out of your 3 posts, this is one of them
U cant really grow taller in a sense, your height is genetically predetermined, but to make sure your height is stunted from your predicted height, just hop on 10-12 IUs of GH daily
second account lost the first one sadlyout of your 3 posts, this is one of them
only thing work here is hgh and ai
other stuff works too just look it up a bit deeper I know its more niche but it works
False
How so? Maybe the biological process of which Exogenous HGH is capped in my comment was wrong, but height is genetically predetermined; Chondrocytes can only multiply and stack for so long before they stop no?
Partly false
It will stunt growth not make u taller
it wont stuff like anavar and even test and tren has some heightgrowth properties just don't let your estrogen clim up high
Shoe soles and pray
what would you think you most someone could add to there height with correct pharma?
Doesn’t exist
What do you mean by this? (If he was talking about localised growth plate aromatisation, might have misunderstood)
AI inhibits intracellular estradiol
How can you prove this? And does it matter if the AI is steroidal or not for this
Tren in a heightmaxxing stack? Retard, most counterproductive thing ever
height isnt genetically predetermined, if it was acromegaly in height wouldnt be a thing retard, and secondly ur height is mostly determined by epigenetics but not fully like i said.
no it doesnt matter, just needs to be cell permeable which all are, anas letro exemes all are good.
6k cals a day
tren is useless matter fact counterproductive,anavar same thing,just keep test gh drop t3/t4 and drop mk if u alr pinnin gh retard, abalo gh ai low dose test is good enough.
So I could do proper doses of test at 16 without having to worry abt growth plate closure if I used an ai? And does primo have the same effect with stopping aromatisation at growth plates
Height fraud and save for LL surgery. All else is cope at 18+
just abuse em, u would worry about e2 mediated fusion if u think that would let u run 1g of test then ud still fuse from androgen mediated bone age acceleration, just use 300 to 400 max test with ai and ud be good.
Oh yeah let me see u pin 60 IUs of HGH and get acromegaly in height over the span of a couple years u fucking retard, obviously im talking about people without GHD or a Pituatary tumor.
Literally via the same pathway? It doesnt cap out on its proliferation, more is always gonna lead to more proliferation and more hypertrophy unless ur pinnin like 40iu then yeah obviously gonna lead to less of an roi, u dont even know how the growth plates work yet ur over here talking sounding like an absolute retard, jfl
????? Doesnt answer my question; But I dont expect a pseudo-science tard to answer it clearly anyways.
pubmed.ncbi.nlm.nih.gov
pmc.ncbi.nlm.nih.gov
pmc.ncbi.nlm.nih.gov
pubmed.ncbi.nlm.nih.gov
pubmed.ncbi.nlm.nih.gov
pubmed.ncbi.nlm.nih.gov
Yeah bro keep giving the ai slop bro, if all this shit was right there wouldnt be acromegaly as igf1 density is finite, lol no one daid it aint finite, if u need signficantly more than 4iu to cap out igf1 activity plus u moron ghr doesnt only induce growth thru igf1, but i mean dude again i aint gonna waste my time trying to prove u wrong, keep coping with ur 4iu brah and gl with chatgptmaxxing copy paste jfl????? Doesnt answer my question; But I dont expect a pseudo-science tard to answer it clearly anyways.
Growth Hormone binds to Growth Hormone Receptors in Chondrocytes which release Local IGF1, This local IGF-1 then binds to IGF-1 receptors (IGF1R) on chondrocytes, activating PI3K-AKT and MAPK/ERK signaling, which regulates Proliferation-
IGF1R density is finite (Rosenfeld et al., 1984), meaning there is a limited capacity for IGF1 signaling in chondrocytes. If receptor numbers were not finite, growth plate proliferation would be unlimited and epiphyseal senescence would not happen. Additionally, U cannot diddle with your Penis and expect Biology to change its laws for you because your parents are shortfucks, you utter stooge.
IGF1R is also an RTK which is responsible for certain pathways
PI3K = ATK ---> Cell Growth
RAS = RAF = MEK = ERK ---> Proliferation
Your retarded position inherently depends on the fact that AKT/ERK Activation leads to more Cell Proliferation and Chondrocyte Division, higher then whats genetically capped; This is retarded, as is yourself, because this Pathway, Alongside every other Pathway to exist, is Saturable, meaning its genetically limited. Additionally, when AKT/ERK is strongly regulated, it causes Negative Feedback for Certain Pathways, such as PTEN and MAPK
- Hyperactive AKT leads to the decrease of IGF‑1R at the transcriptional levelAKT down-regulates insulin-like growth factor-1 receptor as a negative feedback - PubMed
As a member of receptor tyrosine kinase (RTK) family, insulin-like growth factor-1 (IGF1) receptor (IGF1R) activates several downstream pathways to transmit proliferative signals from extracellular stimulation. AKT as a major effector plays a pivotal role in integrating various survival...
- Mounting evidence indicates that the mTORC1/S6K axis not only promotes growth-promoting signaling but also mediates potent negative feedback loops that restrain upstream signaling through insulin/IGF receptor and other tyrosine kinase receptors in both normal and oncogene-transformed cellsSuppression of feedback loops mediated by PI3K/mTOR induces multiple over-activation of compensatory pathways: an unintended consequence leading to drug resistance - PMC
The development of drug resistance by cancer cells is recognized as a major cause for drug failure and disease progression. PI3K/Akt/mTOR pathway is aberrantly stimulated in many cancer cells and thus it has emerged as a target for therapy. However, ...
- AKT activation causes feedback inhibition of receptor tyrosine kinases, including IGF1R, indicating that hyperactivation of the signaling pathway engages intrinsic negative feedback mechanisms that limit further signal propagationAKT inhibition relieves feedback suppression of receptor tyrosine kinase expression and activity - PMC
Activation of the PI3K-AKT pathway in tumors is modulated by negative feedback, including mTORC1-mediated inhibition of upstream signaling. We now show that AKT inhibition induces the expression and phosphorylation of multiple receptor tyrosine ...
Incase u still want to continue in your deluded pseudo-science, there are multiple studies on Exogenous HGH Therapy (and dont worry, theyre above 10 IUs) which show that HGH Therapy does not increase APH, But only speed up Growth Plate Maturation.
- Final height was significantly correlated with target height in both groups. These preliminary observations indicate that GH treatment does not generally increase final height over target height in short non-GH-deficient children.Final height after growth hormone therapy in non-growth-hormone-deficient children with short stature - PubMed
We report the effect of growth hormone (GH) treatment for 4 to 10 years in 15 prepubertal non-GH-deficient short children (10 boys, 5 girls, aged 7.4 to 13.2 years). In 7 patients, GH was administered at a dosage of 0.5 U/kg per week (group 1: 4 boys, 3 girls) and in 8 patients (group 2: 6 boys...
- GH therapy during the prepubertal period did not improve the final height of boys with non-GH-deficient short stature. GH therapy without GS decreased pubertal height gain, resulting in reduced final height. Combination therapy with GH and GS using cyproterone acetate decelerated the bone maturation during puberty which might be accelerated by GH therapy, but did not improve the final height which might have been attained without treatment.Combination therapy with GH and cyproterone acetate does not improve final height in boys with non-GH-deficient short stature - PubMed
GH therapy during the prepubertal period did not improve the final height of boys with non-GH-deficient short stature. GH therapy without GS decreased pubertal height gain, resulting in reduced final height. Combination therapy with GH and GS using cyproterone acetate decelerated the bone...
- The effect of growth hormone therapy on final height in 28 short boys without growth hormone deficiency was evaluated retrospectively. The boys had received growth hormone for at least 2 years and were close to final height when therapy was stopped. The mean estimated final height was very close to that predicted from the pretherapy bone age. The fact that bone age advanced a mean of 4.9 years during a mean of 3.5 years of therapy may account for the lack of effect on final height.Effect of growth hormone therapy on final versus predicted height in short twelve- to sixteen-year-old boys without growth hormone deficiency - PubMed
The effect of growth hormone therapy on final height in 28 short boys without growth hormone deficiency was evaluated retrospectively. The boys had received growth hormone for at least 2 years and were close to final height when therapy was stopped. The mean estimated final height was very close...
And just a note for next time when u wish to be a retard and argue about Gigantism and Acromegaly in Height, realize that even Doctors dont know what causes them to grow, No doctor on this earth can say "Its a Micro-Duplication of a Chromosome" Or "Its a Mutation in the aryl hydrocarbon receptor-interacting Gene" or "broooo theyre producing 200000mg of rHGH"
.Aryl hydrocarbon????? Doesnt answer my question; But I dont expect a pseudo-science tard to answer it clearly anyways.
Growth Hormone binds to Growth Hormone Receptors in Chondrocytes which release Local IGF1, This local IGF-1 then binds to IGF-1 receptors (IGF1R) on chondrocytes, activating PI3K-AKT and MAPK/ERK signaling, which regulates Proliferation-
IGF1R density is finite (Rosenfeld et al., 1984), meaning there is a limited capacity for IGF1 signaling in chondrocytes. If receptor numbers were not finite, growth plate proliferation would be unlimited and epiphyseal senescence would not happen. Additionally, U cannot diddle with your Penis and expect Biology to change its laws for you because your parents are shortfucks, you utter stooge.
IGF1R is also an RTK which is responsible for certain pathways
PI3K = ATK ---> Cell Growth
RAS = RAF = MEK = ERK ---> Proliferation
Your retarded position inherently depends on the fact that AKT/ERK Activation leads to more Cell Proliferation and Chondrocyte Division, higher then whats genetically capped; This is retarded, as is yourself, because this Pathway, Alongside every other Pathway to exist, is Saturable, meaning its genetically limited. Additionally, when AKT/ERK is strongly regulated, it causes Negative Feedback for Certain Pathways, such as PTEN and MAPK
- Hyperactive AKT leads to the decrease of IGF‑1R at the transcriptional levelAKT down-regulates insulin-like growth factor-1 receptor as a negative feedback - PubMed
As a member of receptor tyrosine kinase (RTK) family, insulin-like growth factor-1 (IGF1) receptor (IGF1R) activates several downstream pathways to transmit proliferative signals from extracellular stimulation. AKT as a major effector plays a pivotal role in integrating various survival...
- Mounting evidence indicates that the mTORC1/S6K axis not only promotes growth-promoting signaling but also mediates potent negative feedback loops that restrain upstream signaling through insulin/IGF receptor and other tyrosine kinase receptors in both normal and oncogene-transformed cellsSuppression of feedback loops mediated by PI3K/mTOR induces multiple over-activation of compensatory pathways: an unintended consequence leading to drug resistance - PMC
The development of drug resistance by cancer cells is recognized as a major cause for drug failure and disease progression. PI3K/Akt/mTOR pathway is aberrantly stimulated in many cancer cells and thus it has emerged as a target for therapy. However, ...
- AKT activation causes feedback inhibition of receptor tyrosine kinases, including IGF1R, indicating that hyperactivation of the signaling pathway engages intrinsic negative feedback mechanisms that limit further signal propagationAKT inhibition relieves feedback suppression of receptor tyrosine kinase expression and activity - PMC
Activation of the PI3K-AKT pathway in tumors is modulated by negative feedback, including mTORC1-mediated inhibition of upstream signaling. We now show that AKT inhibition induces the expression and phosphorylation of multiple receptor tyrosine ...
Incase u still want to continue in your deluded pseudo-science, there are multiple studies on Exogenous HGH Therapy (and dont worry, theyre above 10 IUs) which show that HGH Therapy does not increase APH, But only speed up Growth Plate Maturation.
- Final height was significantly correlated with target height in both groups. These preliminary observations indicate that GH treatment does not generally increase final height over target height in short non-GH-deficient children.Final height after growth hormone therapy in non-growth-hormone-deficient children with short stature - PubMed
We report the effect of growth hormone (GH) treatment for 4 to 10 years in 15 prepubertal non-GH-deficient short children (10 boys, 5 girls, aged 7.4 to 13.2 years). In 7 patients, GH was administered at a dosage of 0.5 U/kg per week (group 1: 4 boys, 3 girls) and in 8 patients (group 2: 6 boys...
- GH therapy during the prepubertal period did not improve the final height of boys with non-GH-deficient short stature. GH therapy without GS decreased pubertal height gain, resulting in reduced final height. Combination therapy with GH and GS using cyproterone acetate decelerated the bone maturation during puberty which might be accelerated by GH therapy, but did not improve the final height which might have been attained without treatment.Combination therapy with GH and cyproterone acetate does not improve final height in boys with non-GH-deficient short stature - PubMed
GH therapy during the prepubertal period did not improve the final height of boys with non-GH-deficient short stature. GH therapy without GS decreased pubertal height gain, resulting in reduced final height. Combination therapy with GH and GS using cyproterone acetate decelerated the bone...
- The effect of growth hormone therapy on final height in 28 short boys without growth hormone deficiency was evaluated retrospectively. The boys had received growth hormone for at least 2 years and were close to final height when therapy was stopped. The mean estimated final height was very close to that predicted from the pretherapy bone age. The fact that bone age advanced a mean of 4.9 years during a mean of 3.5 years of therapy may account for the lack of effect on final height.Effect of growth hormone therapy on final versus predicted height in short twelve- to sixteen-year-old boys without growth hormone deficiency - PubMed
The effect of growth hormone therapy on final height in 28 short boys without growth hormone deficiency was evaluated retrospectively. The boys had received growth hormone for at least 2 years and were close to final height when therapy was stopped. The mean estimated final height was very close...
And just a note for next time when u wish to be a retard and argue about Gigantism and Acromegaly in Height, realize that even Doctors dont know what causes them to grow, No doctor on this earth can say "Its a Micro-Duplication of a Chromosome" Or "Its a Mutation in the aryl hydrocarbon receptor-interacting Gene" or "broooo theyre producing 200000mg of rHGH"
bro i swear ur ragebaiting me but iaint gonna fall for it, keep using ur crap ass gpt like a fucking faggot thinking u own pharmacology and biology when u wont last 1 sentence without some ai generated crap.
Anything but responding to the actual scientific evidence provided jesus christYeah bro keep giving the ai slop bro, if all this shit was right there wouldnt be acromegaly as igf1 density is finite, lol no one daid it aint finite, if u need signficantly more than 4iu to cap out igf1 activity plus u moron ghr doesnt only induce growth thru igf1, but i mean dude again i aint gonna waste my time trying to prove u wrong, keep coping with ur 4iu brah and gl with chatgptmaxxing copy paste jfl
your retarded, noone is gaining height on 4 IUs u faggot. I made an entire thread proving under 10 is retarded, go kill yourself and do us a favor pleaseYeah bro keep giving the ai slop bro, if all this shit was right there wouldnt be acromegaly as igf1 density is finite, lol no one daid it aint finite, if u need signficantly more than 4iu to cap out igf1 activity plus u moron ghr doesnt only induce growth thru igf1, but i mean dude again i aint gonna waste my time trying to prove u wrong, keep coping with ur 4iu brah and gl with chatgptmaxxing copy paste jfl
its actually not look into it
Androgens don’t really make you taller, their effects on igf-1 are minor, testosterone or anavar maybe because they are the mildest but the amount of cortisol increase and oxidative stress tren puts your body under is counterproductive to height growth
use glathatione to mitigate the sides
Not ideal and why even take tren to try and look for anything to lower its side effects? The only thing that may affect from Tren is androgen’s and your best bet is just testosterone.
I do IM
