MESO-Rx

Anabolic Steroids

Can taking testosterone cause epiphysial plate closure?

To answer your question...... BOTH testosterone and estrogen close these plates! Just because you "nuke" estrogen (retarded in itself for a myriad of reasons) doesn't mean the test won't stunt you.

Do not nuke estrogen! It is neuro protective as well as cardio protective. You also won't be able to get hard and fuck (all you should be thinking about at your age)

There is no fucking way in hell you have even close to being able to develop a physique that justifies gear yet. If you were already on TRT then fuck it blast away...... But I doubt that.
 
Taking steroids before your youth growth pattern has completed is just as fucking idiotic as "nuking estrogen".

Eat more, lift more, sleep more.

You don't need fucking steroids yet. I see you have cheerfully gone ahead and gotten on juice anyway from your posting history so I have no idea why I am wasting my time answering your post.

You don't want to hear anything but what you already think you know.
 
Branco said:
provided you’re also making sure to nuke your estrogen levels?
Click to expand...
Its age and hormone related. The theory is that if you take steroids while young and before you have reached full adult height the conversion to estrogen could stunt your growth. Arnold is well known to have started taking dianabol when he was between 13 and 15 years old and dbol is among the highest aromatizing agents. He turned out fine. I'm not sure how much of that theory is actual science and how much propaganda put out to scare you.

So to your needs, you are considering doing a cycle and nuking estrogen to ensure you don't stunt your growth. Your logic makes sense in a way but its not practical or even a good idea. In your case stick with steroids that do not aromatize primo anavar etc and keep doses reasonable and call it a day. If you start fucking with estrogen you are going to have a real mess on your hands. I do not advise you do that.
 
Methyl Mike said:
Its age and hormone related. The theory is that if you take steroids while young and before you have reached full adult height the conversion to estrogen could stunt your growth. Arnold is well known to have started taking dianabol when he was between 13 and 15 years old and dbol is among the highest aromatizing agents. He turned out fine. I'm not sure how much of that theory is actual science and how much propaganda put out to scare you.

So to your needs, you are considering doing a cycle and nuking estrogen to ensure you don't stunt your growth. Your logic makes sense in a way but its not practical or even a good idea. In your case stick with steroids that do not aromatize primo anavar etc and keep doses reasonable and call it a day. If you start fucking with estrogen you are going to have a real mess on your hands. I do not advise you do that.
Click to expand...
Arnold was a shrimp. Look here compared to others.

main-qimg-4ed07856efe037819e070c235dcb2307-c
 
Methyl Mike said:
Its age and hormone related. The theory is that if you take steroids while young and before you have reached full adult height the conversion to estrogen could stunt your growth. Arnold is well known to have started taking dianabol when he was between 13 and 15 years old and dbol is among the highest aromatizing agents. He turned out fine. I'm not sure how much of that theory is actual science and how much propaganda put out to scare you.

So to your needs, you are considering doing a cycle and nuking estrogen to ensure you don't stunt your growth. Your logic makes sense in a way but its not practical or even a good idea. In your case stick with steroids that do not aromatize primo anavar etc and keep doses reasonable and call it a day. If you start fucking with estrogen you are going to have a real mess on your hands. I do not advise you do that.
Click to expand...
Docs use AI's on children as growth treatment, so lowering your E should definitelly help.
Some people mention here that T also closes your plates, i don't know about that, maybe someone can post some studies.
The idea behind all of this is to get extra androgens during puberty for extra androgenic developement, while keeping AI at the lower bound, so you don't stunt your growth. I don't really think there are studies done on children with this protocol, so it's uncharted territory.
 
Estrogen is the primary mediator of epiphyseal growth plate closure. This has been proven in human genetic oddities who lacked the aromatase enzyme gene and therefore had littoe to no estrogen (but still androgens). These handful of oddities never stopped growing taller until they were administered estrogens. These cases resulted in exploration of using aromatase inhibitors to increase height in underdeveloped children, with excellent results.

Furthermore, it appears that its the alpha subtype of the estrogen receptor that is the most important for growth plate fusion. One genetic oddity reviewed by doctors had a gene mutation that resulted in no ER-alpha receptors but still had ER-beta and still had aromatase enzymes and circulating estrogens. This oddity never stopped growing taller. I do not know how (or if) they made him stop growing but i guess theres surgical ways to remove the growth plates in such an extreme case, as administering estrogens wouldnt help given the absence of the necessary receptor.

Androgens are used to accelerate growth rates in children. Testosterone and oxandrolone being the most common. Of course, aromatization to estrogen will accelerate growth plate fusion. Growth hormone is also used to accelerate longitudinal growth.

To understand how this all works you need to understand how epiphyseal growth plates work. They have 4 regions that make up the growth plate: germative layer, proliferation layer, hypertrophic layer, and the zone of provisional calcification.

In the germative layer mesenchymal stem cells are recruited and differentiated into chondrocytes (cartilage cells).

The newly differentiated chondrocytes then undergo proliferation (cellular division), at this stage in the process IGF-1 seems to have its most important role, higher IGF-1 results in increased proliferation of chondrocytes and its likely through this stage and process that HGH increases height growth.

Next the chondrocytes undergo hypertrophy and rapidly increase in size. It seems here androgens may exert their effect most significantly but IGF-1 is also still very relevant. The chondrocytes also begin secreting large amounts of extracellular matrix which is primarily made up of collagen into the spaces around them.

After this the chondrocytes undergo cellular apoptosis (die), following that vascular invasion occurs, with it comes osteoblasts, the osteoblasts enter the voids left within the ECM by the dead chondrocytes and secrete osteocin into the voids, osteocin is bone material and is made up primarily of calcium with other minerals. It seems estrogens exert their biggest effect on the osteoblasts.

In this entire situation you have 2 processes occuring, chondrogenesis and osteogenesis. When the rate of osteogenesis exceeds the rate of chondrogenesis the height of the griwth plate shrinks. The height of the growth plate is the distance from the germative layer to the zone of provisional ossification. The smaller the distance becomes the closer your griwth plate is to fusion, fusion occurs when the osteoblasts reach the germative layer and calcify everything thereby forever ending the process of chondrogenesis in the growth plate.

With this in mind, increasing chondrogenesis while reducing osteogenesis will increase the height of the growth plate, prolonging the growth period.

Ive yet to see a study on this combo but per my understanding mild androgen like oxandrolone plus an aromatase inhibitor plus HGH (or say, MK-677) would be the ultimate trifector for achieving supraphysiological height growth.

Of course theres all kinds of potential side effects outside of the scope that im covering.
 
Human_backhoe said:
www.frontiersin.org

Frontiers | Letrozole Monotherapy in Pre- and Early-Pubertal Boys Does Not Increase Adult Height

BackgroundAromatase inhibitors (AIs) have been used in boys with idiopathic short stature (ISS) to promote growth despite the lack of actual data regarding t...
www.frontiersin.org www.frontiersin.org
Click to expand...
"This, however, does not rule out a beneficial effect of AI-therapy on adult height if the intervention is targeted exclusively to pubertal boys, and the treatment is continued until late stages of puberty."
 
Givemeroidsorgivemedeath said:
Docs use AI's on children as growth treatment, so lowering your E should definitelly help.
Some people mention here that T also closes your plates, i don't know about that, maybe someone can post some studies.
The idea behind all of this is to get extra androgens during puberty for extra androgenic developement, while keeping AI at the lower bound, so you don't stunt your growth. I don't really think there are studies done on children with this protocol, so it's uncharted territory.
Click to expand...
exactly
this was what i hypothesized
 
Megadick3000 said:
Estrogen is the primary mediator of epiphyseal growth plate closure. This has been proven in human genetic oddities who lacked the aromatase enzyme gene and therefore had littoe to no estrogen (but still androgens). These handful of oddities never stopped growing taller until they were administered estrogens. These cases resulted in exploration of using aromatase inhibitors to increase height in underdeveloped children, with excellent results.

Furthermore, it appears that its the alpha subtype of the estrogen receptor that is the most important for growth plate fusion. One genetic oddity reviewed by doctors had a gene mutation that resulted in no ER-alpha receptors but still had ER-beta and still had aromatase enzymes and circulating estrogens. This oddity never stopped growing taller. I do not know how (or if) they made him stop growing but i guess theres surgical ways to remove the growth plates in such an extreme case, as administering estrogens wouldnt help given the absence of the necessary receptor.

Androgens are used to accelerate growth rates in children. Testosterone and oxandrolone being the most common. Of course, aromatization to estrogen will accelerate growth plate fusion. Growth hormone is also used to accelerate longitudinal growth.

To understand how this all works you need to understand how epiphyseal growth plates work. They have 4 regions that make up the growth plate: germative layer, proliferation layer, hypertrophic layer, and the zone of provisional calcification.

In the germative layer mesenchymal stem cells are recruited and differentiated into chondrocytes (cartilage cells).

The newly differentiated chondrocytes then undergo proliferation (cellular division), at this stage in the process IGF-1 seems to have its most important role, higher IGF-1 results in increased proliferation of chondrocytes and its likely through this stage and process that HGH increases height growth.

Next the chondrocytes undergo hypertrophy and rapidly increase in size. It seems here androgens may exert their effect most significantly but IGF-1 is also still very relevant. The chondrocytes also begin secreting large amounts of extracellular matrix which is primarily made up of collagen into the spaces around them.

After this the chondrocytes undergo cellular apoptosis (die), following that vascular invasion occurs, with it comes osteoblasts, the osteoblasts enter the voids left within the ECM by the dead chondrocytes and secrete osteocin into the voids, osteocin is bone material and is made up primarily of calcium with other minerals. It seems estrogens exert their biggest effect on the osteoblasts.

In this entire situation you have 2 processes occuring, chondrogenesis and osteogenesis. When the rate of osteogenesis exceeds the rate of chondrogenesis the height of the griwth plate shrinks. The height of the growth plate is the distance from the germative layer to the zone of provisional ossification. The smaller the distance becomes the closer your griwth plate is to fusion, fusion occurs when the osteoblasts reach the germative layer and calcify everything thereby forever ending the process of chondrogenesis in the growth plate.

With this in mind, increasing chondrogenesis while reducing osteogenesis will increase the height of the growth plate, prolonging the growth period.

Ive yet to see a study on this combo but per my understanding mild androgen like oxandrolone plus an aromatase inhibitor plus HGH (or say, MK-677) would be the ultimate trifector for achieving supraphysiological height growth.

Of course theres all kinds of potential side effects outside of the scope that im covering.
Click to expand...
But u need chondrocytes to make a new cartilage and osteoblast gets made on chondrocytes the cartilage of it so, how is it possible to have more osteoblast than chondrocytes when they need the cartilage from the chondrocytes?
 
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