how so? care to explain?

Scroll through my threads for ur answer I’m tired of debating niggas that roids close ur plates prematurely

 

[Zagro]

my opinion is that androgens ALONE arent good for longitudinal growth. look at androgens effects on mineralization and then look at how negligible the results of non aromatizable androgens are on longitudinal bone growth or even isolated lab setting growth plate cartilage. tho tren upregulating igf-1 (not proven in bone cells) may be controversial after reading this study

Nope completely agreed, and i regret taking androgens with goals as height as literally 90% of the major side-effects and needed supplements come from here you lose HUNDREDS of dollars spending shit on ancillaries and supplements to combat the side effects of AAS on top of the existing cost of legit high-quality oils and the second the cheap "legit" oral you purchased has dbol or the oil has test, ment etc anything aromatising or that binds ERa directly you're pretty much cooked.

I would say androgens alone are possibly one of the worst things you can do for height and i wish i stayed with my beloved rhGH that ive been talking about ever since 2024 and just added other good ROI comps on top, fuck whoever came up with the idea of high dose test or test at all, tren or combining 10 different NAAAS because it looks like you're spending more effort.

Although i would argue that you HAVE to opt for polypharmacy if you use anything for goals such as height, it is practically a need and if you do it correctly having something for androgens wouldn't hurt, like zero test base+ non-aromatising moderately strong androgen that doesn't rape SHBG (maybe even better this way) like anavar (weak) winstrol (rapes SHBG) anadrol (binds ERa) so maybe halotestin really is a good choice here with the minimum needed ancillaries

 

[disco]

IGF-1/GH Axis:
rHGH - 16 ius ed

Androgens:
Test Base - 5 mg ed
Primo - 20 mg ed
Oxandrolone - 10 mg (morning/pre)
Fluoxymesterone - 2.5 mg ed (21 days on 7 off)
Tren - 30 mg pw microdose

E2:
Exemestane - 25 mg eod
Letrozole - 1.25 mg eod
Tamoxifen/Nolvadex - 20 mg ed

FGFR Axis:
Balversa - 3 mg ed (14 days on 7 off)

Skin and Hair:
RU58841 - 20-50 mg per day (5% solution)
Minox - 2.5 mg ed
Isotret - 20mg ed (incase of acne outbreak)
Asthaxanthin - 8 mg ed
GHK-cu - 2 mg ed

Ancillaries:
Empagliflozin
T3
T4
Sevelamer Carbonate
High EPA/DHA Fish Oil
Melatonin
Telmi
Cabergoline
P5P
Aspirin
NAC
TUDCA
Taurine
Lutein
Zeaxanthin
Plus Tons of other shit I will not mention

This will be my second blast as my current first cycle is a lot milder. Any advice is appreciated.

What age?

 

[Zagro]

I'm curious what's the basis for your understanding of this and how do you like kind of draw the line btw actual facts and speculation or conjecture as I have always struggled with ts

Understanding the topic you're speaking on helps, like how progesterone competes with 5a-reductase thus if high/supraphysiological levels of progesterone are reached (insanely easily with mtren and easy with tren, so highly likely) it will compete against DHT and lower levels, the significance of that effect depends on many factors such as what you're using for example. Less testosterone converting into dihydrotestesterone means more estrogen conversion instead so you end up with fucked E2/DHT ratios locally aswell so even more local E2 and less local DHT to potentially compete against that local E2.

I just go off memory and think about how viable something is; rats given trenbolone end up with slightly shorter length, so i think about any nuances around the usage of trenbolone, the needed ancillaries and what trenbolone is and what it does. So i know trenbolone increases prolactin and hyperprolactinemia in children tends to stunt their growth and from afaik that is mechanistically viable and they don't use anything that lower prolactin on the rats treated with trenbolone so that's one caveat from the study.

Second caveat is that they haven't nuked E2 nor is it stated or do i think that their testosterone is fully suppressed because i have already done the math of the doses used and the active trenbolone that remains with the attached enanthate ester and that is quite low and once a week aswell which is not quite stable as enanthate esters are usually dosed more frequently so essentially the rat is constantly receiving a low dose as a baby rat/pup and fucking up everything along the way.

I also know that progesterone competes with 5a-reductase which will fuck things up further when supraphysiological, tren has pretty strong progesterone properties and its molecular skeleton is build upon estrogen too and has negative metabolites that can bind ERa although not strong enough meaning a particular compound such as tamoxifen may make that specific metabolite beneficial by helping it act upon the AF1 of ERa which is positive, but they don't give the rats anything else as no polypharmacy is done.

Progesterone and estrogen oppose eachother from what i know, that means progesterone can reduce the effects of estrogen maybe (this is done without confirmation, and where i begin extrapolating).

As you can see 95% of it are facts and most of the shit i said is true and backed by the current literature, only when it comes to specifics within the growth plate itself, everything switches to relying on mechanistical studies and backing up so not proven in vivo thus extrapolation, but we gotta work with what we have.

I rambled again and didn't quite answer your question but i was supposed to sleep 3-4 hours ago and am raped cognitively, this above is just a part of what went through my mind whilst reading this particular study, maybe it helps you understand better