T3 for bone (repost)

sigmablud42069

sigmablud42069

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yo btw ngas this is better formatted and explained repost
Introduction:
T3 the active thyroid hormone is produced in your body by deiodinases turning T4 the prohormone into T3 and is responsible for many metabolic processes, bone and muscle homeostasis. I mainly see it being talked about as a fat burner, in the space, but in my opinion it could be used as an osteoanabolic if combined with the right ancills.

Some basic knowledge abt how bone growth occurs (idk kinda water but wtv):
Type 1 collagen creates a matrix in which osteoblasts pump calcium and other minerals in creating the solid bone. Osteoclasts break down old bone and signal to osteoblasts to create more new bone.

How it works:
T3 breaks down bone at supraphysiological levels by causing an excess of osteoclasts and an increase in osteoclast activity. However it also increases many functions of bone growth, being hypertrophic cell differentiation, increasing osteoblasts, type 1 collagen expression, IGF-1 expression and increasing IGF-1 and HGH signalling. There are two major medications that decrease osteoclast activity, biphosphonates and cathepsin K inhibitors. Biphosphonates work by killing osteoclasts while cathepsin K inhibitors work by inhibiting cathepsin K, the enzyme with which osteoclasts break down bone, cathespin K breaks down type 1 collagen allowing your body to absorb the left over actual calcium bone tissue. Cathespin K inhibitors just remove this enzyme stopping osteoclasts from being able to break down bone. Cathepsin K inhibitors are better than biphosphonates as they allow osteoclasts to continue to signal to osteoblasts. So by combining cathepsin K inhibitors with high T3 you should get all the osteoanabolic promoting effects of T3 without any of the bone breakdown.

Why it would be good for bone growth:
Facial bone growth is formed through periosteal apposition, the process of a collagen matrix being formed then getting filled with bone (as mentioned above). T3 specifically upregulates all processes around this (again as mentioned above) It would also be good for height and could keep your plates open as it increases PTH signalling and hypertrophic cell differentiation which is the process which turns mesenchymal stem cells into cartilage. As well as the other general processes of increasing osteoblasts, while decreasing osteoclast function.

Safety concerns:
T3 has metabolic and heart effects at supraphysiological levels and cathepsin K inhibitors cause arterial wall damage, (1.3x stroke risk in some old people) i’d say not really a issue for young healthy people but if your roiding you definitely need to control cholesterol. It increases calcification of arteries and makes them brittle. T3 also breaks down muscle so I would roid while running high dose T3 to mitigate any muscle lost

Sigmablud42069’s high iq musings part 2, next PTH analogues

@Genio
@roidfaper66
 
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Ur thyroid is responsible for alot in ur body u could say t3 is good for alot of things

reality is its not going to make a difference in the end for bone growth
 
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Ur thyroid is responsible for alot in ur body u could say t3 is good for alot of things

reality is its not going to make a difference in the end for bone growth
Have you even read the post lol. Hyper and hypo thyroidism leads to osteoporosis and your saying it doesn’t make a difference
 
Have you even read the post lol. Hyper and hypo thyroidism leads to osteoporosis and your saying it doesn’t make a difference
Didnt read it cus I knew its dumb

The change wont be significant
 
Last edited:
high iq.

Low dose t4+t3 are great ancillaries for development stacks.
 
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yo btw ngas this is better formatted and explained repost
Introduction:
T3 the active thyroid hormone is produced in your body by deiodinases turning T4 the prohormone into T3 and is responsible for many metabolic processes, bone and muscle homeostasis. I mainly see it being talked about as a fat burner, in the space, but in my opinion it could be used as an osteoanabolic if combined with the right ancills.

Some basic knowledge abt how bone growth occurs (idk kinda water but wtv):
Type 1 collagen creates a matrix in which osteoblasts pump calcium and other minerals in creating the solid bone. Osteoclasts break down old bone and signal to osteoblasts to create more new bone.

How it works:
T3 breaks down bone at supraphysiological levels by causing an excess of osteoclasts and an increase in osteoclast activity. However it also increases many functions of bone growth, being hypertrophic cell differentiation, increasing osteoblasts, type 1 collagen expression, IGF-1 expression and increasing IGF-1 and HGH signalling. There are two major medications that decrease osteoclast activity, biphosphonates and cathepsin K inhibitors. Biphosphonates work by killing osteoclasts while cathepsin K inhibitors work by inhibiting cathepsin K, the enzyme with which osteoclasts break down bone, cathespin K breaks down type 1 collagen allowing your body to absorb the left over actual calcium bone tissue. Cathespin K inhibitors just remove this enzyme stopping osteoclasts from being able to break down bone. Cathepsin K inhibitors are better than biphosphonates as they allow osteoclasts to continue to signal to osteoblasts. So by combining cathepsin K inhibitors with high T3 you should get all the osteoanabolic promoting effects of T3 without any of the bone breakdown.

Why it would be good for bone growth:
Facial bone growth is formed through periosteal apposition, the process of a collagen matrix being formed then getting filled with bone (as mentioned above). T3 specifically upregulates all processes around this (again as mentioned above) It would also be good for height and could keep your plates open as it increases PTH signalling and hypertrophic cell differentiation which is the process which turns mesenchymal stem cells into cartilage. As well as the other general processes of increasing osteoblasts, while decreasing osteoclast function.

Safety concerns:
T3 has metabolic and heart effects at supraphysiological levels and cathepsin K inhibitors cause arterial wall damage, (1.3x stroke risk in some old people) i’d say not really a issue for young healthy people but if your roiding you definitely need to control cholesterol. It increases calcification of arteries and makes them brittle. T3 also breaks down muscle so I would roid while running high dose T3 to mitigate any muscle lost

Sigmablud42069’s high iq musings part 2, next PTH analogues

@Genio
@roidfaper66
w guide mirin. i will look more into this soon :feelsokman:
 
  • +1
Reactions: sigmablud42069
yo btw ngas this is better formatted and explained repost
Introduction:
T3 the active thyroid hormone is produced in your body by deiodinases turning T4 the prohormone into T3 and is responsible for many metabolic processes, bone and muscle homeostasis. I mainly see it being talked about as a fat burner, in the space, but in my opinion it could be used as an osteoanabolic if combined with the right ancills.

Some basic knowledge abt how bone growth occurs (idk kinda water but wtv):
Type 1 collagen creates a matrix in which osteoblasts pump calcium and other minerals in creating the solid bone. Osteoclasts break down old bone and signal to osteoblasts to create more new bone.

How it works:
T3 breaks down bone at supraphysiological levels by causing an excess of osteoclasts and an increase in osteoclast activity. However it also increases many functions of bone growth, being hypertrophic cell differentiation, increasing osteoblasts, type 1 collagen expression, IGF-1 expression and increasing IGF-1 and HGH signalling. There are two major medications that decrease osteoclast activity, biphosphonates and cathepsin K inhibitors. Biphosphonates work by killing osteoclasts while cathepsin K inhibitors work by inhibiting cathepsin K, the enzyme with which osteoclasts break down bone, cathespin K breaks down type 1 collagen allowing your body to absorb the left over actual calcium bone tissue. Cathespin K inhibitors just remove this enzyme stopping osteoclasts from being able to break down bone. Cathepsin K inhibitors are better than biphosphonates as they allow osteoclasts to continue to signal to osteoblasts. So by combining cathepsin K inhibitors with high T3 you should get all the osteoanabolic promoting effects of T3 without any of the bone breakdown.

Why it would be good for bone growth:
Facial bone growth is formed through periosteal apposition, the process of a collagen matrix being formed then getting filled with bone (as mentioned above). T3 specifically upregulates all processes around this (again as mentioned above) It would also be good for height and could keep your plates open as it increases PTH signalling and hypertrophic cell differentiation which is the process which turns mesenchymal stem cells into cartilage. As well as the other general processes of increasing osteoblasts, while decreasing osteoclast function.

Safety concerns:
T3 has metabolic and heart effects at supraphysiological levels and cathepsin K inhibitors cause arterial wall damage, (1.3x stroke risk in some old people) i’d say not really a issue for young healthy people but if your roiding you definitely need to control cholesterol. It increases calcification of arteries and makes them brittle. T3 also breaks down muscle so I would roid while running high dose T3 to mitigate any muscle lost

Sigmablud42069’s high iq musings part 2, next PTH analogues

@Genio
@roidfaper66
Nice only thought of it as a fat burner
 
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Reactions: sigmablud42069

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