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Blackpill Do I ascend or rope? (3 Viewers)

Blackpill Do I ascend or rope?

slogxER

Ropefueler
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15.5 years old, I am a sort of late bloomer and all.

I have a few options

Now I cant moneymaxx until I am 16 minimum, then I will have to save to buy HGH and reta and last 10-13IU HGH and some reta for 8 months. Then probably hop on some androgens.
So I will have to softmaxx until like 16, then hard-softmaxx (gear/PEDs) but then if HGH + roids dont ascend me and I dont have money to get surgeries, do i just call it a day (rope). Or shall I end up softmaxxing, then roid, in hopes to ascend then live in peace after?

or if that does not work out, do i moneymaxx and get surgery (with a risk of being botched like a dr taban clinic, or do i just rope)
Since when peptides and gear became hardmaxx
 

birthdefect

pray to the purple powder
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Oh and btw, presented by the beautiful birthdefect birthdefect :

Z x weight(KGS) / 7 x 3 = daily gh iu dose
Z = any number between 0.24-0.47​

THE HGH FORMULA

Just a range to choose. Test will be good(and prolly better in a stand alone comp ig) and cheaper. Eitherway u should do a solid stack.
i love you nigga
thank you for sharing this knowledge with the needy goyim
will be copying this formatting so i can use it elsewhere
 

birthdefect

pray to the purple powder
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thanks for giving me the opportunity to write my 1500th post

on 13 IU HGH you will die
mirin intellect
idk if he specified his weight since i dnrd, but 13 iu is perfectly ok depending on weight
aforementioned formula that VelocityAnt¹ VelocityAnt¹ posted would give you 14.1 iu daily max dose for a goy that weighed 70kg
 

birthdefect

pray to the purple powder
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congrats OP has acromegaly and insulin resistance now
neither occurs from +2.0 igf1 z score, which is the actual goal
prior formula is derived from dosing from the nih overview on gh dosing, which includes dosing practises on idiopathic short stature patients
1771228054238.png

disqualified
 

Dexter

🩺 | .gg’s doctor, M.D.
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neither occurs from +2.0 igf1 z score, which is the actual goal
prior formula is derived from dosing from the nih overview on gh dosing, which includes dosing practises on idiopathic short stature patients
View attachment 28893
disqualified
clinical gh dosing in teens w deficiency is 0.16-0.23/mg/kg/week, occasionally up to 0.3mg/kg/week
for 70kg teen, using 0.3mg/kg/week we get 9 ish IU/day
that is already upper end therapeutic dosing for a diagnosed pathology
13 iu means 0.43 mg/kg/week and that too for a deficient teen and not a normal one with normal gh axis

GH has direct anti insulin effects independent of IGF1
increases hepatic gluconeogenesis
decreases peripheral glucose uptake
increases lipolysis which elevates FFA and worsens insulin signaling
suppresses insulin receptor substrate pathways

my claim of acro was an exaggeration. but chronic supraphysiologic GH alone induces insulin resistance even when IGF1 is "within range". GH is not metabolically benign


And since GH stimulates systemic cell proliferation via IGF1,
long term elevated IGF1 has epidemiological associations with increased risk of certain malignancies

and about that formula, it assumes
linear GH -> IGF-1 response (false)
uniform hepatic sensitivity (false)
identical clearance rates (false)
stable endogenous GH suppression (false)
identical pubertal hormonal environments (false)

IGF1 response to GH varies massively between individuals,
two people can take the same IU dose and have completely different IGF1 levels.
thats why endocrinologists titrate based on serial IGF1 labs, glucose tolerance, lipids, thyroid status etc. and not a formula on some incel forum
 

birthdefect

pray to the purple powder
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clinical gh dosing in teens w deficiency is 0.16-0.23/mg/kg/week, occasionally up to 0.3mg/kg/week
for 70kg teen, using 0.3mg/kg/week we get 9 ish IU/day
that is already upper end therapeutic dosing for a diagnosed pathology
13 iu means 0.43 mg/kg/week and that too for a deficient teen and not a normal one with normal gh axis

GH has direct anti insulin effects independent of IGF1
increases hepatic gluconeogenesis
decreases peripheral glucose uptake
increases lipolysis which elevates FFA and worsens insulin signaling
suppresses insulin receptor substrate pathways

my claim of acro was an exaggeration. but chronic supraphysiologic GH alone induces insulin resistance even when IGF1 is "within range". GH is not metabolically benign


And since GH stimulates systemic cell proliferation via IGF1,
long term elevated IGF1 has epidemiological associations with increased risk of certain malignancies

and about that formula, it assumes
linear GH -> IGF-1 response (false)
uniform hepatic sensitivity (false)
identical clearance rates (false)
stable endogenous GH suppression (false)
identical pubertal hormonal environments (false)

IGF1 response to GH varies massively between individuals,
two people can take the same IU dose and have completely different IGF1 levels.
thats why endocrinologists titrate based on serial IGF1 labs, glucose tolerance, lipids, thyroid status etc. and not a formula on some incel forum
with deficiency you're right, but this isnt about deficiency
its about being short without an underlying cause, aka idiopathic short stature, which is dosed at the rate i provided
in clinical settings, insulin resistance and diabetes isnt usually a problem, but in severe cases afaik metformin is used
you are correct about people having super different responses to gh, which is why i always specify in actual conversations that they should focus on the z score and not the actual iu dose. the formula is intentionally simple and just uses standard guidelines

wdym it has anti insulin effects independent of igf1? isnt that a given considering igf1 is literally insulin like in its metabolic action?
 

Dexter

🩺 | .gg’s doctor, M.D.
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with deficiency you're right, but this isnt about deficiency
its about being short without an underlying cause, aka idiopathic short stature, which is dosed at the rate i provided
in clinical settings, insulin resistance and diabetes isnt usually a problem, but in severe cases afaik metformin is used
you are correct about people having super different responses to gh, which is why i always specify in actual conversations that they should focus on the z score and not the actual iu dose. the formula is intentionally simple and just uses standard guidelines

wdym it has anti insulin effects independent of igf1? isnt that a given considering igf1 is literally insulin like in its metabolic action?
Yes ISS dosings can go up to .44mg/kg/week iirc
but,
ISS is still treated under pediatric endocrinology supervision, patients are monitored every 3 to6 months, IGF1 is kept within age adjusted reference range, glucose metabolism is monitored, therapy is stopped if adverse effects occur
13 IU is .43mg/kg/wk
this is at upper end of ISS protocol, dnd those protocols are not casual enhancement regimens but are carefully monitored.
so the issue isn’t whether 0.43 mg/kg/week exists in literature, it is whether a 16y old self administering 13 IU daily without confirmed ISS diagnosis, without endocrine monitoring (a proper one, i doubt OP even knows what a lipid profile is) is medically equivalent to supervised ISS treatment (it isnt)


clinical settings, insulin resistance and diabetes isnt usually a problem
in pediatric ISS therapy mild insulin resistance is common, fasting insulin often rises, glucose tolerance may worsen slightly, most cases remain compensated
Because doses are controlled, duration is limited, monitoring occurs and patients are screened
That doesnt mean supraphysiologic GH is metabolically benign
metformin is sometimes used, yes, but thats managing a side effect and npt a proof of harmlessness


focus on the z score and not the actual iu dose.
this is closer to clinical reasoning imo

the GH IGF1 response curve is nonlinear and saturable
some individuals require low doses to reach +2 Z. others overshoot easily

but

maintaining someone chronically at +2 Z score is near the upper physiologic boundary
it increases mitogenic signaling via IGF1 receptor
activates PI3K/Akt and MAPK pathways
promotes cell proliferation and antiapoptotic signaling

i may have missed points but whatever, it's a bad day
 

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