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Full hyperthyroidism stack
As in my last hyperthyroidism stack I went over on why and how we can make hyperthyroidism anabolic for appositional growth and what drugs we could use now in this video I’ll be speaking fully on what we can use while on the stack every drug to prevent up regulation of sots or dkk1 or excessive bone resorption and how these drugs synergy together to do this ok.( suggesting reading first post as I go over how we fix some of the issues like osteoblast not maturing etc in detail I’ll go over it again in this post too but not in as much detail on that subject as I already covered it. ) and moderately easy to source.
The main drugs we will use to induce hyperthyroidism:
25mcg t3 4x a day with 150 mcg t4 once a day this will suppress our TSH production thus removing its inhibitory effects on LRP-5 and flk-1 thus up regulating wnt and vefg2/angiogenesis as I mentioned in my first hyperthyroidism post. Now we also have the anabolic effects of t3 such as the up regulation of bmp2 by 1.7 fold and bmp4 by 1.5 fold while also increasing local igf-1 production, expression of fgf1/2 and hyper activation of erk1/2 ( forcing constant mitoses in pre osteoblasts ) enhancing pth anabolism in osteoblast via up regulating PTHr1 and up regulates CXCL12 ( pulls bone marrow stromal cells ) into the surface of bone from the marrow and forces them to differentiate into osteoblasts rather then fat cells .
These are the main ways how hyperthyroidism causes its anabolic effects in bones now I will be listing it’s catabolic effects and how we can prevent them with compounds and doses .
Sots up regulation/ forcing maturation in the pre osteoblast and preventing early apoptosis in osteoblast :
In hyperthyroidism sots production can increase by over 20-30% this happens because the body is trying to prevent bone overgrowth from the hyperactive osteoblast and anabolism caused by hyperthyroidism here I will be listing drugs we can use to supers sots and prevent this break on the anabolism .
Romosozumab: romo is a sots antibody that specifically binds to the wnt inhibitor Sclerostin made by osteocytes to put a break on bone growth . Romo is also been shown to actively decrease RANKL and increase opg thus preventing also the masive over activation of osteoclast caused by hyperthyroidism we even see in a study that I will link below that a sots antibody not only improved the bone formation rate in hyperthyroidic mice by 90% and mineral apposition rate by 20% over a base line level that is already hyper active as hyperthyroidism increases bone formation over normal models by 100-150% as seen in this picture:
The incense in mineral apposition rate suggests that sots antibody was strong enough to force maturation of the pre osteoblast despite the hyperactive erk1/2 and p38 mapk while also preventing early apoptosis in osteoblast by suppressing BAD protein via bcl-2 and bcl-xl up regulation .
50-75% of the recommended dose ( 220 mg being the recommend. ) ( u can also take the full dose as well
)
Dkk1 increase and drugs to inhibit this( as seen in this picture dkk1 increased 20-25% from the sots anti body treatment in hyperthyroidism model ) :
Dkk1 is another wnt inhibitor its its heavily up regulated in hyperthyroidism when treated with a sots inhibitor as this is the seconds line of defence the body will try to use to suppress excessive bone growth when sots is inhibited it’s even seen in real life with romo the gains slow down drastically of room after 6 months of therapy beacons of the up regulation of dkk1 and fully platou by 12 months because of this so inhibition of dkk1 can even not only have huge synergy with the sots down regulation ( 3-4x the gains then with a sots anti body as seen in models ) but also prolong the usage time of romo as the gains won’t plateau by 12 months now because dkk1 will be also suppressed.
Abaloparatide:
Abalo is a pthr1 agonist that specifically caused a sharp brief spike in cAMP thus resulting in the up regulation of PAK what also then caused the inhibitory phosphorylation of BAD thus again preventing pre mature apoptosis and also dives up the production of Blc-2 and blc-xl as well while also lowering Rankl and increasing opg to suppress the massive hyperactive osteoclast caused from hyperthyroidism. But the unique thing I love about abalo is that as seen in this study we see a 90% reduction in dkk-1 mRNA from pth hormone alone.
100-200 mcg ed 100 mcg 2x a day if using 200mcg and 1x if only using 100 mcg
Second drug what we will use to inhibit dkk1 is brotezmin :
Boz is a proteasome inhibiror I have mentioned it a lot in my post as it has the ability to not only suppress sots and dkk1 but also prevent the break down of b-catirin Runx2 sp7 and hif1 but right now we will focus entirely on how it lowers sots and dkk1 as proven by these studies:
Boz also has amazing synergy with a compound called fingolimod I made a whole post dedicated to these 2 synergy effects so If u want full explanation on how they work together check it out but in short summary boz prevent the break down of Runx2 while fingolimod up regulates Runx2 its self . Boz also down regulars Rankl via down regulating NK-Bk and increasing opg. ( note it’s also a potent inhbitor of sots as shown in the study it decreased it by over 50% systemically )
Doses :
Boz needs to be run in a cycle like this
Days 1-4-8-11 then a 10 day break 1.75-2mg on each of those days .
Fingolimod 0.25-0.5mg every day
Tocilizumab:
Tob is a IL-6 inhibitor and a TNF-a down regulator it’s used in rheumatoid arthritis where systemic levels of IL-6 and TNF-a are caused to spike thus resuming in the up regulation of dkk1 this also happens in hyperthyroidism IL-6 and TNF-a massively spike resulting in a up regulation of dkk1 independent of the sots negative feed back loop. Tob has been reported to detect systemic levels of dkk1 by up to 25-31% as seen in this study :
Doses:
100-150 mg subq every other week
Lithium carbonate :
While lithium carbonate doesn’t directly inhibit dkk1 it indirectly prevent its inhibitor actions on b-Catitin by suppressing GSK-3b thus preventing the break down and degradation of b-catitin as one of dkk1s way of suppressing wnt is via up regulation of GSK-3b.
800 mg ed
Roxadustant + dfo+ viagra
I’ve made plenty of posts on roxa and it’s anabolic effects on bone via hif-1/vegf up regulation and it’s positive effects on wnt up regulating by stabilising b-catitin via not only the hif1 stabilisation but also down regulating dkk1 a bit (10-15%).
Dfo is an iron striper meaning it strips iron from ur cells also casing a up regulation in hif1 via mimicimc a low oxygen environment these 2 drugs synergies together super well because Roxadustant strips away the PHD enzyme that lets the vfl protein recognise hif 1/2 and DOF strips away the iron cofactor ( the enzymes needed for vfl to function ) this causes like a massive spike in hif1/2 and mimics a super low oxygen environment and it causes a huge up regulation of wnt and vegf.
While also adding in viagra to mimic the effects of hif-1 up regulation via inhibition of NO-cGMP what would then trigger pro angiogenic genes what up regulation of hif1 would normally do and also up regulating Hif-1 its self via P1TK and mTOR.
Roxa 0.5mg per kg every other day .
Dfo 5-7 mg per kg on days of roxa .
Viagra 50-100 mg ed
( potentially inhibitory effects )
Ghrelin:
Ghrelin has been shown in a study to down regulate dkk-1 but it wasn’t specifically in bones hence why I’m putting it as potentially but from this study it did inhibit dkk-1 just not in bones so take this as with a grain of salt:
Drugs u could use :
Ghrp6/2 150-200 mcg 3x a day
Mk677 25 mg + oral kokatozole and 250 ml grape fruit juice a day to nuke CYP3A4 thus increasing the half life of mk from 6h to 36 ( this also means tbf u can take mk eod )
Another one potentially usable :
Metformin has been shown to also decrease the expression of dkk1 and sots in osteocytes in diabetic mice model ( normally they make more of these catabolic compounds still aplicabile to us as hyperthyroidism also drives this increase as it’s also driven by inflammation stress etc .) thus we can maybe utilise a high dose of Metformin when we’re off boz on the 10 day break ( not even needed to start right on the first day as the boz effects last 3 days) so on the third day of the break we can dose Metformin 750mg 3x a day to have some inhibitory effects on dkk1 as seen in this model:
The massive surge and increase in osteoclast and how we can turn this anabolic:
Cat k inhibition:
I’ve made a detailed post about inhibition of cat k and its powerful effects on bones via preserving the coupling loop ( preserving osteoclast but just inhibiting their ability to break down the matrix of the bone thus leaving us to reap the anabolic effects osteoclast also have by up regulating wnt10,S1P,CT-1,complement compound 3 and Cthrc-1 while also keeping anabolic compounds embedded in the bone matrix and not degrading them like bmp2 igf-1 and ostocalin.
This would also have really good synergy with the fact that hyperthyroidism causes a massive surge in osteoclast recruitment while meaning they can keep pumping out these anabolic path ways and fuel our already over active osteoblast while the osteoclast can’t even break down the bone matrix .
It’s so good at keeping this anabolic synergy that in castrated models of monkeys odn alone increased cortical thickens by up to 21% and a 3.5-6 fold increase in periosteal bone formation even in adult monkeys so we can only imagine how much more the increase in bone formation while keeping in mind everything I said above would be .
Doses ODN: 50 mg 1x a week or 100 mg split in 2 doses per week ( 50 Monday 50 Thursday )
The hgh/igf-1 axis and utilising the increase in the ghr and local igf-1 sensitivity to our advance.
High dose hgh + lantus for way above super physiological levels of igf-1 ( systemic ) and also a huge increase in local igf-1 mRNA by up to 2-4x fold in osteoblast driving proliferation and and maturation by up regulating Runx2 and sp7 while also up regulating mTOR allowing osteoblast to lay down matrix faster and more efficiently while also increasing the survival of osteoblast by down regulating TNF-a expression locally while also the drugs above that we used to suppress dkk1 will also lift this inhibitory effect hgh and igf-1 causes as a way for the body to prevent over growth from them is via up regulation of dkk1.
Doses:
12+ ius ( min ) hgh + 25-30 ius lantus everyday
Or
Oral kokatozole 100 mg and 250 ml grape fruit juice to nuke CYP3A4 while taking 25 mg mk677 ed or eod with 2.5 mg cjc dac 2x a week or 250 mcg cjc no dac 3x a day while also taking if u can’t afford adding in the hg in the stack .
Linoleic acid ( LA) ppra-a/b path way :
I also suggest adding LA to this stack because non of these drugs actually target the ppra-a/b path way enough and it has been proven in rodent models when activated via subq LA injections to not only cause a massive 220% increase in periosteal apposition growth but also 15% periosteal perimeter increase and 38% cortical thickness gains with out any effects on endocortial bone meaning the whole expansions and gains of the bone were pure appositional growth as seen in this photo from the study :
Doses 0.05mg per kg ( 5-6mg ) split into 3-5 doses thru out the day so if u do 6 mg and pin 3 x a day u do 2mg per pin .
The over active PGE2 problem :
Hyperthyroidism also has been shown to overly activate the secretion of PGE2 thus forcing both the over activation of PE2 and PE4 thus boosting both bone formation and re absorption but unfortunately the EP4 de-sensitises way faster and quicker then EP2 due to the structure of the EP2 receptors having less phosphorylation sites thus leading re absorption outpace bone building .
One solution I thought of and is even proven to be anabolic for the periosteum is the usage of low dose flubiprofen . I have spoken about flubiprofen in my other videos but it inhibits PGE2 via inhibiting cox2 and also by trapping it inside the cell by inhibiting the enzyme cpla2a from creating arachidonic acid and also inhibiting the cells ability to push PGE2 into surrounding tissues via blocking MRP4 .
Flubiprofen has also been shown to decrease ostoclast number by having inhbitor effects on NG-Kb via down regulation of TRAF6 while also increasing periosteal bone formation rate by 30-40% as seen in this study:
Doses:
If on any CYP3A4 inhbitor I recommend just 8.5 mg of flubiprofen every 2 days as it would Increse its half life and if not then 5-7x a week . ( potentially use this in cycles such as 2 months on 1-2 months off to not fully supress the huge surge of ostoclasts from the PGE2 activation while also reaping the benefits from its anabolic effects on the months on )
Thanks for reading and remember to follow me on TikTok o have Changes my user from 19nor_abuse to androgen_reap3r
As in my last hyperthyroidism stack I went over on why and how we can make hyperthyroidism anabolic for appositional growth and what drugs we could use now in this video I’ll be speaking fully on what we can use while on the stack every drug to prevent up regulation of sots or dkk1 or excessive bone resorption and how these drugs synergy together to do this ok.( suggesting reading first post as I go over how we fix some of the issues like osteoblast not maturing etc in detail I’ll go over it again in this post too but not in as much detail on that subject as I already covered it. ) and moderately easy to source.
The main drugs we will use to induce hyperthyroidism:
25mcg t3 4x a day with 150 mcg t4 once a day this will suppress our TSH production thus removing its inhibitory effects on LRP-5 and flk-1 thus up regulating wnt and vefg2/angiogenesis as I mentioned in my first hyperthyroidism post. Now we also have the anabolic effects of t3 such as the up regulation of bmp2 by 1.7 fold and bmp4 by 1.5 fold while also increasing local igf-1 production, expression of fgf1/2 and hyper activation of erk1/2 ( forcing constant mitoses in pre osteoblasts ) enhancing pth anabolism in osteoblast via up regulating PTHr1 and up regulates CXCL12 ( pulls bone marrow stromal cells ) into the surface of bone from the marrow and forces them to differentiate into osteoblasts rather then fat cells .
These are the main ways how hyperthyroidism causes its anabolic effects in bones now I will be listing it’s catabolic effects and how we can prevent them with compounds and doses .
Sots up regulation/ forcing maturation in the pre osteoblast and preventing early apoptosis in osteoblast :
In hyperthyroidism sots production can increase by over 20-30% this happens because the body is trying to prevent bone overgrowth from the hyperactive osteoblast and anabolism caused by hyperthyroidism here I will be listing drugs we can use to supers sots and prevent this break on the anabolism .
Romosozumab: romo is a sots antibody that specifically binds to the wnt inhibitor Sclerostin made by osteocytes to put a break on bone growth . Romo is also been shown to actively decrease RANKL and increase opg thus preventing also the masive over activation of osteoclast caused by hyperthyroidism we even see in a study that I will link below that a sots antibody not only improved the bone formation rate in hyperthyroidic mice by 90% and mineral apposition rate by 20% over a base line level that is already hyper active as hyperthyroidism increases bone formation over normal models by 100-150% as seen in this picture:
The incense in mineral apposition rate suggests that sots antibody was strong enough to force maturation of the pre osteoblast despite the hyperactive erk1/2 and p38 mapk while also preventing early apoptosis in osteoblast by suppressing BAD protein via bcl-2 and bcl-xl up regulation .
50-75% of the recommended dose ( 220 mg being the recommend. ) ( u can also take the full dose as well
) Dkk1 increase and drugs to inhibit this( as seen in this picture dkk1 increased 20-25% from the sots anti body treatment in hyperthyroidism model ) :
Dkk1 is another wnt inhibitor its its heavily up regulated in hyperthyroidism when treated with a sots inhibitor as this is the seconds line of defence the body will try to use to suppress excessive bone growth when sots is inhibited it’s even seen in real life with romo the gains slow down drastically of room after 6 months of therapy beacons of the up regulation of dkk1 and fully platou by 12 months because of this so inhibition of dkk1 can even not only have huge synergy with the sots down regulation ( 3-4x the gains then with a sots anti body as seen in models ) but also prolong the usage time of romo as the gains won’t plateau by 12 months now because dkk1 will be also suppressed.
Abaloparatide:
Abalo is a pthr1 agonist that specifically caused a sharp brief spike in cAMP thus resulting in the up regulation of PAK what also then caused the inhibitory phosphorylation of BAD thus again preventing pre mature apoptosis and also dives up the production of Blc-2 and blc-xl as well while also lowering Rankl and increasing opg to suppress the massive hyperactive osteoclast caused from hyperthyroidism. But the unique thing I love about abalo is that as seen in this study we see a 90% reduction in dkk-1 mRNA from pth hormone alone.
100-200 mcg ed 100 mcg 2x a day if using 200mcg and 1x if only using 100 mcg
Second drug what we will use to inhibit dkk1 is brotezmin :
Boz is a proteasome inhibiror I have mentioned it a lot in my post as it has the ability to not only suppress sots and dkk1 but also prevent the break down of b-catirin Runx2 sp7 and hif1 but right now we will focus entirely on how it lowers sots and dkk1 as proven by these studies:
Boz also has amazing synergy with a compound called fingolimod I made a whole post dedicated to these 2 synergy effects so If u want full explanation on how they work together check it out but in short summary boz prevent the break down of Runx2 while fingolimod up regulates Runx2 its self . Boz also down regulars Rankl via down regulating NK-Bk and increasing opg. ( note it’s also a potent inhbitor of sots as shown in the study it decreased it by over 50% systemically )
Doses :
Boz needs to be run in a cycle like this
Days 1-4-8-11 then a 10 day break 1.75-2mg on each of those days .
Fingolimod 0.25-0.5mg every day
Tocilizumab:
Tob is a IL-6 inhibitor and a TNF-a down regulator it’s used in rheumatoid arthritis where systemic levels of IL-6 and TNF-a are caused to spike thus resuming in the up regulation of dkk1 this also happens in hyperthyroidism IL-6 and TNF-a massively spike resulting in a up regulation of dkk1 independent of the sots negative feed back loop. Tob has been reported to detect systemic levels of dkk1 by up to 25-31% as seen in this study :
Doses:
100-150 mg subq every other week
Lithium carbonate :
While lithium carbonate doesn’t directly inhibit dkk1 it indirectly prevent its inhibitor actions on b-Catitin by suppressing GSK-3b thus preventing the break down and degradation of b-catitin as one of dkk1s way of suppressing wnt is via up regulation of GSK-3b.
800 mg ed
Roxadustant + dfo+ viagra
I’ve made plenty of posts on roxa and it’s anabolic effects on bone via hif-1/vegf up regulation and it’s positive effects on wnt up regulating by stabilising b-catitin via not only the hif1 stabilisation but also down regulating dkk1 a bit (10-15%).
Dfo is an iron striper meaning it strips iron from ur cells also casing a up regulation in hif1 via mimicimc a low oxygen environment these 2 drugs synergies together super well because Roxadustant strips away the PHD enzyme that lets the vfl protein recognise hif 1/2 and DOF strips away the iron cofactor ( the enzymes needed for vfl to function ) this causes like a massive spike in hif1/2 and mimics a super low oxygen environment and it causes a huge up regulation of wnt and vegf.
While also adding in viagra to mimic the effects of hif-1 up regulation via inhibition of NO-cGMP what would then trigger pro angiogenic genes what up regulation of hif1 would normally do and also up regulating Hif-1 its self via P1TK and mTOR.
Roxa 0.5mg per kg every other day .
Dfo 5-7 mg per kg on days of roxa .
Viagra 50-100 mg ed
( potentially inhibitory effects )
Ghrelin:
Ghrelin has been shown in a study to down regulate dkk-1 but it wasn’t specifically in bones hence why I’m putting it as potentially but from this study it did inhibit dkk-1 just not in bones so take this as with a grain of salt:
Drugs u could use :
Ghrp6/2 150-200 mcg 3x a day
Mk677 25 mg + oral kokatozole and 250 ml grape fruit juice a day to nuke CYP3A4 thus increasing the half life of mk from 6h to 36 ( this also means tbf u can take mk eod )
Another one potentially usable :
Metformin has been shown to also decrease the expression of dkk1 and sots in osteocytes in diabetic mice model ( normally they make more of these catabolic compounds still aplicabile to us as hyperthyroidism also drives this increase as it’s also driven by inflammation stress etc .) thus we can maybe utilise a high dose of Metformin when we’re off boz on the 10 day break ( not even needed to start right on the first day as the boz effects last 3 days) so on the third day of the break we can dose Metformin 750mg 3x a day to have some inhibitory effects on dkk1 as seen in this model:
The massive surge and increase in osteoclast and how we can turn this anabolic:
Cat k inhibition:
I’ve made a detailed post about inhibition of cat k and its powerful effects on bones via preserving the coupling loop ( preserving osteoclast but just inhibiting their ability to break down the matrix of the bone thus leaving us to reap the anabolic effects osteoclast also have by up regulating wnt10,S1P,CT-1,complement compound 3 and Cthrc-1 while also keeping anabolic compounds embedded in the bone matrix and not degrading them like bmp2 igf-1 and ostocalin.
This would also have really good synergy with the fact that hyperthyroidism causes a massive surge in osteoclast recruitment while meaning they can keep pumping out these anabolic path ways and fuel our already over active osteoblast while the osteoclast can’t even break down the bone matrix .
It’s so good at keeping this anabolic synergy that in castrated models of monkeys odn alone increased cortical thickens by up to 21% and a 3.5-6 fold increase in periosteal bone formation even in adult monkeys so we can only imagine how much more the increase in bone formation while keeping in mind everything I said above would be .
Doses ODN: 50 mg 1x a week or 100 mg split in 2 doses per week ( 50 Monday 50 Thursday )
The hgh/igf-1 axis and utilising the increase in the ghr and local igf-1 sensitivity to our advance.
High dose hgh + lantus for way above super physiological levels of igf-1 ( systemic ) and also a huge increase in local igf-1 mRNA by up to 2-4x fold in osteoblast driving proliferation and and maturation by up regulating Runx2 and sp7 while also up regulating mTOR allowing osteoblast to lay down matrix faster and more efficiently while also increasing the survival of osteoblast by down regulating TNF-a expression locally while also the drugs above that we used to suppress dkk1 will also lift this inhibitory effect hgh and igf-1 causes as a way for the body to prevent over growth from them is via up regulation of dkk1.
Doses:
12+ ius ( min ) hgh + 25-30 ius lantus everyday
Or
Oral kokatozole 100 mg and 250 ml grape fruit juice to nuke CYP3A4 while taking 25 mg mk677 ed or eod with 2.5 mg cjc dac 2x a week or 250 mcg cjc no dac 3x a day while also taking if u can’t afford adding in the hg in the stack .
Linoleic acid ( LA) ppra-a/b path way :
I also suggest adding LA to this stack because non of these drugs actually target the ppra-a/b path way enough and it has been proven in rodent models when activated via subq LA injections to not only cause a massive 220% increase in periosteal apposition growth but also 15% periosteal perimeter increase and 38% cortical thickness gains with out any effects on endocortial bone meaning the whole expansions and gains of the bone were pure appositional growth as seen in this photo from the study :
Doses 0.05mg per kg ( 5-6mg ) split into 3-5 doses thru out the day so if u do 6 mg and pin 3 x a day u do 2mg per pin .
The over active PGE2 problem :
Hyperthyroidism also has been shown to overly activate the secretion of PGE2 thus forcing both the over activation of PE2 and PE4 thus boosting both bone formation and re absorption but unfortunately the EP4 de-sensitises way faster and quicker then EP2 due to the structure of the EP2 receptors having less phosphorylation sites thus leading re absorption outpace bone building .
One solution I thought of and is even proven to be anabolic for the periosteum is the usage of low dose flubiprofen . I have spoken about flubiprofen in my other videos but it inhibits PGE2 via inhibiting cox2 and also by trapping it inside the cell by inhibiting the enzyme cpla2a from creating arachidonic acid and also inhibiting the cells ability to push PGE2 into surrounding tissues via blocking MRP4 .
Flubiprofen has also been shown to decrease ostoclast number by having inhbitor effects on NG-Kb via down regulation of TRAF6 while also increasing periosteal bone formation rate by 30-40% as seen in this study:
Doses:
If on any CYP3A4 inhbitor I recommend just 8.5 mg of flubiprofen every 2 days as it would Increse its half life and if not then 5-7x a week . ( potentially use this in cycles such as 2 months on 1-2 months off to not fully supress the huge surge of ostoclasts from the PGE2 activation while also reaping the benefits from its anabolic effects on the months on )
Thanks for reading and remember to follow me on TikTok o have Changes my user from 19nor_abuse to androgen_reap3r
I’m genuinely to lazy to fix it I’ll unironically pay ppl 20% of my coaching shit if they help me format better
