Kojo
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I'm not going to make this thread like a traditional guide that's super professional and rhetorically appealing for readers. I'm just going to explain things.
WITHOUT FURTHER ADO.
-- In a normal Skeletal framework, Mammals grow and develop bone in 2 ways. But we will be focusing on Longitudinal Growth of Bone.
-- Now that the I've covered the absolute basics, I will go deeper into the histology of this process, How they actually fuse, How they help you grow and what makes you grow.
I will also explain misunderstandings that a lot of people here have about this whole thing because of a lack of research, which is fine.
-- So what happens when we take a deep look at these growth promoting zones at the cellular level?
-- Into the nitty gritty of the Chondrocyte Maturation Phases. (VERY IMPORTANT!!)
-- Hormonal Influence on Growth:
-- MYTH BUSTING:
I know it is a LOT but it is a good read, and literally explains everything you need to know about bone growth and height. After reading this, you will more than likely need NO other research outside of clarifying my claims (basic literature anyways easy to see what I'm saying is true).
I just want to unite this community on the knowledge of bone growth but it probably wont happen because of stupid prideful 14 year olds like you probably reading this right now
If people here can see this thread and get this down, this forum can genuinely be more productive for convos like these. A lot of this community is genuinely just tiktok niggers saying bullshit
Thank you for reading bhai's I'll answer questions below we can have a discussion if anyone wants to counter this thread. Remember I'm not omniscient, there may be things I don't know either and that goes for everyone here
WITHOUT FURTHER ADO.
-- In a normal Skeletal framework, Mammals grow and develop bone in 2 ways. But we will be focusing on Longitudinal Growth of Bone.
Longitudinal Bone Growth is a process that all mammals go through to grow in length. This process happens at the ends of long bones where zones of Cartilage are present, called the growth plate. Or Rather, The Physis.
These Cartilage deposits house chondrocytes which go through phases of maturation to finally, ossify and produce bone. In turn, making you taller. However, there are limits to this procedure. As these zones eventually fuse and turn into bone from ages 16-19 in males and can no longer produce any bone growth due to the hormone ESTRADIOL. This process is called, Endochondral Ossification.
These Cartilage deposits house chondrocytes which go through phases of maturation to finally, ossify and produce bone. In turn, making you taller. However, there are limits to this procedure. As these zones eventually fuse and turn into bone from ages 16-19 in males and can no longer produce any bone growth due to the hormone ESTRADIOL. This process is called, Endochondral Ossification.
-- Now that the I've covered the absolute basics, I will go deeper into the histology of this process, How they actually fuse, How they help you grow and what makes you grow.
I will also explain misunderstandings that a lot of people here have about this whole thing because of a lack of research, which is fine.
-- So what happens when we take a deep look at these growth promoting zones at the cellular level?
Now when your parents have sex and they produce you incels, you are born with Skeletal Stem Cells that give rise to Mesenchymal Stem Cells that can differentiate into 2 things relating to bone.
-- Chondroblasts
-- Osteoblasts
Chondroblasts mature into Chondrocytes and reside in a Type 2 Collagen Matrix which is what the growth plate is comprised of.
Osteoblasts play a key role in maintaining bone density in the Osteoblast-Osteoclast cycle, in which bone is broken down and rebuilt.
These two cells have their own lane, however, Osteoblasts do cross over into the Chondrocyte realm. As osteoblasts provide bone matrix for Matured Chondrocytes that went through the MATURATION PHASE.
-- Chondroblasts
-- Osteoblasts
Chondroblasts mature into Chondrocytes and reside in a Type 2 Collagen Matrix which is what the growth plate is comprised of.
Osteoblasts play a key role in maintaining bone density in the Osteoblast-Osteoclast cycle, in which bone is broken down and rebuilt.
These two cells have their own lane, however, Osteoblasts do cross over into the Chondrocyte realm. As osteoblasts provide bone matrix for Matured Chondrocytes that went through the MATURATION PHASE.
-- Into the nitty gritty of the Chondrocyte Maturation Phases. (VERY IMPORTANT!!)
There are 4 phases involved in the phase of Longitudinal Bone Growth through chondrocyte maturation. In order:
-- The Resting Zone. This is where reserve chondrocytes are housed, they functionally serve as a self-renewing stem cell pool for chondrocytes as they supply the growth plate with more chondrocytes engineered towards Proliferation.
What's good about the resting zone is, it allows for a CYCLE of Continuous growth. When it pushes out chondrocytes from it's reserve, it multiplies that chondrocyte first and keeps it in the resting zone before pushing the initial cell into the next zone of the growth plate.
This allows the Resting Zone to maintain the amount of Reserve Cells it has. The amount of these you have are genetically predetermined. This entire process is called Differentiation.
-- The Proliferative Zone. Here, those chondrocytes that Left the Resting Zone, move into the Proliferative Zone and start to rapidly multiply, aka proliferate. The chondrocytes stack on top of each other in rows.
The reason people grow fast, and we have our pubertal growth spurt is due to high IGF-1 levels/IGF-1R sensitivity which directly stimulate this cellular phenomenon. The more chondrocytes that divide, the more growth you get (NOT FAH) in terms of growth velocity.
This is also why dwarfs exist, they may have high IGF-1 levels but they have overactive FGFR3 presence, which is the brake on Chondrocyte Proliferation. If you can't proliferate Chondrocytes much, there's not enough material for you to grow fast enough before your plates fuse. Once stacked, these Chondrocytes move into inducing HYPERTROPHY.
-- The Hypertrophic Zone. Now this seems to be the area where not a lot of people did enough research in or could understand properly even though it's very simple but can trip you up. A friend of mine @AtrophicPyra seemed to have a bit of trouble fully understanding this concept in it's relation to Growth Plate Fusion. So I will explain how this entire zone functions.
It is very simple. After chondrocytes have proliferated to their maximal capacity, they move into the zone of Hypertrophy. Hypertrophy put simply, is the growing in size of something like tissues/cells. In this zone, those chondrocytes swell in size due to osmosis which is pulling water into the chondrocytes (stay hydrated boyos) to increase their size. Not number, Size.
Everyone always talks about increasing proliferation, but this is a very underrated subject of bone growth and literally the most important of the 4. It is the LAST zone so it honestly determines a majority of the growth you get.
If those chondrocytes do not swell enough, all the proliferation that was done in the proliferative phase wasn't for much. I'm not saying it means NOTHING, but it doesn't mean as much as it should have. This is because when the chondrocytes swell in size, they go through a series of maturation and degeneration, eventually dying off.
Before you see "DIE" and think this is bad, this is really good. The chondrocytes need to die off and leave empty spaces (Lacunae) So that those spaces are invaded by blood vessels and osteoblasts that start replacing the space with bone by pushing the bone matrix that osteoblasts create into the diaphysis. Consequently, lengthening the diaphysis. This is Endochondral Ossification.
So just speaking logically, if there is a bigger space for bone to invade, that means more bone is added which quite literally means more growth. This is why it's essential for cells to hypertropy a fuck ton before dying. This is NOT Growth Plate Fusion.
FULL DIAGRAM:
-- The Resting Zone. This is where reserve chondrocytes are housed, they functionally serve as a self-renewing stem cell pool for chondrocytes as they supply the growth plate with more chondrocytes engineered towards Proliferation.
What's good about the resting zone is, it allows for a CYCLE of Continuous growth. When it pushes out chondrocytes from it's reserve, it multiplies that chondrocyte first and keeps it in the resting zone before pushing the initial cell into the next zone of the growth plate.
This allows the Resting Zone to maintain the amount of Reserve Cells it has. The amount of these you have are genetically predetermined. This entire process is called Differentiation.
-- The Proliferative Zone. Here, those chondrocytes that Left the Resting Zone, move into the Proliferative Zone and start to rapidly multiply, aka proliferate. The chondrocytes stack on top of each other in rows.
The reason people grow fast, and we have our pubertal growth spurt is due to high IGF-1 levels/IGF-1R sensitivity which directly stimulate this cellular phenomenon. The more chondrocytes that divide, the more growth you get (NOT FAH) in terms of growth velocity.
This is also why dwarfs exist, they may have high IGF-1 levels but they have overactive FGFR3 presence, which is the brake on Chondrocyte Proliferation. If you can't proliferate Chondrocytes much, there's not enough material for you to grow fast enough before your plates fuse. Once stacked, these Chondrocytes move into inducing HYPERTROPHY.
-- The Hypertrophic Zone. Now this seems to be the area where not a lot of people did enough research in or could understand properly even though it's very simple but can trip you up. A friend of mine @AtrophicPyra seemed to have a bit of trouble fully understanding this concept in it's relation to Growth Plate Fusion. So I will explain how this entire zone functions.
It is very simple. After chondrocytes have proliferated to their maximal capacity, they move into the zone of Hypertrophy. Hypertrophy put simply, is the growing in size of something like tissues/cells. In this zone, those chondrocytes swell in size due to osmosis which is pulling water into the chondrocytes (stay hydrated boyos) to increase their size. Not number, Size.
Everyone always talks about increasing proliferation, but this is a very underrated subject of bone growth and literally the most important of the 4. It is the LAST zone so it honestly determines a majority of the growth you get.
If those chondrocytes do not swell enough, all the proliferation that was done in the proliferative phase wasn't for much. I'm not saying it means NOTHING, but it doesn't mean as much as it should have. This is because when the chondrocytes swell in size, they go through a series of maturation and degeneration, eventually dying off.
Before you see "DIE" and think this is bad, this is really good. The chondrocytes need to die off and leave empty spaces (Lacunae) So that those spaces are invaded by blood vessels and osteoblasts that start replacing the space with bone by pushing the bone matrix that osteoblasts create into the diaphysis. Consequently, lengthening the diaphysis. This is Endochondral Ossification.
So just speaking logically, if there is a bigger space for bone to invade, that means more bone is added which quite literally means more growth. This is why it's essential for cells to hypertropy a fuck ton before dying. This is NOT Growth Plate Fusion.
FULL DIAGRAM:
-- Hormonal Influence on Growth:
In this section, I will cover Testosterone, Growth Hormone, Insulin Growth Factor-1 and Estradiol.
-- Testosterone: Testosterone is the main male sex hormone responsible for driving pubertal changes into Adolescence for young boys. What we will be focusing on is it's effect on height.
Testosterone is the primary reason for the Male Growth Spurt, but also the primary reason for the stoppage of growth through fusing the growth plates. This hormone fuses the growth plates through converting into another hormone called Estradiol, otherwise known as Estrogen. (Family of hormones it belongs to, similar to Androgens. Estrogens for females Androgens for Males.)
So how does testosterone convert into Estradiol? It does so by the enzyme called Aromatase. Testosterone binds to the aromatase enyzme, converting a portion of it into Estradiol. This enzyme is present in body fat. This is why it is optimal to be stay in a healthy weight range during your pubertal years to reduce the abundance of this enzyme.
Testosterone induces the growth spurt through a hormone we spoke of earlier called IGF-1. IGF-1 stimulates chondrocytes to differentiate from the resting zone and proliferate in the proliferative zone resulting in a rapid increase in these processes. Testosterone shoots IGF-1 levels up, and additionally makes IGF-1 Receptors much more sensitive to IGF-1 which is why the growth is extreme.
-- Growth Hormone. Growth Hormone is an active hormone that produces the stimulation IGF-1. No GH, no IGF-1. This hormone is secreted as pulses from the pituitary gland, in which the hypothalamus signals to the pituitary gland through Growth Hormone Releasing Hormone to release GH.
Once GH makes it to the liver, it binds to GH receptors on Liver Cells which signals to the liver to produce IGF-1. There are other GH benefits but I want to focus on growth. GH also binds to GH receptors in the chondrocytes, and is very necessary for growth as GH prevents chondrocytes from undergoing apoptosis, also promoting resting zone cells to differentiate.
This also explains why you idiots should not be using "Muh igf-1 lr3" don't rape your growth plates. GH is very necessary for chondrocytes. Also, GH is necessary for chondrocyte proliferation. This does not aromatise so it will not fuse growth plates. The same can be said for IGF-1.
GH also has it's own Negative feedback loop built into it called somatostatin that the hypothalamus secretes in order to make sure there isn't an overload of GH being sent. It modulates the release of GH, patients that do not have this factor usually have Gigantism if they have the pair of the pituitary also releasing excess GH in itself. This hormone travels to the pituitary. Other names are GHIH.
-- Estradiol. Estradiol is the hormone that produces the signal for growth plate closure. The cessation of growth. This hormone is synthesised through a conversion of testosterone into Estradiol through the enzyme aromatase. There's not much to say about estradiol in improving growth, it's honestly just a net negative on your growth.
Yes estradiol can have positive effects on growth as it is shown to increase IGF-1 levels but honestly why aren't you even running rhGH if you're in your growth years? Lmfao
There are also 2 Estrogen receptors in the growth plates, Estrogen receptor alpha and beta. Keeping it simple, Beta for bad, Alpha for amazing. I know it's childish but it helps you remember which one is which. Both are bad in some capacity, but Era actually drives skeletal growth and enhances skeletal growth and maturation. Whilst ERb acts as an antagonist to ERa activity and drives the plates to senescence whilst ERa has preventative qualities. Both still have roles in eventual growth stoppage.
--IGF-1. IGF-1 is the growth factor that actually grows things in the body. All cells that grow, grow due to this hormone. Responsible for cell hypertrophy, division and differentiation. There's not much to say about it honestly it's very self-intuitive.
-- Testosterone: Testosterone is the main male sex hormone responsible for driving pubertal changes into Adolescence for young boys. What we will be focusing on is it's effect on height.
Testosterone is the primary reason for the Male Growth Spurt, but also the primary reason for the stoppage of growth through fusing the growth plates. This hormone fuses the growth plates through converting into another hormone called Estradiol, otherwise known as Estrogen. (Family of hormones it belongs to, similar to Androgens. Estrogens for females Androgens for Males.)
So how does testosterone convert into Estradiol? It does so by the enzyme called Aromatase. Testosterone binds to the aromatase enyzme, converting a portion of it into Estradiol. This enzyme is present in body fat. This is why it is optimal to be stay in a healthy weight range during your pubertal years to reduce the abundance of this enzyme.
Testosterone induces the growth spurt through a hormone we spoke of earlier called IGF-1. IGF-1 stimulates chondrocytes to differentiate from the resting zone and proliferate in the proliferative zone resulting in a rapid increase in these processes. Testosterone shoots IGF-1 levels up, and additionally makes IGF-1 Receptors much more sensitive to IGF-1 which is why the growth is extreme.
-- Growth Hormone. Growth Hormone is an active hormone that produces the stimulation IGF-1. No GH, no IGF-1. This hormone is secreted as pulses from the pituitary gland, in which the hypothalamus signals to the pituitary gland through Growth Hormone Releasing Hormone to release GH.
Once GH makes it to the liver, it binds to GH receptors on Liver Cells which signals to the liver to produce IGF-1. There are other GH benefits but I want to focus on growth. GH also binds to GH receptors in the chondrocytes, and is very necessary for growth as GH prevents chondrocytes from undergoing apoptosis, also promoting resting zone cells to differentiate.
This also explains why you idiots should not be using "Muh igf-1 lr3" don't rape your growth plates. GH is very necessary for chondrocytes. Also, GH is necessary for chondrocyte proliferation. This does not aromatise so it will not fuse growth plates. The same can be said for IGF-1.
GH also has it's own Negative feedback loop built into it called somatostatin that the hypothalamus secretes in order to make sure there isn't an overload of GH being sent. It modulates the release of GH, patients that do not have this factor usually have Gigantism if they have the pair of the pituitary also releasing excess GH in itself. This hormone travels to the pituitary. Other names are GHIH.
-- Estradiol. Estradiol is the hormone that produces the signal for growth plate closure. The cessation of growth. This hormone is synthesised through a conversion of testosterone into Estradiol through the enzyme aromatase. There's not much to say about estradiol in improving growth, it's honestly just a net negative on your growth.
Yes estradiol can have positive effects on growth as it is shown to increase IGF-1 levels but honestly why aren't you even running rhGH if you're in your growth years? Lmfao
There are also 2 Estrogen receptors in the growth plates, Estrogen receptor alpha and beta. Keeping it simple, Beta for bad, Alpha for amazing. I know it's childish but it helps you remember which one is which. Both are bad in some capacity, but Era actually drives skeletal growth and enhances skeletal growth and maturation. Whilst ERb acts as an antagonist to ERa activity and drives the plates to senescence whilst ERa has preventative qualities. Both still have roles in eventual growth stoppage.
--IGF-1. IGF-1 is the growth factor that actually grows things in the body. All cells that grow, grow due to this hormone. Responsible for cell hypertrophy, division and differentiation. There's not much to say about it honestly it's very self-intuitive.
-- MYTH BUSTING:
-- "Chondrocyte Hypertrophy is bad for FAH" -- I've literally never heard of this notion outside of today that really pushed me to make this thread. Literally where did this even come from, people are misunderstanding shit on this forum without thorough research. Yes, hypertrophy of chondrocytes causes them to die, this is NOT a bad thing.
They are supposed to mature and die off so that we can even grow. If they don't do that, you don't grow. There's also this completely contradictory notion of "Chondrocytes getting into the hypertrophic phase prematurely and dying off early" this is just a made up sensation that comes from nowhere.
If anything this literally is contradictory, the entire phase of growth is about maturation, chondrocytes can't prematurely mature and die off before maturation.. They only die AFTER maturing, so it's not PREmature. If anything, doing this process faster allows you to keep growing more and more so you can restart the cycle of pushing chondrocytes from the resting phase into the proliferative and then hypertrophic phase.
-- "Androgenic Mediated Fusion OUTSIDE of Estradiol signalling" -- This one is less brosciency and made up and is more about limited knowledge and a misunderstanding of things. I've seen arguments using studies where trenbolone is used in the study, but looking at the actual ending data of the study there is barely any difference in the length of the bones. Like literally barely. Trenbolone also has strong progestogenic properties that can upregulate ER sensitivity. (look at T compared to C for reference)
-- "Muh rhGH or androgens deplete the resting zone" -- This is the newest one yet and is actual utter bullshit and genuinely shows anyone who is saying that hasn't done a molecule of research into the growth plate histology like at all. It's literally made up. There's no literature supporting the idea that resting zone chondrocytes get "depleted" without the existence of estradiol whether you mean totally or even to some degree. The entire point of this zone is to KEEP going growing and NOT deplete.
As I explained earlier, they are self-sustaining stem cells. Their job is to produce chondrocytes for maturation to continually push height growth. When resting zone cells get used for proliferation, before leaving, it divides and leaves an identical version of itself in the resting zone pool of chondrocytes to literally do the opposite of what you're saying it does.
And if it ever happens to be the case that Resting Zone cells are "differentiating too fast" there are negative feedback loops in place that modulate the differentiation rate.
Now onto really critical info about the resting zone since I guess no one wanted to do any research into it, the resting zone cells have a lifespan like ALL cells do. They all die eventually via programmed cell death. This is called apoptosis. However, this isn't the driver of growth plate fusion and actually takes a long while to happen. The role of estradiol in humans is to rapidly decrease the lifespan of resting zone cells, which is why we stop growing.
Because once those cells die, there is no growth at all. Growth has to stop, and then Estradiol fuses the rest of the zones subsequently. THIS is how resting zone cells get "depleted". This doesn't happen through "muh androgens" or muh igf-1/high dose gh stop talking from your ass.
To also address the muh runx2 argument, runx2 quite literally synthesis aromatase which leads to e2 so your "androgenic fusion through runx2" is nothing more than e2 signalling. And even then there's no evidence runx2 closes plates outside of the aromatase expression it has which you should be nuking your e2/aromatase regardless in your growing years. Trailing off of the runx2 argument, people think runx2 inducing hypertrophy means growth plate closure.
BOYS, Chondrocyte hypertrophy --> cell death --> ossification is not the same as ossification that affects your final adult height through e2. When the chondrocytes die after hypertrophy, the cycle simply starts again and you keep growing bone more and more through the growth cycle. E2 kills off the RESTING ZONE. Which is why it is completely different. Get this through your thick heads.
They are supposed to mature and die off so that we can even grow. If they don't do that, you don't grow. There's also this completely contradictory notion of "Chondrocytes getting into the hypertrophic phase prematurely and dying off early" this is just a made up sensation that comes from nowhere.
If anything this literally is contradictory, the entire phase of growth is about maturation, chondrocytes can't prematurely mature and die off before maturation.. They only die AFTER maturing, so it's not PREmature. If anything, doing this process faster allows you to keep growing more and more so you can restart the cycle of pushing chondrocytes from the resting phase into the proliferative and then hypertrophic phase.
-- "Androgenic Mediated Fusion OUTSIDE of Estradiol signalling" -- This one is less brosciency and made up and is more about limited knowledge and a misunderstanding of things. I've seen arguments using studies where trenbolone is used in the study, but looking at the actual ending data of the study there is barely any difference in the length of the bones. Like literally barely. Trenbolone also has strong progestogenic properties that can upregulate ER sensitivity. (look at T compared to C for reference)
-- "Muh rhGH or androgens deplete the resting zone" -- This is the newest one yet and is actual utter bullshit and genuinely shows anyone who is saying that hasn't done a molecule of research into the growth plate histology like at all. It's literally made up. There's no literature supporting the idea that resting zone chondrocytes get "depleted" without the existence of estradiol whether you mean totally or even to some degree. The entire point of this zone is to KEEP going growing and NOT deplete.
As I explained earlier, they are self-sustaining stem cells. Their job is to produce chondrocytes for maturation to continually push height growth. When resting zone cells get used for proliferation, before leaving, it divides and leaves an identical version of itself in the resting zone pool of chondrocytes to literally do the opposite of what you're saying it does.
And if it ever happens to be the case that Resting Zone cells are "differentiating too fast" there are negative feedback loops in place that modulate the differentiation rate.
Now onto really critical info about the resting zone since I guess no one wanted to do any research into it, the resting zone cells have a lifespan like ALL cells do. They all die eventually via programmed cell death. This is called apoptosis. However, this isn't the driver of growth plate fusion and actually takes a long while to happen. The role of estradiol in humans is to rapidly decrease the lifespan of resting zone cells, which is why we stop growing.
Because once those cells die, there is no growth at all. Growth has to stop, and then Estradiol fuses the rest of the zones subsequently. THIS is how resting zone cells get "depleted". This doesn't happen through "muh androgens" or muh igf-1/high dose gh stop talking from your ass.
To also address the muh runx2 argument, runx2 quite literally synthesis aromatase which leads to e2 so your "androgenic fusion through runx2" is nothing more than e2 signalling. And even then there's no evidence runx2 closes plates outside of the aromatase expression it has which you should be nuking your e2/aromatase regardless in your growing years. Trailing off of the runx2 argument, people think runx2 inducing hypertrophy means growth plate closure.
BOYS, Chondrocyte hypertrophy --> cell death --> ossification is not the same as ossification that affects your final adult height through e2. When the chondrocytes die after hypertrophy, the cycle simply starts again and you keep growing bone more and more through the growth cycle. E2 kills off the RESTING ZONE. Which is why it is completely different. Get this through your thick heads.
I know it is a LOT but it is a good read, and literally explains everything you need to know about bone growth and height. After reading this, you will more than likely need NO other research outside of clarifying my claims (basic literature anyways easy to see what I'm saying is true).
I just want to unite this community on the knowledge of bone growth but it probably wont happen because of stupid prideful 14 year olds like you probably reading this right now
If people here can see this thread and get this down, this forum can genuinely be more productive for convos like these. A lot of this community is genuinely just tiktok niggers saying bullshitThank you for reading bhai's I'll answer questions below we can have a discussion if anyone wants to counter this thread. Remember I'm not omniscient, there may be things I don't know either and that goes for everyone here
@nwed @AtrophicPyra @eyezen @brootaldood @its.over.
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