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Iron
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How can we make hyperthyroidism advantageous to bone building ( apparitional growth ) ?
Ok so in this post today I’ll be explaining how hyperthyroidism + a combo of other drugs would create a hyper anabolic bone environment for appositional growth please ok ans please keep in mind this is a really high risk combo ok and use it at your own risks I’m huse here to share my theory with u all ok ?
Hyperthyroidism effects on bones:
The TSH path way :
Hyperthyroidism has many interesting effects on bones one main one is that it’s ability to drive ostoblast activity and osteoclast thru the roof via Tra receptor activation and many other ways that I will be covering today. One way hypothyroidism causes an increase in ostoblast activity is via the TSH supression when we take exogenous t3 and t4 at high doses this causes a negative feedback loop in the body thus nuking TSH this is ideal in this circumstance as TSH binds to receptors on ostoblast and acts as a direct inhbitor on bone turnover. TSH does this by suppressing the expression of LRP-5 and flk-1 thus TSH is a potent inhbitor of the wnt/b-catenin and a angiogenesis inhibitor ok so now that we covered one way how hyperthyroidism over activates osteoblasts let’s look at more ways it does this.
The T3 path way ( anabolic) :
T3 is the active thyroid hormone that binds directly to ostoblast thyroid receptors ( Trs ) or TNF ( receptor-associated factors ) when t3 binds to the Trs in ostoblast ( Tra ) or directly pushes MSCs to differentiate and commit into becoming become ostoblast. T3 does this by up regulating runx2 and osterix via ( p38 mapk ) and suppressing PPARy directly also forcing the MSCs into becoming bone building cells not fat cells. T3 is also anabolic to bones via increasing bmp2mRNA expression by over 1.7 fold, bmp4mRNA by 1.5 , increasing the expression of FGf1 and FGF2 thus making MCS more responsive to growth signals and commitment to becoming ostoblast not fat cells , the increase in local igf-1 and making GHr and igf-1r more sensitive to gh and igf-1 , excess t3 also causes hyper activation of ekr1/2 thus forcing mitoses in ostoblast ( immature ones will explain later how we can fix this and why this is a benefit for us when paired with romo ) flooding the bone matrix and periosteum with pre ostoblast.
The t3 path way ( catabolic effects ):
One main reason why hyperthyroidism causes bone loss is due to the fact that when Trs ( Trb especially ) it forces a huge release of RANKL and IL-6 this causes a huge release of osteoclast to become hyper active and eat at the bone matrix and the fact that the over activation of erk1/2 and p38 mapk forces pre ostoblast into mitoses while in an immature state not being able to fully mature into ostoblast thus not being about to lay down bone strong structural bone properly they lay down woven bone and the fact that the body tries to stop this over activation of both ostoblast and ostoclast by trying to Inhbit and slow down ostoblast via up regulation of sots and dkk-1 yet it still fails to slow down the osteoblast formation and numbers .
Ok so how do we make sure to not end up with bone loss then from this?
My theory is that these main drugs that cover this :
1: Romo
Romo is a sots anti body we will use this to make up for the fact that sots increases in hyperthyroidism and to stabilise the wnt path way even more and it up regulates survival proteins like ( Bcl-2) and the massive influx of b- catenin from the sots and dkk1 inhbition ( will use a proteasome inhibitor will speak on this later ) will force the immature ostoblast to start maturing and also the Bcl-2 there to neutralises the inflammatory and apoptotic signals caused by over active erk1/2 while also Romo being able to suppress RANKL and increse OPG
2:Abalo
Abalo will be used to force osteoblast to secrete ALP and osteocalcin while also the cAMP spike causes the activation of PKA what then drives the inhibitory phosphorylation of BAD ( pro apoptotic protein ) at the ser 112 site this stops the programmed death of the osteoblast and the stabilisation of again Bcl-2 and Bcl-xl allowing osteoblast to mature and also live for longer and it also prevent the depletion of bcl-2 and bcl-xl via activation of CREB ( camp response binding element ) this down regulate the transcription and the ( bcl-2 and bcl-xl block ) bax thus leading to a decrease of bax proteins available meaning the cell can’t build the pores required for mitochondrial leakage to happen. Also pth hormone has been documented to lower dkk1 mRNA by up to 90% and systemic dkk1 by 20-30% potentially meaning abalo would do the same maybe even more effectively .
3:Brotezobin
Brote ( Brotezobin ) is a proteasome inhibitor this allows the surge of anabolic factors like runx2 and b-catetin to not be broken down by the proteasome while it also down regulates dkk1 and sots further more aiding in osteoblast activity and survival while it also inhibits RANKL via preventing the break down of IkB what then accumulates and locks the NF-kB thus not allowing it to enter the nucleus and stepping the massive surge of RANKL.
4: Cat k inhbition
Odanacatib: is a cat k inhbitor this drug ( I made a post on this if u wanna get to know more about it go read on it ) stops the active enzyme cat k from braking down type I collagen what makes up 90% of bone matrix meaning even if the osteoclast try to eat at the bone they will be unable to dissolve it but not only that but the osteoclast will keep the positive anabolic feed back loop bc of coupling meaning osteoclast will keep secreting anabolic signals like S1P CT-1 Cthrc-1 complement component 3 wnt10 and bmp6 while also not being to degrade the other anabolic compound embedded in the bone matrix like igf-1 bmp2 and ostoecalin.
The combination of all these drugs would prevent the mature death of osteoblasts and the ability for the over activation of ostoclast to destroy thr bomes while keeping the anabolism from over activating the Trs .
And another drug what I made a post about again what could be paired with this for appositional growth is LA ( linoleic acid ) I made a post on it and how it increse periostial bone formation by 220% , increased Cortial thickness by 38% and periostial perimeter by 15% while having 0 effects on Endocortial thickness meaning it’s extremely biast towards the periosteum of bones.
Thank you for reading if u have any questions dm me and we can talk about it also i will start coaching join the dc link in my bio and tag me ( dc user methylated_0 ) or shoot me a dm thanks for reading again and I love you l guys
Ok so in this post today I’ll be explaining how hyperthyroidism + a combo of other drugs would create a hyper anabolic bone environment for appositional growth please ok ans please keep in mind this is a really high risk combo ok and use it at your own risks I’m huse here to share my theory with u all ok ?
Hyperthyroidism effects on bones:
The TSH path way :
Hyperthyroidism has many interesting effects on bones one main one is that it’s ability to drive ostoblast activity and osteoclast thru the roof via Tra receptor activation and many other ways that I will be covering today. One way hypothyroidism causes an increase in ostoblast activity is via the TSH supression when we take exogenous t3 and t4 at high doses this causes a negative feedback loop in the body thus nuking TSH this is ideal in this circumstance as TSH binds to receptors on ostoblast and acts as a direct inhbitor on bone turnover. TSH does this by suppressing the expression of LRP-5 and flk-1 thus TSH is a potent inhbitor of the wnt/b-catenin and a angiogenesis inhibitor ok so now that we covered one way how hyperthyroidism over activates osteoblasts let’s look at more ways it does this.
The T3 path way ( anabolic) :
T3 is the active thyroid hormone that binds directly to ostoblast thyroid receptors ( Trs ) or TNF ( receptor-associated factors ) when t3 binds to the Trs in ostoblast ( Tra ) or directly pushes MSCs to differentiate and commit into becoming become ostoblast. T3 does this by up regulating runx2 and osterix via ( p38 mapk ) and suppressing PPARy directly also forcing the MSCs into becoming bone building cells not fat cells. T3 is also anabolic to bones via increasing bmp2mRNA expression by over 1.7 fold, bmp4mRNA by 1.5 , increasing the expression of FGf1 and FGF2 thus making MCS more responsive to growth signals and commitment to becoming ostoblast not fat cells , the increase in local igf-1 and making GHr and igf-1r more sensitive to gh and igf-1 , excess t3 also causes hyper activation of ekr1/2 thus forcing mitoses in ostoblast ( immature ones will explain later how we can fix this and why this is a benefit for us when paired with romo ) flooding the bone matrix and periosteum with pre ostoblast.
The t3 path way ( catabolic effects ):
One main reason why hyperthyroidism causes bone loss is due to the fact that when Trs ( Trb especially ) it forces a huge release of RANKL and IL-6 this causes a huge release of osteoclast to become hyper active and eat at the bone matrix and the fact that the over activation of erk1/2 and p38 mapk forces pre ostoblast into mitoses while in an immature state not being able to fully mature into ostoblast thus not being about to lay down bone strong structural bone properly they lay down woven bone and the fact that the body tries to stop this over activation of both ostoblast and ostoclast by trying to Inhbit and slow down ostoblast via up regulation of sots and dkk-1 yet it still fails to slow down the osteoblast formation and numbers .
Ok so how do we make sure to not end up with bone loss then from this?
My theory is that these main drugs that cover this :
1: Romo
Romo is a sots anti body we will use this to make up for the fact that sots increases in hyperthyroidism and to stabilise the wnt path way even more and it up regulates survival proteins like ( Bcl-2) and the massive influx of b- catenin from the sots and dkk1 inhbition ( will use a proteasome inhibitor will speak on this later ) will force the immature ostoblast to start maturing and also the Bcl-2 there to neutralises the inflammatory and apoptotic signals caused by over active erk1/2 while also Romo being able to suppress RANKL and increse OPG
2:Abalo
Abalo will be used to force osteoblast to secrete ALP and osteocalcin while also the cAMP spike causes the activation of PKA what then drives the inhibitory phosphorylation of BAD ( pro apoptotic protein ) at the ser 112 site this stops the programmed death of the osteoblast and the stabilisation of again Bcl-2 and Bcl-xl allowing osteoblast to mature and also live for longer and it also prevent the depletion of bcl-2 and bcl-xl via activation of CREB ( camp response binding element ) this down regulate the transcription and the ( bcl-2 and bcl-xl block ) bax thus leading to a decrease of bax proteins available meaning the cell can’t build the pores required for mitochondrial leakage to happen. Also pth hormone has been documented to lower dkk1 mRNA by up to 90% and systemic dkk1 by 20-30% potentially meaning abalo would do the same maybe even more effectively .
3:Brotezobin
Brote ( Brotezobin ) is a proteasome inhibitor this allows the surge of anabolic factors like runx2 and b-catetin to not be broken down by the proteasome while it also down regulates dkk1 and sots further more aiding in osteoblast activity and survival while it also inhibits RANKL via preventing the break down of IkB what then accumulates and locks the NF-kB thus not allowing it to enter the nucleus and stepping the massive surge of RANKL.
4: Cat k inhbition
Odanacatib: is a cat k inhbitor this drug ( I made a post on this if u wanna get to know more about it go read on it ) stops the active enzyme cat k from braking down type I collagen what makes up 90% of bone matrix meaning even if the osteoclast try to eat at the bone they will be unable to dissolve it but not only that but the osteoclast will keep the positive anabolic feed back loop bc of coupling meaning osteoclast will keep secreting anabolic signals like S1P CT-1 Cthrc-1 complement component 3 wnt10 and bmp6 while also not being to degrade the other anabolic compound embedded in the bone matrix like igf-1 bmp2 and ostoecalin.
The combination of all these drugs would prevent the mature death of osteoblasts and the ability for the over activation of ostoclast to destroy thr bomes while keeping the anabolism from over activating the Trs .
And another drug what I made a post about again what could be paired with this for appositional growth is LA ( linoleic acid ) I made a post on it and how it increse periostial bone formation by 220% , increased Cortial thickness by 38% and periostial perimeter by 15% while having 0 effects on Endocortial thickness meaning it’s extremely biast towards the periosteum of bones.
Thank you for reading if u have any questions dm me and we can talk about it also i will start coaching join the dc link in my bio and tag me ( dc user methylated_0 ) or shoot me a dm thanks for reading again and I love you l guys
