AI and GH Will NOT Make You Grow Taller

[Deleted member 34054]

Introduction​

Growth plates, or epiphyseal plates, are essential for bone growth. The chondrocytes in these plates undergo stages of proliferation, hypertrophy, and apoptosis, all regulated by GH, IGF-1, testosterone, and estrogen. This review delves into how these hormones affect chondrocyte activity and why growth plates close, ending height growth.

Mechanisms of Chondrocyte Regulation​

Chondrocytes in growth plates go through a cycle: they divide in the proliferative zone, enlarge in the hypertrophic zone, and die off to be replaced by bone in the ossification zone. GH and IGF-1 are crucial for these processes, promoting division, enlargement, and bone formation. This cartilage-to-bone replacement, known as endochondral ossification, is vital for height growth during childhood and adolescence .

Pubertal Changes and Growth Plate Senescence​

During puberty, typically between ages 15-19 in developed countries and 12-15 in less developed ones, growth accelerates but then slows as chondrocytes become less responsive to growth signals. Environmental and genetic factors cause faster telomere shortening, making chondrocytes more prone to aging and apoptosis, leading to growth plate closure and the end of height increase .

Pathways Influencing Chondrocyte Response​

The STAT and PI3K-Akt pathways are key for GH and IGF-1 signaling in chondrocytes. However, these pathways become less effective as chondrocytes age. Therefore, giving GH to older individuals doesn’t have much effect, similar to trying to revive a barren field with water .

Role of Estrogen and Androgens in Growth Plate Closure​

Estrogen is crucial for growth plate closure, binding to receptors on chondrocytes and promoting their maturation and ossification. Some propose using letrozole, an aromatase inhibitor, to keep growth plates open by reducing estrogen. However, this can increase testosterone and dihydrotestosterone (DHT), which also bind to androgen receptors on chondrocytes and promote ossification .

Discussion​

While letrozole might delay growth plate closure, it doesn’t guarantee additional height growth. Mature chondrocytes don’t respond well to GH, making significant height increase unlikely. Using GH after puberty won’t yield much growth and can lead to issues like insulin resistance .

Conclusion​

Using GH and IGF-1 to boost height after puberty is ineffective due to the natural aging of chondrocytes and the closure of growth plates. Letrozole may delay closure but doesn’t ensure extra height growth. Future research should focus on understanding chondrocyte aging and finding ways to improve their responsiveness during key growth periods.

References​

1. Baron, J., et al. (2006). The Growth Plate. Journal of Endocrinology, 189(1), 27-40. Link
2. Lui, J.C., et al. (2019). Biological parameters of the human growth plate. Journal of Biological Chemistry, 294(24), 9137-9148. Link
3. Nilsson, O., et al. (2015). Evidence that estrogen hastens growth plate senescence. Journal of Molecular Endocrinology, 54(1), 61-69. Link
4. Hiyama, A., et al. (2021). Growth plate senescence and epiphyseal fusion: Mechanisms and implications. Frontiers in Endocrinology, 12, 705. Link
5. Tian, J., et al. (2019). Molecular mechanisms of endochondral ossification and its role in skeletal diseases. Journal of Molecular Endocrinology, 62(2), 1-14. Link

 

[Deleted member 34054]

Thread was rewritten by ChatGPT

 

[Orc]

Thread was rewritten by ChatGPT

it's fine as long as the information is accurate.

something that's often overlooked here is that the average age of the participants in hgh trials is around 10 years of age, they're pre-puberty, not nearing the end of it like most posters here.

 

[niqfan625]

Introduction​

Growth plates, or epiphyseal plates, are essential for bone growth. The chondrocytes in these plates undergo stages of proliferation, hypertrophy, and apoptosis, all regulated by GH, IGF-1, testosterone, and estrogen. This review delves into how these hormones affect chondrocyte activity and why growth plates close, ending height growth.

Mechanisms of Chondrocyte Regulation​

Chondrocytes in growth plates go through a cycle: they divide in the proliferative zone, enlarge in the hypertrophic zone, and die off to be replaced by bone in the ossification zone. GH and IGF-1 are crucial for these processes, promoting division, enlargement, and bone formation. This cartilage-to-bone replacement, known as endochondral ossification, is vital for height growth during childhood and adolescence .

Pubertal Changes and Growth Plate Senescence​

During puberty, typically between ages 15-19 in developed countries and 12-15 in less developed ones, growth accelerates but then slows as chondrocytes become less responsive to growth signals. Environmental and genetic factors cause faster telomere shortening, making chondrocytes more prone to aging and apoptosis, leading to growth plate closure and the end of height increase .

Pathways Influencing Chondrocyte Response​

The STAT and PI3K-Akt pathways are key for GH and IGF-1 signaling in chondrocytes. However, these pathways become less effective as chondrocytes age. Therefore, giving GH to older individuals doesn’t have much effect, similar to trying to revive a barren field with water .

Role of Estrogen and Androgens in Growth Plate Closure​

Estrogen is crucial for growth plate closure, binding to receptors on chondrocytes and promoting their maturation and ossification. Some propose using letrozole, an aromatase inhibitor, to keep growth plates open by reducing estrogen. However, this can increase testosterone and dihydrotestosterone (DHT), which also bind to androgen receptors on chondrocytes and promote ossification .

Discussion​

While letrozole might delay growth plate closure, it doesn’t guarantee additional height growth. Mature chondrocytes don’t respond well to GH, making significant height increase unlikely. Using GH after puberty won’t yield much growth and can lead to issues like insulin resistance .

Conclusion​

Using GH and IGF-1 to boost height after puberty is ineffective due to the natural aging of chondrocytes and the closure of growth plates. Letrozole may delay closure but doesn’t ensure extra height growth. Future research should focus on understanding chondrocyte aging and finding ways to improve their responsiveness during key growth periods.

References​

1. Baron, J., et al. (2006). The Growth Plate. Journal of Endocrinology, 189(1), 27-40. Link
2. Lui, J.C., et al. (2019). Biological parameters of the human growth plate. Journal of Biological Chemistry, 294(24), 9137-9148. Link
3. Nilsson, O., et al. (2015). Evidence that estrogen hastens growth plate senescence. Journal of Molecular Endocrinology, 54(1), 61-69. Link
4. Hiyama, A., et al. (2021). Growth plate senescence and epiphyseal fusion: Mechanisms and implications. Frontiers in Endocrinology, 12, 705. Link
5. Tian, J., et al. (2019). Molecular mechanisms of endochondral ossification and its role in skeletal diseases. Journal of Molecular Endocrinology, 62(2), 1-14. Link

Can say from doing this myself heightmaxxing is cope

 

[LooksThinker]

Introduction​

Growth plates, or epiphyseal plates, are essential for bone growth. The chondrocytes in these plates undergo stages of proliferation, hypertrophy, and apoptosis, all regulated by GH, IGF-1, testosterone, and estrogen. This review delves into how these hormones affect chondrocyte activity and why growth plates close, ending height growth.

Mechanisms of Chondrocyte Regulation​

Chondrocytes in growth plates go through a cycle: they divide in the proliferative zone, enlarge in the hypertrophic zone, and die off to be replaced by bone in the ossification zone. GH and IGF-1 are crucial for these processes, promoting division, enlargement, and bone formation. This cartilage-to-bone replacement, known as endochondral ossification, is vital for height growth during childhood and adolescence .

Pubertal Changes and Growth Plate Senescence​

During puberty, typically between ages 15-19 in developed countries and 12-15 in less developed ones, growth accelerates but then slows as chondrocytes become less responsive to growth signals. Environmental and genetic factors cause faster telomere shortening, making chondrocytes more prone to aging and apoptosis, leading to growth plate closure and the end of height increase .

Pathways Influencing Chondrocyte Response​

The STAT and PI3K-Akt pathways are key for GH and IGF-1 signaling in chondrocytes. However, these pathways become less effective as chondrocytes age. Therefore, giving GH to older individuals doesn’t have much effect, similar to trying to revive a barren field with water .

Role of Estrogen and Androgens in Growth Plate Closure​

Estrogen is crucial for growth plate closure, binding to receptors on chondrocytes and promoting their maturation and ossification. Some propose using letrozole, an aromatase inhibitor, to keep growth plates open by reducing estrogen. However, this can increase testosterone and dihydrotestosterone (DHT), which also bind to androgen receptors on chondrocytes and promote ossification .

Discussion​

While letrozole might delay growth plate closure, it doesn’t guarantee additional height growth. Mature chondrocytes don’t respond well to GH, making significant height increase unlikely. Using GH after puberty won’t yield much growth and can lead to issues like insulin resistance .

Conclusion​

Using GH and IGF-1 to boost height after puberty is ineffective due to the natural aging of chondrocytes and the closure of growth plates. Letrozole may delay closure but doesn’t ensure extra height growth. Future research should focus on understanding chondrocyte aging and finding ways to improve their responsiveness during key growth periods.

References​

1. Baron, J., et al. (2006). The Growth Plate. Journal of Endocrinology, 189(1), 27-40. Link
2. Lui, J.C., et al. (2019). Biological parameters of the human growth plate. Journal of Biological Chemistry, 294(24), 9137-9148. Link
3. Nilsson, O., et al. (2015). Evidence that estrogen hastens growth plate senescence. Journal of Molecular Endocrinology, 54(1), 61-69. Link
4. Hiyama, A., et al. (2021). Growth plate senescence and epiphyseal fusion: Mechanisms and implications. Frontiers in Endocrinology, 12, 705. Link
5. Tian, J., et al. (2019). Molecular mechanisms of endochondral ossification and its role in skeletal diseases. Journal of Molecular Endocrinology, 62(2), 1-14. Link

it's fine as long as the information is accurate.

something that's often overlooked here is that the average age of the participants in hgh trials is around 10 years of age, they're pre-puberty, not nearing the end of it like most posters here.

Does taking CJC and aromasin work for height growth as a mid teenager?

 

[Gaygymmaxx]

Can say from doing this myself heightmaxxing is cope

I went extrmely hard as well and was too late, 17 bone age is too late to spend hundreds of dollars, you won't get much past your growth chart snd prediction if you don't start at like 15

 

[Gaygymmaxx]

Does taking CJC and aromasin work for height growth as a mid teenager?

That's valid it should help if ,"mid teen"

What age?

 

[Deleted member 34054]

Does taking CJC and aromasin work for height growth as a mid teenager?

no molecule is going to make you taller

 

[LooksThinker]

That's valid it should help if ,"mid teen"

What age?

15.7 with late puberty

 

[LooksThinker]

no molecule is going to make you taller

over

 

[Deleted member 34054]

0

 

[elemanzelvadre]

Being fat and low igf makes u short u can just save ur predicted height

 

[Deleted member 34054]

Being fat and low igf makes u short

this statement is contradictory. Empirical data shows that obese individuals typically have higher IGF-1 levels, not lower. Additionally, the statement does not consider the percentage of the global population that has growth hormone deficiency

 

[Deleted member 34054]

0

 

[elemanzelvadre]

this statement is contradictory. Empirical data shows that obese individuals typically have higher IGF-1 levels, not lower. Additionally, the statement does not consider the percentage of the global population that has growth hormone deficiency

I dıdnt say obeses are low igf thehy are high e and being skinny makes u low igf both are makes u short

 

[DR. NICKGA]

I literaly say it all the time, why you guys look at this chatgpt generated thread and be like "woaaaah!! I am in shock"



Increasing serum hgh levels in you blood will not result in more growth

 

[Outerz14]

I went extrmely hard as well and was too late, 17 bone age is too late to spend hundreds of dollars, you won't get much past your growth chart snd prediction if you don't start at like 15

It just begun for me

 

[iblamesols]

sing GH and IGF-1 to boost height after puberty

who said anything about after puberty? lol

 

[iblamesols]

. However, this can increase testosterone and dihydrotestosterone (DHT), which also bind to androgen receptors on chondrocytes and promote ossification .

then take fin?

 

[Donkeyballs]

that’s why I mainly support injecting when your hormones (igf-1) are below average/low percentile which many users included I have had and grown some.
If your body has no incentive to grow it won’t obviously, but this also includes hormonal factors. From hgh, I’ve grown 1.5 inches in the last 3-4 months. I also started taking aromasin since last year

 

[justropemaxbro]

basically, it works when during Puberty and it doesn't after puberty?

 

[Deleted member 34054]

I literaly say it all the time, why you guys look at this chatgpt generated thread and be like "woaaaah!! I am in shock"



Increasing serum hgh levels in you blood will not result in more growth

This thread is was not generated by chatgpt i wrote everything and then chatgpt rewrote it for clarification and grammar issues

 

[Deleted member 34054]

basically, it works when during Puberty and it doesn't after puberty?

it only works if youre deficient in hgh

 

[justropemaxbro]

it only works if youre deficient in hgh

Then what would you suggest that I do? and aromasin makes that and closing of the growth plates slower? So why wouldn’t it work?

 

[justropemaxbro]

it only works if youre deficient in hgh

what if I use HGH + AI or test + ai?

 

[slavicpsycho]

Did you copy that one doctor tikoker fag hahaha

 

[ogrepilled]

dnr

 

[pandac]

if u start very early its not cope but none of these niggas are that young

 

[Rigged]

Introduction​

Growth plates, or epiphyseal plates, are essential for bone growth. The chondrocytes in these plates undergo stages of proliferation, hypertrophy, and apoptosis, all regulated by GH, IGF-1, testosterone, and estrogen. This review delves into how these hormones affect chondrocyte activity and why growth plates close, ending height growth.

Mechanisms of Chondrocyte Regulation​

Chondrocytes in growth plates go through a cycle: they divide in the proliferative zone, enlarge in the hypertrophic zone, and die off to be replaced by bone in the ossification zone. GH and IGF-1 are crucial for these processes, promoting division, enlargement, and bone formation. This cartilage-to-bone replacement, known as endochondral ossification, is vital for height growth during childhood and adolescence .

Pubertal Changes and Growth Plate Senescence​

During puberty, typically between ages 15-19 in developed countries and 12-15 in less developed ones, growth accelerates but then slows as chondrocytes become less responsive to growth signals. Environmental and genetic factors cause faster telomere shortening, making chondrocytes more prone to aging and apoptosis, leading to growth plate closure and the end of height increase .

Pathways Influencing Chondrocyte Response​

The STAT and PI3K-Akt pathways are key for GH and IGF-1 signaling in chondrocytes. However, these pathways become less effective as chondrocytes age. Therefore, giving GH to older individuals doesn’t have much effect, similar to trying to revive a barren field with water .

Role of Estrogen and Androgens in Growth Plate Closure​

Estrogen is crucial for growth plate closure, binding to receptors on chondrocytes and promoting their maturation and ossification. Some propose using letrozole, an aromatase inhibitor, to keep growth plates open by reducing estrogen. However, this can increase testosterone and dihydrotestosterone (DHT), which also bind to androgen receptors on chondrocytes and promote ossification .

Discussion​

While letrozole might delay growth plate closure, it doesn’t guarantee additional height growth. Mature chondrocytes don’t respond well to GH, making significant height increase unlikely. Using GH after puberty won’t yield much growth and can lead to issues like insulin resistance .

Conclusion​

Using GH and IGF-1 to boost height after puberty is ineffective due to the natural aging of chondrocytes and the closure of growth plates. Letrozole may delay closure but doesn’t ensure extra height growth. Future research should focus on understanding chondrocyte aging and finding ways to improve their responsiveness during key growth periods.

References​

1. Baron, J., et al. (2006). The Growth Plate. Journal of Endocrinology, 189(1), 27-40. Link
2. Lui, J.C., et al. (2019). Biological parameters of the human growth plate. Journal of Biological Chemistry, 294(24), 9137-9148. Link
3. Nilsson, O., et al. (2015). Evidence that estrogen hastens growth plate senescence. Journal of Molecular Endocrinology, 54(1), 61-69. Link
4. Hiyama, A., et al. (2021). Growth plate senescence and epiphyseal fusion: Mechanisms and implications. Frontiers in Endocrinology, 12, 705. Link
5. Tian, J., et al. (2019). Molecular mechanisms of endochondral ossification and its role in skeletal diseases. Journal of Molecular Endocrinology, 62(2), 1-14. Link

Nigga are you slow no way ur saying GH and AI dont work...

First off, e2.... No way u think it's as simple as "estrogen closes growth plates" muh muhh nigga. Estrogen interacts with ERa and ERB on chondrocytes, which triggers MAPK/ERK, PI3K/Akt, and Wnt/B-catenin pathways they regulate chondrocyte proliferation and hypertrophy. E2 also upregulates MMPs and VEGF for remodeling plates and boosting blood vessel formation. This isnt "muh e2 simpleee" it's a process that you clearly don’t get

Now Ai your saying they don’t work because reducing estrogen isn’t enough??? lmao what nigga, it stops the conversion of androgens to estrogens... This slows down EVERY estrogen mediated process. this isnt a fucking theory it’s how these drugs work nigga

More e2 = more test/dht doesnt mean plates will close faster... they interact with androgen receptors on chondrocytes, which activatees paths that PROMOTE growth the Wnt/B-catenin path is involved here too higher androgen receptor expression means chondrocytes are more responsive to androgens supports continued growth even when e2 levels are changes

Abt telomeres, E2 affects telomerase activity + TRF1 and TRF2 which MAINTAINS telomere integrity lowering estrogen delays telomere attrition which would increase chondrocyte proliferative capacity + epigenetic changes, DNA methylation and histone modifications change gene expression patterns for growth epigenetic drugs can reverse this, reactivating growth genes youre ignoring a whole field of science

also localized deliver like nanoparticle carriers boosts GH and IGF-1 u could also combine this with telomerase activators and epigenetic modulators could boost chondrocyte proliferation and delay senescence

"insulin resistance"
nigga even ur avg steroid gymbro knows how to counter this side

TLDR: hes on copius amounts of weed

 

[Rigged]

I literaly say it all the time, why you guys look at this chatgpt generated thread and be like "woaaaah!! I am in shock"



Increasing serum hgh levels in you blood will not result in more growth

nope hes wrong again this is the 5th anti hgh thread ive seen u reply on and dickride that i js debunk, well keep this going

 

[DR. NICKGA]

nope hes wrong again this is the 5th anti hgh thread ive seen u reply on and dickride that i js debunk, well keep this going

Its not that i dickride , i AM the one who make this anti hgh threads, it was me idea all along


I am a DR
I can easily destroy you with the power of SCIENCE, facts and logic

But you lucky i spare you dumbass , go then go buy hgh and see it for yourself

Do it, buy it

 

[Rigged]

I am a DR
I can easily destroy you with the power of SCIENCE, facts and logic

But you lucky i spare you dumbass , go then go buy hgh and see it for yourself

Do it

No Dr. Nikga im sorry pls dont embarrass me with ur insane iq

 

[DR. NICKGA]

No Dr. Nikga im sorry pls dont embarrass me with ur insane iq

Do it

Buy hgh and see it for yourself

We will see who is RIGHT And who is NOT

 

[Rigged]

Do it

Buy hgh and see it for yourself

We will see who is RIGHT And who is NOT

my plates r closed, also ik how the science works u dont

 

[DR. NICKGA]

my plates r closed, also ik how the science works u dont

Well well well Nice cope dumbass

Now shut the fuck up

 

[Rigged]

Well well well Nice cope dumbass

Now shut the fuck up

nigga who tf r u talking to ima bitch slap u if i catch u

 

[DR. NICKGA]

nigga who tf r u talking to ima bitch slap u if i catch u

I beat the fuck out of you nigga

 

[Rigged]

I beat the fuck out of you nigga

on dhzz if i catch u its on sight fn

 

[DR. NICKGA]

on dhzz if i catch u its on sight fn

On KING DAVID NIGGA ON KING DAVID

YOU BETTER NOT LET ME CAUGHT YAA ASS LACKING NIGGA

THESE BULLETS WILL PIERCE THROUGHT YOU BRAINS IN SECONDS NIGGA (idk if u have any brains tho)

 

[Rigged]

On KING DAVID NIGGA ON KING DAVID

YOU BETTER NOT LET ME CAUGHT YAA ASS LACKING NIGGA

THESE BULLETS WILL PIERCE THROUGHT YOU BRAINS IN SECONDS NIGGA (idk if u have any brains tho)

ON WHO NIGGA U CALLIN ANOTHER NIGGA YO KING IK U BE SNIFFING HIS DICK
U BE PUTTING UR DICK IN THAT NIGGA ASSHOLE (u dont have a dick u a pussy)
ASS NIGGA BMD U GON BE LOOKIN LIKE A FROSTED SNOWFLAKE AFTER THIS ON SIGHT FN
NUT ON YO FACE LIKE U MY BITCH

 

[DR. NICKGA]

ON WHO NIGGA U CALLIN ANOTHER NIGGA YO KING IK U BE SNIFFING HIS DICK
U BE PUTTING UR DICK IN THAT NIGGA ASSHOLE (u dont have a dick u a pussy)
ASS NIGGA BMD U GON BE LOOKIN LIKE A FROSTED SNOWFLAKE AFTER THIS ON SIGHT FN
NUT ON YO FACE LIKE U MY BITCH

AGRH YOU ITUCKINGGN IGEE4R YOUU TUCKINGG BASTATDDD

YOU GONMA BE GONE NIGGA YOU GONNA BE FUCKINGG GONEE

ONN KIMG DAVID , IF I SEE YOU , A FUCKING MASCARA WILL GONNA HAPLENDDDD , YOU WILL BE FUCKINGG DEATHH FUCKING D E A RH

I WILL UNLOAD ALL THAAT MAGS ON YOU FUCKING FACE , THERE WILL BE NOTHING LEFR OF YOU

JUST WAIT NIGGA JUST WAIT

 

[Rigged]

AGRH YOU ITUCKINGGN IGEE4R YOUU TUCKINGG BASTATDDD

YOU GONMA BE GONE NIGGA YOU GONNA BE FUCKINGG GONEE

ONN KIMG DAVID , IF I SEE YOU , A FUCKING MASCARA WILL GONNA HAPLENDDDD , YOU WILL BE FUCKINGG DEATHH FUCKING D E A RH

I WILL UNLOAD ALL THAAT MAGS ON YOU FUCKING FACE , THERE WILL BE NOTHING LEFR OF YOU

JUST WAIT NIGGA JUST WAIT

U FUCKINBG BAFOOKJMN IM BDOLN EWITH THJFDIK SDHUIT UR OGN GET |FUCKED BICH ASS NIGGA
FUCJK U THINK THIS IS DUMB ASS NIGG
ON BMD U FUCK NIGGA IMA ROLL ON YO PACK NIGGA
SLIME ON SLIME FN CATCH U ON MY STREET GON BE ON YO PERIUOD FN

 

[Mrinfinityx]

Always been over, u cant alter exogenously all ur genetic growth processes at play, even if u would have the control and the ascendancy on one of them as supraphysiological levels of HGH the effect will be barely negligible through HGH resistance and genes retrocontrol, if u are not deficient or stunted in this parameter u will just speed up ur skeletal maturation earlier than expected that s it

Growth hormone resistance - PubMed

Biological ineffectiveness of endogenous or exogenous growth hormone (GH) (i.e. a state or resistance) has been reported in several clinical conditions. The most typical form is Laron-type dwarfism, a hereditary disease which is clinically undistinguishable from isolated GH deficiency and which...

pubmed.ncbi.nlm.nih.gov

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6449614/

Genetics of human growth - PubMed

Genes involved in human growth consist of major growth genes and minor growth genes. Major growth genes have fundamental effects on human growth, and their mutations cause growth failure (or overgrowth) which are recognizable as single gene disorders. Minor growth genes exert relative minor...

pubmed.ncbi.nlm.nih.gov

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4004846/

Exogenous growth hormone inhibits growth hormone-releasing factor-induced growth hormone secretion in normal men.

Previous studies from this laboratory and by others in rats, monkeys, and humans support the concept that growth hormone (GH) can regulate its own secretion through an autofeedback mechanism. With the availability of human growth hormone-releasing factor ...

www.ncbi.nlm.nih.gov

Even acromegaly and gigantism are part of growth genes alteration that u cant replicate exogenously, as in those cases endogenous HGH reaches insane amount of a dose for a long period that u probably couldnt replicate exogenously in safety anyway

Genetics of Acromegaly and Gigantism - PubMed

Growth hormone (GH)-secreting pituitary tumours represent the most genetically determined pituitary tumour type. This is true both for germline and somatic mutations. Germline mutations occur in several known genes (<i>AIP</i>, <i>PRKAR1A</i>, <i>GPR101</i>, <i>GNAS</i>, <i>MEN1</i>...

pubmed.ncbi.nlm.nih.gov

It is utter cope

 

[Mrinfinityx]

Btw It is utterly over for AI copers too, u cant just biohack ur body without altered genes

Overcoming aromatase inhibitor resistance in breast cancer: possible mechanisms and clinical applications - PubMed

Estrogen plays crucial roles in the progression of hormone-dependent breast cancers through activation of nuclear estrogen receptor α (ER). Estrogen is produced locally from circulating inactive steroids and adrenal androgens in postmenopausal women. However, conversion by aromatase is a...

pubmed.ncbi.nlm.nih.gov

Mechanisms of aromatase inhibitor resistance - PubMed

Oestrogen receptor-positive (ER(+)) breast cancer is a major cause of cancer death in women. Although aromatase inhibitors suppress the function of ER and reduce the risk of recurrence, therapeutic resistance is common and essentially inevitable in advanced disease. This Review considers both...

pubmed.ncbi.nlm.nih.gov

Acquired resistance to aromatase inhibitors: where we stand! - PubMed

Aromatase inhibitors (AIs) are one of the principal therapeutic approaches for estrogen receptor-positive (ER⁺) breast cancer in postmenopausal women. They block estrogen biosynthesis through aromatase inhibition, thus preventing tumour progression. Besides the therapeutic success of...

pubmed.ncbi.nlm.nih.gov

Understanding the mechanisms of aromatase inhibitor resistance - PubMed

Aromatase inhibitors (AIs) have a central role in the treatment of breast cancer; however, resistance is a major obstacle to optimal management. Evidence from endocrine, molecular and pathological measurements in clinical material taken before and after therapy with AIs and data from clinical...

pubmed.ncbi.nlm.nih.gov

Mitochondrial stress adaptation promotes resistance to aromatase inhibitor in human breast cancer cells via ROS/calcium up-regulated amphiregulin-estrogen receptor loop signaling - PubMed

Many breast cancer patients harbor high estrogen receptor (ER) expression in tumors that can be treated with endocrine therapy, which includes aromatase inhibitors (AI); unfortunately, resistance often occurs. Mitochondrial dysfunction has been thought to contribute to progression and to be...

pubmed.ncbi.nlm.nih.gov

 

[Rigged]

Btw It is utterly over for AI copers too, u cant just biohack ur body without altered genes

Overcoming aromatase inhibitor resistance in breast cancer: possible mechanisms and clinical applications - PubMed

Estrogen plays crucial roles in the progression of hormone-dependent breast cancers through activation of nuclear estrogen receptor α (ER). Estrogen is produced locally from circulating inactive steroids and adrenal androgens in postmenopausal women. However, conversion by aromatase is a...

pubmed.ncbi.nlm.nih.gov

Mechanisms of aromatase inhibitor resistance - PubMed

Oestrogen receptor-positive (ER(+)) breast cancer is a major cause of cancer death in women. Although aromatase inhibitors suppress the function of ER and reduce the risk of recurrence, therapeutic resistance is common and essentially inevitable in advanced disease. This Review considers both...

pubmed.ncbi.nlm.nih.gov

Acquired resistance to aromatase inhibitors: where we stand! - PubMed

Aromatase inhibitors (AIs) are one of the principal therapeutic approaches for estrogen receptor-positive (ER⁺) breast cancer in postmenopausal women. They block estrogen biosynthesis through aromatase inhibition, thus preventing tumour progression. Besides the therapeutic success of...

pubmed.ncbi.nlm.nih.gov

Understanding the mechanisms of aromatase inhibitor resistance - PubMed

Aromatase inhibitors (AIs) have a central role in the treatment of breast cancer; however, resistance is a major obstacle to optimal management. Evidence from endocrine, molecular and pathological measurements in clinical material taken before and after therapy with AIs and data from clinical...

pubmed.ncbi.nlm.nih.gov

Mitochondrial stress adaptation promotes resistance to aromatase inhibitor in human breast cancer cells via ROS/calcium up-regulated amphiregulin-estrogen receptor loop signaling - PubMed

Many breast cancer patients harbor high estrogen receptor (ER) expression in tumors that can be treated with endocrine therapy, which includes aromatase inhibitors (AI); unfortunately, resistance often occurs. Mitochondrial dysfunction has been thought to contribute to progression and to be...

pubmed.ncbi.nlm.nih.gov

I also like sending studies that barely if at all correlate to the arguement im trying to make, keep it up twin

 

[Mrinfinityx]

I also like sending studies that barely if at all correlate to the arguement im trying to make, keep it up twin

U cant just replicate genes alteration in a way of biohacking urself, ur body will retrocontrol u to ground when u are shooting for ur dreams if genes are physiologically healthy and if u are not stunted or deficient in a certain way prior through catch up if possible

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5002943/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9732115/

U cant just replicate this exogenously

 

[Rigged]

U cant just replicate genes alteration in a way of biohacking urself, ur body will retrocontrol u to ground when u are shooting for ur dreams if genes are physiologically healthy and if u are not stunted or deficient in a certain way prior through catch up if possible

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5002943/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9732115/

U cant just replicate this exogenously

View attachment 3078209

The first study says it takes several hormones but everyone already knows this
2nd study

2nd study isnt about low estrogen its about missing parts of estrogen

Keep it up twin ur inspiring me

 

[Mrinfinityx]

The first study says it takes several hormones but everyone already knows this
2nd study

2nd study isnt about low estrogen its about missing parts of estrogen

Keep it up twin ur inspiring me

There is literally not a single study outside there or any user here that reported extra growth potential in a state of already physiological parameters like serum levels, receptors sensitivity and genes statut prior, just some copers in puberty period who got all hot at their tracking obsession through the process of growth, not a single molecule of this cope

 

[Rigged]

There is literally not a single study outside there or any user here that reported extra growth potential in a state of already physiological parameters like serum levels, receptors sensitivity and genes statut prior, just some copers in puberty period who got all hot at their tracking obsession through the process of growth, not a single molecule of this cope

View attachment 3078259

Also do u really thing org users actually do shit some do 99% of them are js lying which ruins the work/didnt work stat

 

[Mrinfinityx]

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Also do u really thing org users actually do shit some do 99% of them are js lying which ruins the work/didnt work stat

That s it, nobody would even go all in full sayan mode as having the money or courage to experience this for plenty years with a background of the physiological state prior to treatment to justify the mere potential results only linked to treatment on a clear non stunted individual with a precise adult predicted height, so we will never have a clear and undeniable proof of any sort