Holy retard, taking more doesn’t mean better results buddy. First get your weight and according to that do your HGH dose, super high doses will only increase sides. This probably won’t make you grow anyway, I can’t be bothered to explain the complex pharmacology, just search up why HGH + AI is cope. In human studies with normal children it yields literally no results. You should first be starting at low doses and slowly titrating up to see how your body responds. Why are you taking enclo? HGH won’t be affecting your test production. Also how old are you?
I liked reading this and I felt like everyone needed to know that.
i’m taking enclo bcz me and my mate i’m down too pin test but he’s not so he sent me sum forums on other height cycles and his cycle for height was super light what i put in but half that’s why i said everything i know i gotta slowly work my way up in doses im not that dumb im 16 but wont we need a boost in test too make the gh work due too higher levels than normal we gonna need higher test too make it wanna be used for height or sum bs don’t diss i’m fucking dumb but like any cycle would work
I don’t get why you need enclo? Enclo won’t make you jacked or anything btw, it’s going to increase the amount of test from your balls. That test will bind to the SHBG enzyme and lose its anabolic value. If I were you I would run test, HGH and a AI so you don’t close your plates. But you won’t be getting taller from any stack really, most men stop growing at 16 and HGH and AI in normal children doesn’t produce any height growth.
so run test c how much? is there a body weight calculation too use also i wanna blast too maximize height idc abt safe or not if it will work too increase height im gonna risk it so test c daily or every other day hgh daily the ai daily or not?
i have vials of test c free that’s why i’m asking abt test c what’s the biggest difference besides half life? also so running letrozole hgh and test e is the height cycle that most likely too work or anything that would be better
Why do you just have spare test vials lying around? I don’t really know the affects of test on height, test will aromatize so it’s probably going to stunt you at high doses. Makes more sense to just run HGH and a AI to keep plates open (will be toxic to your body tho) and then introduce erda at 4mg, from what I have seen, erda is the only proven compound to grow height in healthy humans. Although you might get uncontrolled growth and get scoliosis or blindness.
yo soy griffith
Send a study or close your mouth, also take into account dosing
Idk why you're running enclo, everything else is fine
so just rope?
no, he's an idiot
so run test test e or c i have genuinely a lot of test c bro
violador...
only do test if you're gonna take any other roid as a buffer to your hgh for igf-1, if not then just don't run test. You should do a non aromatising androgen though then add test at like 50mgew
Short kids in HGH studies have genetic GH defects — not comparable to normal kids
This is such a stupid argument, and I sit on the fence when it comes to GH therapy for increased height. But even I can acknowledge how retarded this is.
Holy your retarded, they use the clinical approved dose that is proven to grow you the most dumbass. Only dumb virgins think that more always equals better. The 2.85cm was for turbomanlets that ran proper treatment for years upon years. The us of a AI doesn’t do shit, keeping your plates open won’t equal to them making your bones grow. If you don’t know shit just shut up, your TikTok info isn’t clinical data. This was on turbo manlets btw, who have genetic factors at play for their height, in normal healthy children we can logically assume the affect of such a therapy would be even more negligible.This is such a stupid argument, and I sit on the fence when it comes to GH therapy for increased height. But even I can acknowledge how retarded this is.
"Normal kids are already at peak gh output" Yes endogenously, increasing GH levels exogenously has no comparison to an endogenous max, not sure what the point here is at all. Literally a non sequitur
The study you sent still shows an increase in predicted fah by 2.85cm. This is gh alone, there's no mention of the use of aromatase inhibitors, or whatever dosage it is. When GH therapy is done they never put humans into supraphysiological doses and always use dosages that would be somewhat equivalent to what their normal gh would be.
Like 0.05iu/kgbw
Also idiopathic short stature doesn't mean they finish growing late, AI's are supposed to prolong height growth. The kids could've stopped at 16 for all we know
How tall are u?
...
I love how people who know nothing about the subject genuinely believe their shitty takes and actually think they're intelligent when they say the things they say. It's called the dunning-krueger effect and you are a classic example of it.
pubmed.ncbi.nlm.nih.gov
good job man bumped me and proved bro imbecile so taking the gh erda would work? also reeeading bros shit holy fuck he’s dumb he said at 16 i get that i might not grow a lot but holy fuck nothing at all if my plates are open and i’m using exogenous growth hormone likeI love how people who know nothing about the subject genuinely believe their shitty takes and actually think they're intelligent when they say the things they say. It's called the dunning-krueger effect and you are a classic example of it.
I always have to do this on this forum so lets go through it.
Claims you have made and have not substantiated upon/aren't true:
"The use of ai doesn't do shit" -> zero justification
"keeping your plates open won't equal to making your bones grow" -> this is an analytic falsehood. This implies that your plates can be "open" and not in a stage of active growth which is analytically impossible.
"they use the clinically* approved dose that is proven to grow you the most dumbass" -> Another falsehood again, you cannot legally just do whatever dosages you want on humans. You have to do the dosages that are supposed to correct the issue that is present.
This doesn't mean they're being put on supraphysiological gh like people here are, it literally means they take a dosing protocol that should match to what they should naturally produce, whether ghd or iss. As everything for studies has to be THERAPEUTIC.
"your TikTok info isn't clinical data." -> I didn't even have to reply to this bullshit it's just hilarious because I'm the furthest you'd get from a "tiktok" info user
"Only dumb virgins think that more always equals better" -> Well no this would be a strawman, I never said more equals better but this principle does apply to most things in the world as most things in general are linear in efficacy. All it takes is observing whether it has that trait.
We know GH has that trait as GH directly is converted into IGF-1 through the liver, and higher IGF-1 levels are the direct cause of the male growth spurt. Since Rising sex steroids buffer igf-1 from pre pubertal to pubertal development. So we can gather just off of basic deduction that higher GH = Better in SOME form. Whether it increases FAH has more specific factors into play.
If we take the premise that height is majorly an effect caused by high/optimal chondrocyte proliferation and hypertrophy, <- The former factors happening for longer, you logically come to the conclusion that GH + any compound that allows you to stay in this mode of growth for longer is effective for increasing FAH.
Of course you can't put a number on it but this simple proves the point through deduction.
Testosterone-induced increase of insulin-like growth factor I levels depends upon normal levels of growth hormone - PubMed
Pubertal development is associated with a rise in plasma insulin-like growth factor I (IGF-I) levels that is related both to the increase in sex steroids and/or to the sex steroid-induced augmentation in endogenous growth hormone (GH) secretion. In order to investigate the relationship between...
Edit: Just a clarifying addition onto what I was saying about test because I know you're an idiot that probably won't see where the argument went, test -> igf-1 is the same thing as gh -> igf-1 in effect. Because igf-1 is the mediator for the growth.
The entire reason males even grow as tall as they do is because of the pubertal growth spurt which directly increases the proliferation and hypertrophy of CC's. Keep coping, and I even sit on the fence about this but even I know you're a retard that's making a shitty argument against it, I don't think anyone should strictly be on either side of this debate.
It's Low IQ imo. Both sides "genetics" vs "HGH" are true.
i titrate my gh up too 14 starting at 6 3and3 and letrozole start at .625 then work up too 1.25? and erda i gotta do more research but from what originally what im gathering from it idc abt that risks it’s worth if u want just give me a cycle
I won't give you a cycle I can just recommend good compounds, I like everyone to always do their own research even though I will explain things for you.good job man bumped me and proved bro imbecile so taking the gh erda would work? also reeeading bros shit holy fuck he’s dumb he said at 16 i get that i might not grow a lot but holy fuck nothing at all if my plates are open and i’m using exogenous growth hormone like
it depends on what you mean by "active growth", response to local signaling and hormones? or meaningful growth? those are two different things, if you mean they would still respond to the same local signaling and hormonal signals that make cartilage, then sure but if you mean active growth such that that "active growth" causes a meaningful increase in FAH, then open growth plates do not necessitate that. also testosterone -> IGF-1 is not the same as HGH -> IGF-1, completely different pathways, while testosterone only indirectly increases the secretion of GH from the pituitary and thus increasing IGF-1, GH itself directly transcribes IGF-1 significantly independent of testosterones GHRH increasing effects through the partial modulation of the NMDA receptor drive. also, once GH dosing reaches a certain point, increasing the dosage only leads to diminishing results, as there is a limit on how much the chondrocytes can proliferate and also a limit on the finite chondroprogenitor pool number in the resting zone itselfI love how people who know nothing about the subject genuinely believe their shitty takes and actually think they're intelligent when they say the things they say. It's called the dunning-krueger effect and you are a classic example of it.
I always have to do this on this forum so lets go through it.
Claims you have made and have not substantiated upon/aren't true:
"The use of ai doesn't do shit" -> zero justification
"keeping your plates open won't equal to making your bones grow" -> this is an analytic falsehood. This implies that your plates can be "open" and not in a stage of active growth which is analytically impossible.
"they use the clinically* approved dose that is proven to grow you the most dumbass" -> Another falsehood again, you cannot legally just do whatever dosages you want on humans. You have to do the dosages that are supposed to correct the issue that is present.
This doesn't mean they're being put on supraphysiological gh like people here are, it literally means they take a dosing protocol that should match to what they should naturally produce, whether ghd or iss. As everything for studies has to be THERAPEUTIC.
"your TikTok info isn't clinical data." -> I didn't even have to reply to this bullshit it's just hilarious because I'm the furthest you'd get from a "tiktok" info user
"Only dumb virgins think that more always equals better" -> Well no this would be a strawman, I never said more equals better but this principle does apply to most things in the world as most things in general are linear in efficacy. All it takes is observing whether it has that trait.
We know GH has that trait as GH directly is converted into IGF-1 through the liver, and higher IGF-1 levels are the direct cause of the male growth spurt. Since Rising sex steroids buffer igf-1 from pre pubertal to pubertal development. So we can gather just off of basic deduction that higher GH = Better in SOME form. Whether it increases FAH has more specific factors into play.
If we take the premise that height is majorly an effect caused by high/optimal chondrocyte proliferation and hypertrophy, <- The former factors happening for longer, you logically come to the conclusion that GH + any compound that allows you to stay in this mode of growth for longer is effective for increasing FAH.
Of course you can't put a number on it but this simple proves the point through deduction.
Testosterone-induced increase of insulin-like growth factor I levels depends upon normal levels of growth hormone - PubMed
Pubertal development is associated with a rise in plasma insulin-like growth factor I (IGF-I) levels that is related both to the increase in sex steroids and/or to the sex steroid-induced augmentation in endogenous growth hormone (GH) secretion. In order to investigate the relationship between...
Edit: Just a clarifying addition onto what I was saying about test because I know you're an idiot that probably won't see where the argument went, test -> igf-1 is the same thing as gh -> igf-1 in effect. Because igf-1 is the mediator for the growth.
The entire reason males even grow as tall as they do is because of the pubertal growth spurt which directly increases the proliferation and hypertrophy of CC's. Keep coping, and I even sit on the fence about this but even I know you're a retard that's making a shitty argument against it, I don't think anyone should strictly be on either side of this debate.
It's Low IQ imo. Both sides "genetics" vs "HGH" are true.
Another really shit response, albeit you somewhat know what you're talking about and haven't said anything totally wrong but the issue is you strawmanning me. So lets do the same with you.
""Once GH dosing reaches a certain point, increasing the dosage only leads to diminishing results" -> Unjustified claim" its simple biology really, as i said theres a finite number of cells in the resting zone and cells eventually cant divide anymore, so under what basis are you saying that GH doesn't grant diminishing results after a certain point?Another really shit response, albeit you somewhat know what you're talking about and haven't said anything totally wrong but the issue is you strawmanning me. So lets do the same with you.
"if you mean active growth such that active growth causes a meaningful increase in fah then open growth plates do not necessitate that" 1. There's additional factors to this claim I made that's completely being left out
2. I didn't imply you just get meaningful growth, at least in a short period of time. Meaningful growth meaning any measurable growth in inches like 0.5+. By technicality you will be growing as you spoke of plate signalling and developing bone but it won't be at a good enough rate for measurable growth. Which is why this is a two-pronged argument.
"Testosterone -> IGF-1 is not the same as HGH -> IGF-1, completely different pathways" -> Another strawman, you didn't understand the point. They're effectively the same as the common denominator here is an increase in the production of igf-1 with the proportional increase of the medium that increases IGF-1. We know it's different pathways.
"Once GH dosing reaches a certain point, increasing the dosage only leads to diminishing results" -> Unjustified claim
"As there is a limit on how much the chondrocytes can proliferate" This claim and the posterior claim are complete non sequiturs lol. There's also only a limit to chondrocyte proliferation because of the fact that resting zone cells get fused in the first place, not because chondrocytes just "stop proliferating"
"also a limit on the finite chondroprogenitor pool number in the resting zone itself" -> This claim is honestly a buzzphrase in this discussion from people that don't actually understand bone growth histology
Rz cells go through asymmetric division, meaning once an rz cell divides, One of the copies stay in the stem cell reservoir. So you effectively have the same number of cells continuously. Yes there's a finite number of rz cells but more specifically proliferative lifespan is what that actually means.
But this isn't conducive to what we're talking about, this is more about aging and apoptosis. The body naturally wants to kill of cells at SOME point. So these cells die eventually due to aging, not e2 fusion.
They don't die or fuse in the pubertal timespan outside of e2 which is exactly why aromatase deficient males still have open growth plates even in ages like 24. Cell death =/= Fusion is what's being explained here. It's actually an old belief that when you stop growing it's because cells "die" but it was discovered it's because of e2 turning the cells into bone not necessarily killing them.
Of course proliferative chondrocytes die, because they lay out the bone formation after dividing, growing and then leaving lacunae to be ossified. That isn't the same as rz cells though, they technically won't die off for a while as long as they aren't ossified by e2.
So yes RZ cells aren't infinite because all cells die at some point in life but that's less about growth plate mechanics and e2, more so about aging.
So no you can keep proliferating chondrocytes for a good while as long as your plates are open and you're at supraphysiological levels of IGF-1.
also if you're going to attack me on fallacies such as strawman i suggest you look at the post that i initially responded to where you were responding to somebody else and you committed ad hominem multiple times. So don't lecture me on fallacies, responding to what is implied using normal presumed definitions (such as "effect") != strawman but rather a misunderstanding due to imprecise wording one being responded toAnother really shit response, albeit you somewhat know what you're talking about and haven't said anything totally wrong but the issue is you strawmanning me. So lets do the same with you.
"if you mean active growth such that active growth causes a meaningful increase in fah then open growth plates do not necessitate that" 1. There's additional factors to this claim I made that's completely being left out
2. I didn't imply you just get meaningful growth, at least in a short period of time. Meaningful growth meaning any measurable growth in inches like 0.5+. By technicality you will be growing as you spoke of plate signalling and developing bone but it won't be at a good enough rate for measurable growth. Which is why this is a two-pronged argument.
"Testosterone -> IGF-1 is not the same as HGH -> IGF-1, completely different pathways" -> Another strawman, you didn't understand the point. They're effectively the same as the common denominator here is an increase in the production of igf-1 with the proportional increase of the medium that increases IGF-1. We know it's different pathways.
"Once GH dosing reaches a certain point, increasing the dosage only leads to diminishing results" -> Unjustified claim
"As there is a limit on how much the chondrocytes can proliferate" This claim and the posterior claim are complete non sequiturs lol. There's also only a limit to chondrocyte proliferation because of the fact that resting zone cells get fused in the first place, not because chondrocytes just "stop proliferating"
"also a limit on the finite chondroprogenitor pool number in the resting zone itself" -> This claim is honestly a buzzphrase in this discussion from people that don't actually understand bone growth histology
Rz cells go through asymmetric division, meaning once an rz cell divides, One of the copies stay in the stem cell reservoir. So you effectively have the same number of cells continuously. Yes there's a finite number of rz cells but more specifically proliferative lifespan is what that actually means.
But this isn't conducive to what we're talking about, this is more about aging and apoptosis. The body naturally wants to kill of cells at SOME point. So these cells die eventually due to aging, not e2 fusion.
They don't die or fuse in the pubertal timespan outside of e2 which is exactly why aromatase deficient males still have open growth plates even in ages like 24. Cell death =/= Fusion is what's being explained here. It's actually an old belief that when you stop growing it's because cells "die" but it was discovered it's because of e2 turning the cells into bone not necessarily killing them.
Of course proliferative chondrocytes die, because they lay out the bone formation after dividing, growing and then leaving lacunae to be ossified. That isn't the same as rz cells though, they technically won't die off for a while as long as they aren't ossified by e2.
So yes RZ cells aren't infinite because all cells die at some point in life but that's less about growth plate mechanics and e2, more so about aging.
So no you can keep proliferating chondrocytes for a good while as long as your plates are open and you're at supraphysiological levels of IGF-1.
I'm gonna respond to your shit paragraph rn, you clearly still just don't know what you're talking about and are trying to save face on a topic you don't fully understand.
except you can never truly prove someone is an "idiot" based off of just arguing with them on a studied topic on an online forum, so it is an ad hominem.
It isn't imprecise wording, neither did you show it was.
you're the one committing strawmans by claiming that im the one making strawmans.It isn't imprecise wording, neither did you show it was.
Also, I didn't give any argument about the quantification about the effect, ANOTHER strawman you're making right now. The effect is the effect in identity not in quantity. Nice strawman. You just can't stop strawmanning can you
They eventually can't divide anymore due to cell death from aging. More specifically telomere shortening. When it is said in bone histology that these cells are "finite" it simply means they can't keep reproducing themselves forever I mean that would be stupid, because when you die all cells die due to a lack of essential nutrients like oxygen and blood. But finitude can literally mean 20 years, 30 years 40 years there's not direct number on it. but it's not limited to puberty or a short span of time.
I didn't ignore senescence, that's quite literally what that entire response was responding to. Another indicator that you do not understand or can comprehend the topic
It's overly used without people actually knowing what it means, anyone who brings up the finitude of rz cells in the context of a heightmaxxing conversation does not know what they're talking about as that literally is a non issue.
Are you genuinely stupid? You're making up definitions for words now lmao an effect simply is a consequence brought about by a cause
I literally didn't say they grew because later because of supraphysiological gh so i'm not sure why you said "and not supraphys gh"
No that's not what I was talking about, I can agree there was a misunderstanding here with me not being specific enough. I was talknig about the proliferation/division in the rz zone not having a limit.
LMFAOO YOU'RE LITERALLY A RETARD
I simply said test and gh produce the same effect. And that effect is IGF-1. HOW MUCH igf-1 is produce is an additional factor that does not come under the definition of "effect". That's additional clarification of the qualities of the effect.
Just fucking LAUGHING at you trying to use colloquialism to define a word but then trying to ridicule me for apparently being "colloquial" about the word effect when I wasn't at it's YOU being colloquial about it
Don't even start on logic, you don't know shit about logic
You made an argument against a claim i didn't make, therefore it is a strawman
But if i’m fine with how i will feel this would make me grow?
no, because letrozole will close your growth plates faster and high dose hgh won't make you taller if your plates are already fused you'll just get organ growth and permanent side effects for nothing.
if i run .625 letrozole 12.5 enclo and keep my gh dose high it would work for the full 52 weeks?
