R
RealLifecel
Iron
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- Jul 13, 2025
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This is a discussion post for people that have time and want to learn, teach, give input, provoke thoughts or have their thoughts provoked.
If you are toxic and hate on people just because they are mistaken or do not know something gtfo.
I have been looking into all craniofacial growth mechanisms and identified which factors drive them and at which age they stop and why.: Sutures and growth plates close at 17-19/18-22 which eliminates two major growth mechanisms. What is left is periosteal apposition and pathogenic growth via GH excess aka. "acromegaly".
Your bone is also in a constant homeostasis (homeostasis means balance, imagine it like a 50/50 "balance"). This balance exists because you have some catabolic (means deconstruct, destroy, remove, take away...) cells in your bone called osteoclasts and some anabolic (means build, grow, add, construct...) cells in your bone called osteoblasts. Both of them are supposed to be in a balanced ratio (homeostasis) which ensures that the bone constantls deconstructs and constructs itself simultaneously.
However you can throw off this balance unnaturally in the favour of our goals. If you reduce the osteoCLASTS (catabolic) and increase the osteoBLASTS (anabolic) you throw off the 50/50 balance, disrupt the homeostasis and create a "anabolic environment". An environment that net grows, constructs.
Steroids bind to androgen receptors. Androgen receptors are distributed all over your body. In your skeletal muscles, your prostate, your skin, your hair follicles, your liver and your bones. Regarding the bones they are distributed in a "male pattern" though (the same way they are distributed on your scalp in a "male pattern". That is why hormonally caused hair loss presents itself in the same pattern in everyone). You have more androgen receptors in your zygos, mandible/gonials, chin and browridge than elsewhere. So if you were to take steroids they would dock to those specific areas, upregulate osteoblasts creating an anabolic environment and:
Cause the outter layer of the bone called the "periosteum" to slowly add layer on layer on layer.
Steroids docking to those ARs also makes the periosteum (the outter layer on the bone) produce IGF1 locally which is even more potent for bone growth than systemic IGF1 from the liver.
Regarding the "pathogenic growth via GH excess aka. acromegaly" it basically means giving yourself a mini acromegaly. Additionally HGH does not just upregulate systemic IGF 1 via the liver but also docks to GH receptors in bone directly and produces IGF1 locally which as said: Is more potent than systemic IGF1.
(Then there is ofc mechanical stuff like MSE, MARPE, thumbpulling, mouthguard, chewing. And unorthodox stuff like bonesmashing or vibrational stuff, bee pollen I think?)
That is the theoretical part. How this plays out practically? I have no clue. How to apply this practically? I do not know.
I do not know whether the androgenic or the anabolic aspect of the compound is what matters. I do not know whether it is about the the gear being non-selective and thus being more prone to docking everywhere and guaranteeing that all the bone is being docked to. Or whether it is the opposite, the gear being very selective like SARMs. Because the effect of Ostarine and S4 on bone density has been more potent than testosterone and DHT for example.
As you can tell I really need some dialogues to bring me forward.
DNR and "You are just wrong" will not get me anywhere, save your time and be a better person.
Thanks for reading and looking forward to your feedback.
If you are toxic and hate on people just because they are mistaken or do not know something gtfo.
I have been looking into all craniofacial growth mechanisms and identified which factors drive them and at which age they stop and why.: Sutures and growth plates close at 17-19/18-22 which eliminates two major growth mechanisms. What is left is periosteal apposition and pathogenic growth via GH excess aka. "acromegaly".
Your bone is also in a constant homeostasis (homeostasis means balance, imagine it like a 50/50 "balance"). This balance exists because you have some catabolic (means deconstruct, destroy, remove, take away...) cells in your bone called osteoclasts and some anabolic (means build, grow, add, construct...) cells in your bone called osteoblasts. Both of them are supposed to be in a balanced ratio (homeostasis) which ensures that the bone constantls deconstructs and constructs itself simultaneously.
However you can throw off this balance unnaturally in the favour of our goals. If you reduce the osteoCLASTS (catabolic) and increase the osteoBLASTS (anabolic) you throw off the 50/50 balance, disrupt the homeostasis and create a "anabolic environment". An environment that net grows, constructs.
Steroids bind to androgen receptors. Androgen receptors are distributed all over your body. In your skeletal muscles, your prostate, your skin, your hair follicles, your liver and your bones. Regarding the bones they are distributed in a "male pattern" though (the same way they are distributed on your scalp in a "male pattern". That is why hormonally caused hair loss presents itself in the same pattern in everyone). You have more androgen receptors in your zygos, mandible/gonials, chin and browridge than elsewhere. So if you were to take steroids they would dock to those specific areas, upregulate osteoblasts creating an anabolic environment and:
Cause the outter layer of the bone called the "periosteum" to slowly add layer on layer on layer.
Steroids docking to those ARs also makes the periosteum (the outter layer on the bone) produce IGF1 locally which is even more potent for bone growth than systemic IGF1 from the liver.
Regarding the "pathogenic growth via GH excess aka. acromegaly" it basically means giving yourself a mini acromegaly. Additionally HGH does not just upregulate systemic IGF 1 via the liver but also docks to GH receptors in bone directly and produces IGF1 locally which as said: Is more potent than systemic IGF1.
(Then there is ofc mechanical stuff like MSE, MARPE, thumbpulling, mouthguard, chewing. And unorthodox stuff like bonesmashing or vibrational stuff, bee pollen I think?)
That is the theoretical part. How this plays out practically? I have no clue. How to apply this practically? I do not know.
I do not know whether the androgenic or the anabolic aspect of the compound is what matters. I do not know whether it is about the the gear being non-selective and thus being more prone to docking everywhere and guaranteeing that all the bone is being docked to. Or whether it is the opposite, the gear being very selective like SARMs. Because the effect of Ostarine and S4 on bone density has been more potent than testosterone and DHT for example.
As you can tell I really need some dialogues to bring me forward.
DNR and "You are just wrong" will not get me anywhere, save your time and be a better person.
Thanks for reading and looking forward to your feedback.
