hardmaxing solutions for feminine features at 14

[geekr]

i

yeah ur dumb, if you did look through textbooks you would realize no amount of testosterone can change what your genes already do

its mostly for size, thats why im asking for surgeries

 

[birthdefect]

Genuinely it would make him more retarded

Would fry homies brain development

arent there studies that show having nuked e2 doesnt do much cognitively? idk about long term effects tho
you think you could completely nuke e2 and then supplement with alfatradiol to keep most of e2s benefits without it raping the plates?
i lowkey wrote a thread on this on gg

 

[gmoneyyyy21]

Im a 14 year old male and hates my feminine features,
I need advice on how to larp a lefort 1 or 3 osteotomy
I also need advice on dht derivatives like masteron and winstrol, as well as if its true that access androgens can close growth plates
please give me more surgeries and steroids/hormones I can look into
I am currently on anavar and mk 677
and I will be taking 8iu gh and 300 test in a year to 6 months

and no I don't care about fertility or living past 30, so please don't reply just to tell me how stupid I am.

Lets see how cooked u r

 

[Deleted member 297038]

buddy

i

its mostly for size, thats why im asking for surgeries

no jaw surgery is needed (or will be given) for cosmetic benefit in puberty, its only if you have a genuine problem. you can't just larp having an extreme orthodontic problem.

 

[geekr]

Lets see how cooked u r

have to put a towel over my mirror, fuh nah

 

[exsttttt]

Lowering your E2 will not meaningfully prolong growth plate closure.

1: Growth plate closure is dictated by tissue specific E2 exposure over time. Randomly lowering it won’t stop that process.

2: As I said before you need E2 for your body to convert HGH to IGF-1. It is very difficult to use AIs, I don’t care what the forum says they are hard to use effectively even when on gear.

3: “added years of linear growth” do you think with and AI you just get additional YEARS where your growth progresses at a linear rate(?

We’ve with HGH+AI starting at 14 we don’t see statistically significant growth. 1-2 at BEST.

And it comes with consequences.

Stop this pseudo intellectual facade.

you said it urself, fusion is dictated by local e2 activity exposure over time, hes just getting started, as long as gp havent fused, ai remains a viable way to delay said fusion, quite frankly just before u mention any other retarded reason why it wont work, why would ai be used alongside gh in idiopathic short stature, at even 15-16 yo in some cases? and u saying it only gives 1-2 inches at best isnt true first of all, but its not much more than that, and thats not because ai didnt delay fusion enough. it works as long as they havent fused. and secondly for ur retarded reason, quite funny how u said im retarded when clearly u are here, u DONT need e2 to produce igf1, igf1 always remains, just gets downregulated the further u inhibit e2 simply because e2 increases gh pulsatility and increases ghr expression in the liver in turn making the liver more sensitive to that same gh. even nuking e2 into undetectable levels only downregulates systemic igf1 by about 20ish %, also liver igf1 doesnt mean crap, local igf1 is by far more important. and for ur third mention, i never said ai will extend that same high velocity in ur peak teenage years and carry it into those extra years, it will slow, but not halt.

as for your said " consequences" the only possible sides from nuking, not lowering e2 into the lower end of the range, but nuking it, would be slight decrease in bone density ( which could be resolved after puberty anyway) and slight brain development delay, few studies done on ai and brain development mention no signficant impact on brain health nor development, i mean aromatase deficient people arent textbook retarded are they?

 

[BR32]

everyone here is flaming you for a good reason ngl, Let puberty do its natrual cause until 16-17. The only thing i would suggest is hgh but if your daring you can run test but i really dont reccomend going down this rabbit hole so early best to stick to hgh and as you develop more of an understanding to peptides and pharma you will be more inclined to learn and research AAS and not run them retardly. Thats how it always starts "its just peptides" "just some gh" then its test then tren.

I remember when I first pinned peptides

I told myself "I'll never pin anything else"

 

[birthdefect]

I remember when I first pinned peptides

I told myself "I'll never pin anything else"

i mean tbf the distinction between peptide, protein, and steroid hormones is mostly arbitrary to the user
certain small molecule modulators tho i see the concern

 

[BR32]

arent there studies that show having nuked e2 doesnt do much cognitively? idk about long term effects tho
you think you could completely nuke e2 and then supplement with alfatradiol to keep most of e2s benefits without it raping the plates?
i lowkey wrote a thread on this on gg

maybe dawg idk

Theres issues w jsut inhibiting aromatase alone

physiologic tissue specific E2 etc

none of this is prolly a good idea

besides is E2 the thing thats really the plate closing bottleneck? nah its genetics

 

[gmoneyyyy21]

you said it urself, fusion is dictated by local e2 activity exposure over time, hes just getting started, as long as gp havent fused, ai remains a viable way to delay said fusion, quite frankly just before u mention any other retarded reason why it wont work, why would ai be used alongside gh in idiopathic short stature, at even 15-16 yo in some cases? and u saying it only gives 1-2 inches at best isnt true first of all, but its not much more than that, and thats not because ai didnt delay fusion enough. it works as long as they havent fused. and secondly for ur retarded reason, quite funny how u said im retarded when clearly u are here, u DONT need e2 to produce igf1, igf1 always remains, just gets downregulated the further u inhibit e2 simply because e2 increases gh pulsatility and increases ghr expression in the liver in turn making the liver more sensitive to that same gh. even nuking e2 into undetectable levels only downregulates systemic igf1 by about 20ish %, also liver igf1 doesnt mean crap, local igf1 is by far more important. and for ur third mention, i never said ai will extend that same high velocity in ur peak teenage years and carry it into those extra years, it will slow, but not halt.

as for your said " consequences" the only possible sides from nuking, not lowering e2 into the lower end of the range, but nuking it, would be slight decrease in bone density ( which could be resolved after puberty anyway) and slight brain development delay, few studies done on ai and brain development mention no signficant impact on brain health nor development, i mean aromatase deficient people arent textbook retarded are they?

Dnr nigga

 

[birthdefect]

maybe dawg idk

Theres issues w jsut inhibiting aromatase alone

physiologic tissue specific E2 etc

none of this is prolly a good idea

besides is E2 the thing thats really the plate closing bottleneck? nah its genetics

but what does genetics even mean? have you thought about that?
people claim height is genetics, i asked someone what he meant by that, and he said he thought dna synthesis just stopped once bone reached a certain length

the genetic component is sensitivity to hormones and their downstream signalling cascades (e2 downstream signalling cascade can be inhibited anyways but thats besides the point). genetics arent just some devil lurking in the background, they express their effects through different signalling cascades. e2, androgens, and thyroid hormones are pretty much everything involved in bone aging (and ofc their respective downstream cascades). aromatase inhibition logically has to delay bone aging, and in clinical trials they do so indiscriminately with 1mg anastrozole daily. low e2 like this is found to have little to no cognitive impact during puberty, i dont see why the difference would be significant in adulthood, but even if thats a concern my idea could be used since alfatradiol is significantly less feminising than standard e2, thus preventing any growth plate problems

sorry for text wall

 

[exsttttt]

maybe dawg idk

Theres issues w jsut inhibiting aromatase alone

physiologic tissue specific E2 etc

none of this is prolly a good idea

besides is E2 the thing thats really the plate closing bottleneck? nah its genetics

genetics determine hormone levels ie e2, and inhibiting aromatase would be overriding genetics, so yeah genetics isnt hardlocked. if e2 wasnt what fused plates explain why aromatase deficient people fuse late 20s- early 30s, i mean its genetic right? they should have fused normally, at least thats ur logic.