Is Post-Puberty Height Increase Possible? Exploring Hormonal Manipulation to Reactivate “Closed” Growth Plates

marlx

marlx

hitler's top guy
Joined
Jan 14, 2026
Posts
1,070
Reputation
1,538
I’ve been digging into how growth plates work and whether it’s really true that once they’re “closed,” you can’t grow any taller. Here’s the foundation I built by asking simple questions:
  • Growth plates mostly close between ages 15–18, but some cartilage residue can remain into the mid-20s. (Yes)
  • That leftover cartilage isn’t enough on its own to cause natural longitudinal bone growth. (Yes)
  • Estrogen is the main hormone that causes growth plates to close. (Yes)
  • Blocking estrogen can keep growth plates open longer—but not forever, because estrogen is also crucial for bone health. (Yes)
  • Growth stops at the end of puberty mainly due to too little active cartilage combined with normalized levels of growth hormone (GH), IGF-1, and osteoblast activity. (Yes)
  • So if you blocked estrogen and provided GH, IGF-1, and stimulated osteoblasts at the right levels, you could theoretically induce bone growth from that cartilage residue—even after puberty. (Yes)

Basically, this means that the term “closed” growth plates doesn’t necessarily mean zero potential to grow taller. It means natural growth is over without intervention. But with the right hormonal environment—blocking estrogen, boosting GH/IGF-1, and activating osteoblasts—there might be a way to push for longitudinal bone growth after what’s medically considered closure.


Technically, if someone combined aromatase inhibitors (like anastrozole), SERMs (like clomiphene or tamoxifen), HGH, IGF-1 LR3, and possibly PTH analogs, they could create the conditions for a growth spurt with “closed” growth plates.


This is all theoretical, and obviously comes with big safety concerns. But it challenges the dogma that height can’t increase after puberty ends.


I’m curious—what do you think about this?

(This information is certainly not new, but I haven't found one civilized thread about the topic)
 
  • +1
  • JFL
  • Woah
Reactions: lowdimoltn, plutolock, KidFlash and 4 others
TL;DR: "bla bla bla, bla bla bla bla, bla bla, bla bla bla"
 
  • +1
  • JFL
Reactions: civil_tof0000, ImaASCENDsoon, Buterman and 2 others
I’ve been digging into how growth plates work and whether it’s really true that once they’re “closed,” you can’t grow any taller. Here’s the foundation I built by asking simple questions:
  • Growth plates mostly close between ages 15–18, but some cartilage residue can remain into the mid-20s. (Yes)
  • That leftover cartilage isn’t enough on its own to cause natural longitudinal bone growth. (Yes)
  • Estrogen is the main hormone that causes growth plates to close. (Yes)
  • Blocking estrogen can keep growth plates open longer—but not forever, because estrogen is also crucial for bone health. (Yes)
  • Growth stops at the end of puberty mainly due to too little active cartilage combined with normalized levels of growth hormone (GH), IGF-1, and osteoblast activity. (Yes)
  • So if you blocked estrogen and provided GH, IGF-1, and stimulated osteoblasts at the right levels, you could theoretically induce bone growth from that cartilage residue—even after puberty. (Yes)

Basically, this means that the term “closed” growth plates doesn’t necessarily mean zero potential to grow taller. It means natural growth is over without intervention. But with the right hormonal environment—blocking estrogen, boosting GH/IGF-1, and activating osteoblasts—there might be a way to push for longitudinal bone growth after what’s medically considered closure.


Technically, if someone combined aromatase inhibitors (like anastrozole), SERMs (like clomiphene or tamoxifen), HGH, IGF-1 LR3, and possibly PTH analogs, they could create the conditions for a growth spurt with “closed” growth plates.


This is all theoretical, and obviously comes with big safety concerns. But it challenges the dogma that height can’t increase after puberty ends.


I’m curious—what do you think about this?

(This information is certainly not new, but I haven't found one civilized thread about the topic)
I don't think it's possible tbh
 
I'm working on a thread ill keep you updated. It goes super in depth into new findings on growth plates and how to possibly reopen if they have closed in under 3 years.
 
  • +1
Reactions: GABA., labelmayer and marlx
I’ve been digging into how growth plates work and whether it’s really true that once they’re “closed,” you can’t grow any taller. Here’s the foundation I built by asking simple questions:
  • Growth plates mostly close between ages 15–18, but some cartilage residue can remain into the mid-20s. (Yes)
  • That leftover cartilage isn’t enough on its own to cause natural longitudinal bone growth. (Yes)
  • Estrogen is the main hormone that causes growth plates to close. (Yes)
  • Blocking estrogen can keep growth plates open longer—but not forever, because estrogen is also crucial for bone health. (Yes)
  • Growth stops at the end of puberty mainly due to too little active cartilage combined with normalized levels of growth hormone (GH), IGF-1, and osteoblast activity. (Yes)
  • So if you blocked estrogen and provided GH, IGF-1, and stimulated osteoblasts at the right levels, you could theoretically induce bone growth from that cartilage residue—even after puberty. (Yes)

Basically, this means that the term “closed” growth plates doesn’t necessarily mean zero potential to grow taller. It means natural growth is over without intervention. But with the right hormonal environment—blocking estrogen, boosting GH/IGF-1, and activating osteoblasts—there might be a way to push for longitudinal bone growth after what’s medically considered closure.


Technically, if someone combined aromatase inhibitors (like anastrozole), SERMs (like clomiphene or tamoxifen), HGH, IGF-1 LR3, and possibly PTH analogs, they could create the conditions for a growth spurt with “closed” growth plates.


This is all theoretical, and obviously comes with big safety concerns. But it challenges the dogma that height can’t increase after puberty ends.


I’m curious—what do you think about this?

(This information is certainly not new, but I haven't found one civilized thread about the topic)
igf1lr3😭🖖
 
So if you blocked estrogen and provided GH, IGF-1, and stimulated osteoblasts at the right levels, you could theoretically induce bone growth from that cartilage residue—even after puberty. (Yes
.
 
Last edited:
A compound like CJC-1295 DAC is the only way I personally believe post-puberty height growth will ever be possible (i.e. Replicate the results of limb-lengthening surgery without breaking your legs)
 
  • JFL
Reactions: plutolock
A compound like CJC-1295 DAC is the only way I personally believe post-puberty height growth will ever be possible (i.e. Replicate the results of limb-lengthening surgery without breaking your legs)
:forcedsmile:
 
A compound like CJC-1295 DAC is the only way I personally believe post-puberty height growth will ever be possible (i.e. Replicate the results of limb-lengthening surgery without breaking your legs)
Yeah, most GHRPs that don't significantly raise Cortisol or Prolactin are most likely viable for increased heightgrowth during puberty, so basically CJC-1295, even tho I would suggest no DAC here because you can keep up natural GH at its best. Also, Ipamorelin would be viable.

I know IGF1 LR3 has become this TikTok compound that magically does everything, but it has been used for quite some years, especially in bodybuilding, and if you take hGH, you can very well use IGF1 LR3 to benefit from the bilateral effects of the combination of these two. Apart from that, it does have some anabolic effects, just not as strong as it's portrayed to have.
 
I’ve been digging into how growth plates work and whether it’s really true that once they’re “closed,” you can’t grow any taller. Here’s the foundation I built by asking simple questions:
  • Growth plates mostly close between ages 15–18, but some cartilage residue can remain into the mid-20s. (Yes)
  • That leftover cartilage isn’t enough on its own to cause natural longitudinal bone growth. (Yes)
  • Estrogen is the main hormone that causes growth plates to close. (Yes)
  • Blocking estrogen can keep growth plates open longer—but not forever, because estrogen is also crucial for bone health. (Yes)
  • Growth stops at the end of puberty mainly due to too little active cartilage combined with normalized levels of growth hormone (GH), IGF-1, and osteoblast activity. (Yes)
  • So if you blocked estrogen and provided GH, IGF-1, and stimulated osteoblasts at the right levels, you could theoretically induce bone growth from that cartilage residue—even after puberty. (Yes)

Basically, this means that the term “closed” growth plates doesn’t necessarily mean zero potential to grow taller. It means natural growth is over without intervention. But with the right hormonal environment—blocking estrogen, boosting GH/IGF-1, and activating osteoblasts—there might be a way to push for longitudinal bone growth after what’s medically considered closure.


Technically, if someone combined aromatase inhibitors (like anastrozole), SERMs (like clomiphene or tamoxifen), HGH, IGF-1 LR3, and possibly PTH analogs, they could create the conditions for a growth spurt with “closed” growth plates.


This is all theoretical, and obviously comes with big safety concerns. But it challenges the dogma that height can’t increase after puberty ends.


I’m curious—what do you think about this?

(This information is certainly not new, but I haven't found one civilized thread about the topic)
dnr cope cope cope cope
 
Yeah, most GHRPs that don't significantly raise Cortisol or Prolactin are most likely viable for increased heightgrowth during puberty, so basically CJC-1295, even tho I would suggest no DAC here because you can keep up natural GH at its best. Also, Ipamorelin would be viable.


I know IGF1 LR3 has become this TikTok compound that magically does everything, but it has been used for quite some years, especially in bodybuilding, and if you take hGH, you can very well use IGF1 LR3 to benefit from the bilateral effects of the combination of these two. Apart from that, it does have some anabolic effects, just not as strong as it's portrayed to have.
Igf1lr3 for height growth is absolut dog shit, but for muscle, its good, good alternative to gear ngl
 
  • JFL
Reactions: childishkillah
Technically, if someone combined aromatase inhibitors (like anastrozole), SERMs (like clomiphene or tamoxifen), HGH, IGF-1 LR3, and possibly PTH analogs, they could create the conditions for a growth spurt with “closed” growth plates.
:lul:
 
I’ve been digging into how growth plates work and whether it’s really true that once they’re “closed,” you can’t grow any taller. Here’s the foundation I built by asking simple questions:
  • Growth plates mostly close between ages 15–18, but some cartilage residue can remain into the mid-20s. (Yes)
  • That leftover cartilage isn’t enough on its own to cause natural longitudinal bone growth. (Yes)
  • Estrogen is the main hormone that causes growth plates to close. (Yes)
  • Blocking estrogen can keep growth plates open longer—but not forever, because estrogen is also crucial for bone health. (Yes)
  • Growth stops at the end of puberty mainly due to too little active cartilage combined with normalized levels of growth hormone (GH), IGF-1, and osteoblast activity. (Yes)
  • So if you blocked estrogen and provided GH, IGF-1, and stimulated osteoblasts at the right levels, you could theoretically induce bone growth from that cartilage residue—even after puberty. (Yes)

Basically, this means that the term “closed” growth plates doesn’t necessarily mean zero potential to grow taller. It means natural growth is over without intervention. But with the right hormonal environment—blocking estrogen, boosting GH/IGF-1, and activating osteoblasts—there might be a way to push for longitudinal bone growth after what’s medically considered closure.


Technically, if someone combined aromatase inhibitors (like anastrozole), SERMs (like clomiphene or tamoxifen), HGH, IGF-1 LR3, and possibly PTH analogs, they could create the conditions for a growth spurt with “closed” growth plates.


This is all theoretical, and obviously comes with big safety concerns. But it challenges the dogma that height can’t increase after puberty ends.


I’m curious—what do you think about this?

(This information is certainly not new, but I haven't found one civilized thread about the topic)
how short do you have to be to cope this much:oops:
 
pure cope bruh
 
I’ve been digging into how growth plates work and whether it’s really true that once they’re “closed,” you can’t grow any taller. Here’s the foundation I built by asking simple questions:
  • Growth plates mostly close between ages 15–18, but some cartilage residue can remain into the mid-20s. (Yes)
  • That leftover cartilage isn’t enough on its own to cause natural longitudinal bone growth. (Yes)
  • Estrogen is the main hormone that causes growth plates to close. (Yes)
  • Blocking estrogen can keep growth plates open longer—but not forever, because estrogen is also crucial for bone health. (Yes)
  • Growth stops at the end of puberty mainly due to too little active cartilage combined with normalized levels of growth hormone (GH), IGF-1, and osteoblast activity. (Yes)
  • So if you blocked estrogen and provided GH, IGF-1, and stimulated osteoblasts at the right levels, you could theoretically induce bone growth from that cartilage residue—even after puberty. (Yes)

Basically, this means that the term “closed” growth plates doesn’t necessarily mean zero potential to grow taller. It means natural growth is over without intervention. But with the right hormonal environment—blocking estrogen, boosting GH/IGF-1, and activating osteoblasts—there might be a way to push for longitudinal bone growth after what’s medically considered closure.


Technically, if someone combined aromatase inhibitors (like anastrozole), SERMs (like clomiphene or tamoxifen), HGH, IGF-1 LR3, and possibly PTH analogs, they could create the conditions for a growth spurt with “closed” growth plates.


This is all theoretical, and obviously comes with big safety concerns. But it challenges the dogma that height can’t increase after puberty ends.


I’m curious—what do you think about this?

(This information is certainly not new, but I haven't found one civilized thread about the topic)
Banded sleeping is being researched as of late
 
tag me too bhai
I'm working on a thread ill keep you updated. It goes super in depth into new findings on growth plates and how to possibly reopen if they have closed in under 3 years.
 
I’ve been digging into how growth plates work and whether it’s really true that once they’re “closed,” you can’t grow any taller. Here’s the foundation I built by asking simple questions:
  • Growth plates mostly close between ages 15–18, but some cartilage residue can remain into the mid-20s. (Yes)
  • That leftover cartilage isn’t enough on its own to cause natural longitudinal bone growth. (Yes)
  • Estrogen is the main hormone that causes growth plates to close. (Yes)
  • Blocking estrogen can keep growth plates open longer—but not forever, because estrogen is also crucial for bone health. (Yes)
  • Growth stops at the end of puberty mainly due to too little active cartilage combined with normalized levels of growth hormone (GH), IGF-1, and osteoblast activity. (Yes)
  • So if you blocked estrogen and provided GH, IGF-1, and stimulated osteoblasts at the right levels, you could theoretically induce bone growth from that cartilage residue—even after puberty. (Yes)

Basically, this means that the term “closed” growth plates doesn’t necessarily mean zero potential to grow taller. It means natural growth is over without intervention. But with the right hormonal environment—blocking estrogen, boosting GH/IGF-1, and activating osteoblasts—there might be a way to push for longitudinal bone growth after what’s medically considered closure.


Technically, if someone combined aromatase inhibitors (like anastrozole), SERMs (like clomiphene or tamoxifen), HGH, IGF-1 LR3, and possibly PTH analogs, they could create the conditions for a growth spurt with “closed” growth plates.


This is all theoretical, and obviously comes with big safety concerns. But it challenges the dogma that height can’t increase after puberty ends.


I’m curious—what do you think about this?

(This information is certainly not new, but I haven't found one civilized thread about the topic)
u realize bones fuse fully forever right? there is no cartilage residue, even if there was itd be partially fused with bridged bones and that wouldnt let ur cartilage expand and seperate the bone in the middle, only thing thatd work for denovo is probably to open the bones thru surgery and embed an explant cartilage bud inside filled with growth factors and live chondroprogenitor stem cells. and gh/igf1 is nowhere near the most important factor for growth, there is a fuck ton of pathways that the gh/igf1 axis misses, for example igf1 isnt going to induce massive stem cell mitosis like it does in the proliferative zone and growth plates without stem cells are dead plates, u cant just igf1 ur way into a self sustaining plate.
 
u realize bones fuse fully forever right? there is no cartilage residue, even if there was itd be partially fused with bridged bones and that wouldnt let ur cartilage expand and seperate the bone in the middle, only thing thatd work for denovo is probably to open the bones thru surgery and embed an explant cartilage bud inside filled with growth factors and live chondroprogenitor stem cells. and gh/igf1 is nowhere near the most important factor for growth, there is a fuck ton of pathways that the gh/igf1 axis misses, for example igf1 isnt going to induce massive stem cell mitosis like it does in the proliferative zone and growth plates without stem cells are dead plates, u cant just igf1 ur way into a self sustaining plate.
Dnr + when you stop growing that doesn’t mean your bones have fully fused nigga
 
  • +1
Reactions: crmogs🇪🇸
aromatase inhibitors (like anastrozole), SERMs (like clomiphene or tamoxifen), HGH, IGF-1 LR3, and possibly PTH analog
SERDs (fulvestrant) should be considerated, but prob is shit. and take igf1lr3 out there
 
  • +1
Reactions: crmogs🇪🇸
I'm working on a thread ill keep you updated. It goes super in depth into new findings on growth plates and how to possibly reopen if they have closed in under 3 years.
Tag me when done 🙏🙏
 
  • +1
Reactions: crmogs🇪🇸
I'm working on a thread ill keep you updated. It goes super in depth into new findings on growth plates and how to possibly reopen if they have closed in under 3 years.
Interesting do tag me :love:
 
  • +1
Reactions: crmogs🇪🇸
Just rope nigga its over
 
Are you going to proliferate and deplete the extracellular fluid? There’s no resting zone chondrocyte nor proliferating chondrocyte left negro
 

Similar threads

Goat Epstein
Replies
12
Views
85
sherry12
sherry12
JOTAROSON
Replies
33
Views
186
JOTAROSON
JOTAROSON
f0idslay3r
Replies
34
Views
381
MAMB
MAMB

Users who are viewing this thread

Back
Top