[CENTER]
[FONT=Times New Roman][SIZE=26px][B][COLOR=rgb(84, 172, 210)]FULL HYPERTHYROIDISM STACK[/COLOR][/B][/SIZE][/FONT]
[SIZE=18px][B]Turning a hyperthyroid bone-remodelling state anabolic[/B][/SIZE]
[SIZE=15px][I]Sclerostin • DKK1 • osteoclast coupling • HIF-1/VEGF • IGF-1 • PGE2[/I][/SIZE]
[/CENTER]

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[QUOTE]
[B]READ FIRST:[/B] This is a continuation of my first hyperthyroidism post. That post explains the base theory—including the osteoblast-maturation problem—in greater detail. This chapter focuses on the full stack: the compounds intended to counter SOST/sclerostin, DKK1, excessive bone resorption and the other negative-feedback mechanisms triggered by hyperthyroidism.
[/QUOTE]

[I]Formatting-only reconstruction: the claims and doses below are preserved from the original post and have not been independently verified. Every “[INSERT STUDY]” or “[INSERT FIGURE]” marker should be replaced before publishing.[/I]

[SPOILER="Click to expand — Table of Contents"]
[LIST=1]
[*]The central thesis
[*]Core thyroid induction
[*]Blocking SOST / sclerostin
[*]Blocking DKK1
[*]Turning the osteoclast surge anabolic
[*]Exploiting the GH / IGF-1 axis
[*]Adding the PPAR-α/β pathway
[*]Controlling excess PGE2 signalling
[*]Consolidated compound list
[*]Studies and figures
[/LIST]
[/SPOILER]

[HR][/HR]

[CENTER][SIZE=22px][B][COLOR=rgb(250, 197, 28)]THE STACK IN ONE TABLE[/COLOR][/B][/SIZE][/CENTER]

[TABLE=collapse,center,alternate]
[TR]
[TH]Bottleneck[/TH]
[TH]Intervention discussed[/TH]
[TH]Intended effect[/TH]
[/TR]
[TR]
[TD]Core anabolic stimulus[/TD]
[TD]T3 + T4[/TD]
[TD]Suppress TSH; increase BMP, IGF-1, FGF, ERK1/2, CXCL12 and angiogenic signalling[/TD]
[/TR]
[TR]
[TD]SOST / sclerostin feedback[/TD]
[TD]Romosozumab[/TD]
[TD]Release Wnt signalling while shifting RANKL/OPG toward lower resorption[/TD]
[/TR]
[TR]
[TD]DKK1 compensation[/TD]
[TD]Abaloparatide, bortezomib, tocilizumab, lithium[/TD]
[TD]Reduce DKK1 or preserve downstream β-catenin signalling[/TD]
[/TR]
[TR]
[TD]Hypoxia / angiogenesis axis[/TD]
[TD]Roxadustat + DFO + sildenafil[/TD]
[TD]Amplify HIF-1/2, VEGF and Wnt-related signalling[/TD]
[/TR]
[TR]
[TD]Osteoclast-driven matrix loss[/TD]
[TD]Odanacatib[/TD]
[TD]Preserve osteoclast coupling signals while inhibiting cathepsin-K-mediated degradation[/TD]
[/TR]
[TR]
[TD]GH / IGF-1 sensitivity[/TD]
[TD]HGH + insulin, or secretagogue alternative[/TD]
[TD]Increase systemic and local IGF-1 signalling[/TD]
[/TR]
[TR]
[TD]Underused PPAR-α/β pathway[/TD]
[TD]Linoleic acid[/TD]
[TD]Drive periosteal apposition[/TD]
[/TR]
[TR]
[TD]Excess PGE2 / EP4 desensitisation[/TD]
[TD]Low-dose flurbiprofen[/TD]
[TD]Reduce the resorptive side of the PGE2 response[/TD]
[/TR]
[/TABLE]

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[SIZE=22px][B][COLOR=rgb(84, 172, 210)]1. THE CENTRAL THESIS[/COLOR][/B][/SIZE]

Hyperthyroidism does not simply “destroy bone.” It creates an extremely high-turnover environment: bone formation rises, but bone resorption and compensatory inhibitors rise with it.

The thesis of this stack is therefore:

[LIST]
[*][B]Create the anabolic stimulus[/B] with thyroid hormone.
[*][B]Remove the brakes[/B] imposed by SOST/sclerostin and DKK1.
[*][B]Preserve osteoclast-derived coupling signals[/B] while limiting the osteoclast’s ability to degrade bone matrix.
[*][B]Exploit the resulting sensitivity[/B] to HIF-1/VEGF, PTH, GH/IGF-1 and PPAR signalling.
[/LIST]

[CENTER][SIZE=18px][B]In short: accelerate turnover, preserve the formation signal, and block the pathways that make resorption win.[/B][/SIZE][/CENTER]

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[SPOILER="2. Core thyroid induction — T3 + T4"]
[SIZE=18px][B][COLOR=rgb(250, 197, 28)]THE BASE STIMULUS[/COLOR][/B][/SIZE]

The proposed thyroid base is intended to suppress TSH production, removing its claimed inhibitory effects on LRP5 and FLK-1 and thereby increasing Wnt and VEGF/angiogenic signalling.

[B]The anabolic effects attributed to T3 in the original post include:[/B]

[LIST]
[*]BMP2 upregulation of approximately [B]1.7-fold[/B].
[*]BMP4 upregulation of approximately [B]1.5-fold[/B].
[*]Increased local IGF-1 production.
[*]Increased FGF1/FGF2 expression.
[*]Hyperactivation of ERK1/2, driving continued mitosis in pre-osteoblasts.
[*]Greater PTH anabolism through PTHR1 upregulation.
[*]CXCL12 upregulation, drawing bone-marrow stromal cells toward the bone surface and favouring osteoblast rather than adipocyte differentiation.
[/LIST]

[QUOTE]
[B][COLOR=rgb(250, 197, 28)]Dose stated in the original:[/COLOR][/B]
[LIST]
[*]T3: 25 mcg, four times daily.
[*]T4: 150 mcg, once daily.
[/LIST]
[/QUOTE]

[B]The problem:[/B] this anabolic signalling is accompanied by increased SOST, DKK1, osteoclast recruitment and PGE2-driven resorption. The remainder of the stack is designed around those liabilities.
[/SPOILER]

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[SPOILER="3. Blocking SOST / sclerostin — Romosozumab"]
[SIZE=18px][B][COLOR=rgb(250, 197, 28)]THE FIRST NEGATIVE-FEEDBACK BRAKE[/COLOR][/B][/SIZE]

In the proposed model, hyperthyroidism raises SOST production by more than 20–30%. This is interpreted as a compensatory attempt to restrain the hyperactive osteoblast and prevent excessive bone growth.

[B]Romosozumab[/B] is a monoclonal antibody against sclerostin, the osteocyte-derived Wnt inhibitor encoded by SOST. The post argues that romosozumab would do two useful things simultaneously:

[LIST]
[*]Release the sclerostin brake on Wnt-mediated bone formation.
[*]Reduce RANKL and increase OPG, limiting the hyperthyroidism-induced rise in osteoclast activity.
[/LIST]

The cited hyperthyroid-mouse model reportedly showed that a sclerostin antibody produced:

[LIST]
[*]Approximately [B]90% greater bone-formation rate[/B].
[*]Approximately [B]20% greater mineral-apposition rate[/B] over an already hyperactive baseline.
[/LIST]

[CENTER][B][COLOR=rgb(184, 49, 47)]［ INSERT SCLEROSTIN-ANTIBODY FIGURE HERE ］[/COLOR][/B][/CENTER]

The increased mineral-apposition rate is interpreted as evidence that sclerostin inhibition can push pre-osteoblasts toward maturation despite hyperactive ERK1/2 and p38 MAPK. The post also proposes reduced early osteoblast apoptosis through BAD suppression and BCL-2/BCL-XL upregulation.

[QUOTE]
[B][COLOR=rgb(250, 197, 28)]Dose stated in the original:[/COLOR][/B] 50–75% of the standard 220 mg dose, with the full dose also presented as an option.
[/QUOTE]

[B]However:[/B] once sclerostin is suppressed, DKK1 becomes the next major compensatory brake.
[/SPOILER]

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[SPOILER="4. Blocking DKK1 — the main compensatory layer"]
[SIZE=18px][B][COLOR=rgb(250, 197, 28)]WHY ROMOSOZUMAB ALONE PLATEAUS[/COLOR][/B][/SIZE]

DKK1 is another Wnt inhibitor. In the model described here, DKK1 rises by roughly 20–25% after sclerostin-antibody treatment, acting as the body’s second line of defence against excessive bone growth.

This is used to explain why romosozumab gains slow after roughly six months and plateau by twelve months. The post argues that combined SOST and DKK1 suppression could both magnify the effect and extend the useful window.

[CENTER][B][COLOR=rgb(184, 49, 47)]［ INSERT DKK1-COMPENSATION FIGURE HERE ］[/COLOR][/B][/CENTER]

[SIZE=18px][B][COLOR=rgb(84, 172, 210)]4.1 — Abaloparatide[/COLOR][/B][/SIZE]

Abaloparatide is presented as a PTHR1 agonist producing a sharp, brief cAMP spike. The proposed chain is:

[CENTER][B]PTHR1 → cAMP → PAK → inhibitory BAD phosphorylation → increased BCL-2 / BCL-XL[/B][/CENTER]

The intended outcomes are reduced premature osteoblast apoptosis, reduced RANKL, increased OPG and suppression of hyperactive osteoclast activity. The key claim is that PTH signalling reduced DKK1 mRNA by approximately [B]90%[/B] in the cited study.

[QUOTE]
[B][COLOR=rgb(250, 197, 28)]Dose stated in the original:[/COLOR][/B] 100–200 mcg daily; if using 200 mcg, split into 100 mcg twice daily.
[/QUOTE]

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[SIZE=18px][B][COLOR=rgb(84, 172, 210)]4.2 — Bortezomib + fingolimod[/COLOR][/B][/SIZE]

[B]Bortezomib[/B] is a proteasome inhibitor proposed to:

[LIST]
[*]Suppress SOST and DKK1.
[*]Prevent degradation of β-catenin, RUNX2, SP7 and HIF-1.
[*]Reduce RANKL through NF-κB downregulation.
[*]Increase OPG.
[/LIST]

The post cites a greater than 50% systemic reduction in SOST. Its proposed synergy with [B]fingolimod[/B] is straightforward: bortezomib prevents RUNX2 breakdown while fingolimod increases RUNX2 expression.

[QUOTE]
[B][COLOR=rgb(250, 197, 28)]Doses stated in the original:[/COLOR][/B]
[LIST]
[*]Bortezomib: 1.75–2 mg on days 1, 4, 8 and 11, followed by a ten-day break.
[*]Fingolimod: 0.25–0.5 mg daily.
[/LIST]
[/QUOTE]

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[SIZE=18px][B][COLOR=rgb(84, 172, 210)]4.3 — Tocilizumab[/COLOR][/B][/SIZE]

Tocilizumab is an IL-6 receptor inhibitor that also reduces downstream TNF-α signalling. The rationale is that hyperthyroidism raises IL-6 and TNF-α, increasing DKK1 independently of the SOST feedback loop.

The cited rheumatoid-arthritis data reportedly show a [B]25–31% reduction in systemic DKK1[/B].

[QUOTE]
[B][COLOR=rgb(250, 197, 28)]Dose stated in the original:[/COLOR][/B] 100–150 mg subcutaneously every other week.
[/QUOTE]

[HR][/HR]

[SIZE=18px][B][COLOR=rgb(84, 172, 210)]4.4 — Lithium carbonate[/COLOR][/B][/SIZE]

Lithium is not presented as a direct DKK1 inhibitor. Instead, it is intended to suppress GSK-3β and thereby prevent degradation of β-catenin—partially bypassing DKK1’s downstream inhibition of Wnt signalling.

[QUOTE]
[B][COLOR=rgb(250, 197, 28)]Dose stated in the original:[/COLOR][/B] 800 mg daily.
[/QUOTE]

[HR][/HR]

[SIZE=18px][B][COLOR=rgb(84, 172, 210)]4.5 — Roxadustat + DFO + sildenafil[/COLOR][/B][/SIZE]

This combination targets the HIF/VEGF axis from three directions:

[LIST=1]
[*][B]Roxadustat[/B] inhibits prolyl-hydroxylase-domain enzymes, interfering with VHL-mediated recognition and degradation of HIF-1/2.
[*][B]Deferoxamine (DFO)[/B] chelates the iron cofactor required by those enzymes, further mimicking a low-oxygen environment.
[*][B]Sildenafil[/B] increases NO–cGMP signalling, reproducing part of the pro-angiogenic response associated with HIF-1 activation and potentially increasing HIF-1 through PI3K/AKT and mTOR.
[/LIST]

The intended result is a large rise in HIF-1/2, VEGF, angiogenesis and Wnt signalling, with roxadustat also claimed to reduce DKK1 by approximately 10–15%.

[QUOTE]
[B][COLOR=rgb(250, 197, 28)]Doses stated in the original:[/COLOR][/B]
[LIST]
[*]Roxadustat: 0.5 mg/kg every other day.
[*]DFO: 5–7 mg/kg on roxadustat days.
[*]Sildenafil: 50–100 mg daily.
[/LIST]
[/QUOTE]

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[SIZE=18px][B][COLOR=rgb(184, 49, 47)]4.6 — Lower-confidence additions[/COLOR][/B][/SIZE]

[B]Ghrelin signalling:[/B] A cited study reportedly found DKK1 downregulation outside bone tissue. Because it was not a bone model, the post correctly treats this as speculative.

[QUOTE]
[B][COLOR=rgb(250, 197, 28)]Doses stated in the original:[/COLOR][/B]
[LIST]
[*]GHRP-6 or GHRP-2: 150–200 mcg, three times daily.
[*]MK-677: 25 mg, combined with oral ketoconazole and 250 mL grapefruit juice to inhibit CYP3A4 and extend exposure; every-other-day use is proposed.
[/LIST]
[/QUOTE]

[B]Metformin:[/B] Diabetic-mouse data reportedly show reduced DKK1 and SOST expression in osteocytes. The proposed use is during bortezomib’s ten-day break, beginning around day three because the bortezomib effect is claimed to persist for several days.

[QUOTE]
[B][COLOR=rgb(250, 197, 28)]Dose stated in the original:[/COLOR][/B] 750 mg, three times daily during the off-period.
[/QUOTE]
[/SPOILER]

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[SPOILER="5. Turning the osteoclast surge anabolic — Cathepsin-K inhibition"]
[SIZE=18px][B][COLOR=rgb(250, 197, 28)]PRESERVE THE COUPLING LOOP; BLOCK MATRIX DEGRADATION[/COLOR][/B][/SIZE]

Hyperthyroidism recruits large numbers of osteoclasts. Rather than eliminating them, the proposed strategy is to inhibit [B]cathepsin K[/B]: preserve the osteoclast and its anabolic coupling signals while reducing its ability to digest bone matrix.

[B]Coupling signals the post aims to preserve include:[/B]

[LIST]
[*]WNT10B
[*]S1P
[*]CT-1
[*]Complement component 3
[*]CTHRC1
[/LIST]

At the same time, inhibiting matrix degradation is proposed to retain anabolic factors embedded in bone, including BMP2, IGF-1 and osteocalcin.

[B]Odanacatib (ODN)[/B] is the cathepsin-K inhibitor proposed for this role. In castrated adult-monkey models, the original post cites:

[LIST]
[*]Up to [B]21% greater cortical thickness[/B].
[*]A [B]3.5–6-fold increase in periosteal bone formation[/B].
[/LIST]

[CENTER][B][COLOR=rgb(184, 49, 47)]［ INSERT ODANACATIB / MONKEY-MODEL FIGURE HERE ］[/COLOR][/B][/CENTER]

[QUOTE]
[B][COLOR=rgb(250, 197, 28)]Dose stated in the original:[/COLOR][/B] 50 mg once weekly, or 100 mg weekly split into 50 mg Monday and 50 mg Thursday.
[/QUOTE]

[CENTER][SIZE=18px][B]The intended synergy: more osteoclast recruitment → more coupling signals → more fuel for hyperactive osteoblasts, without equivalent matrix breakdown.[/B][/SIZE][/CENTER]
[/SPOILER]

[HR][/HR]

[SPOILER="6. Exploiting the GH / IGF-1 axis"]
[SIZE=18px][B][COLOR=rgb(250, 197, 28)]USE THE INCREASED GHR AND LOCAL IGF-1 SENSITIVITY[/COLOR][/B][/SIZE]

The post proposes high-dose HGH plus long-acting insulin to produce supraphysiological systemic IGF-1 alongside a claimed two- to four-fold increase in local IGF-1 mRNA in osteoblasts.

[B]The intended downstream effects are:[/B]

[LIST]
[*]Greater osteoblast proliferation and maturation through RUNX2 and SP7.
[*]Increased mTOR activity, allowing faster matrix deposition.
[*]Greater osteoblast survival through reduced local TNF-α expression.
[*]Less DKK1-mediated resistance because the preceding compounds are intended to suppress that feedback pathway.
[/LIST]

[QUOTE]
[B][COLOR=rgb(250, 197, 28)]Primary doses stated in the original:[/COLOR][/B]
[LIST]
[*]HGH: at least 12 IU daily.
[*]Insulin glargine: 25–30 IU daily.
[/LIST]
[/QUOTE]

[B]Lower-cost secretagogue alternative stated in the original:[/B]

[LIST]
[*]MK-677: 25 mg daily or every other day.
[*]Ketoconazole: 100 mg orally.
[*]Grapefruit juice: 250 mL.
[*]CJC-1295 DAC: 2.5 mg twice weekly; [B]or[/B]
[*]CJC without DAC: 250 mcg three times daily.
[/LIST]
[/SPOILER]

[HR][/HR]

[SPOILER="7. Adding the PPAR-α/β pathway — Linoleic acid"]
[SIZE=18px][B][COLOR=rgb(250, 197, 28)]A PATHWAY THE REST OF THE STACK DOES NOT DIRECTLY COVER[/COLOR][/B][/SIZE]

Linoleic acid (LA) is included because the remaining compounds do not substantially target the PPAR-α/β pathway.

In the cited rodent model, subcutaneous LA reportedly produced:

[LIST]
[*]A [B]220% increase in periosteal apposition[/B].
[*]A [B]15% increase in periosteal perimeter[/B].
[*]A [B]38% increase in cortical thickness[/B].
[*]No measured effect on endocortical bone—interpreted as predominantly appositional expansion.
[/LIST]

[CENTER][B][COLOR=rgb(184, 49, 47)]［ INSERT LINOLEIC-ACID STUDY FIGURE HERE ］[/COLOR][/B][/CENTER]

[QUOTE]
[B][COLOR=rgb(250, 197, 28)]Dose stated in the original:[/COLOR][/B] 0.05 mg/kg—approximately 5–6 mg—split into three to five injections throughout the day. At 6 mg over three injections, that would be 2 mg per injection.
[/QUOTE]
[/SPOILER]

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[SPOILER="8. Controlling excess PGE2 signalling — Flurbiprofen"]
[SIZE=18px][B][COLOR=rgb(250, 197, 28)]THE EP2 / EP4 DESENSITISATION PROBLEM[/COLOR][/B][/SIZE]

Hyperthyroidism is claimed to increase PGE2 secretion, activating both EP2 and EP4 and initially increasing both bone formation and resorption.

The proposed problem is that EP4 desensitises faster than EP2 because of differences in receptor phosphorylation sites. Resorption can therefore begin to outpace formation.

[B]Low-dose flurbiprofen[/B] is proposed as the countermeasure. The mechanisms listed in the original are:

[LIST]
[*]COX-2 inhibition, reducing PGE2 production.
[*]cPLA2α inhibition, reducing arachidonic-acid generation.
[*]MRP4 inhibition, reducing export of PGE2 into surrounding tissue.
[*]Reduced osteoclast number through TRAF6 / NF-κB downregulation.
[/LIST]

The cited study reportedly showed a [B]30–40% increase in periosteal bone-formation rate[/B].

[CENTER][B][COLOR=rgb(184, 49, 47)]［ INSERT FLURBIPROFEN STUDY FIGURE HERE ］[/COLOR][/B][/CENTER]

[QUOTE]
[B][COLOR=rgb(250, 197, 28)]Dose stated in the original:[/COLOR][/B]
[LIST]
[*]With a CYP3A4 inhibitor: 8.5 mg every two days.
[*]Without one: 5–7 doses weekly.
[*]A possible cycle proposed in the original: two months on, followed by one to two months off.
[/LIST]
[/QUOTE]

The cycling idea is intended to avoid permanently suppressing the osteoclast surge while still capturing the proposed periosteal benefit during treatment periods.
[/SPOILER]

[HR][/HR]

[SPOILER="9. Consolidated compound list — click to expand"]
[TABLE=collapse,center,alternate]
[TR]
[TH]Layer[/TH]
[TH]Compound(s)[/TH]
[TH]Schedule stated in original[/TH]
[/TR]
[TR]
[TD]Thyroid base[/TD]
[TD]T3 + T4[/TD]
[TD]T3 25 mcg four times daily; T4 150 mcg daily[/TD]
[/TR]
[TR]
[TD]Sclerostin[/TD]
[TD]Romosozumab[/TD]
[TD]50–75% of 220 mg; full dose also proposed[/TD]
[/TR]
[TR]
[TD]PTH / DKK1[/TD]
[TD]Abaloparatide[/TD]
[TD]100–200 mcg daily[/TD]
[/TR]
[TR]
[TD]Proteasome / RUNX2[/TD]
[TD]Bortezomib + fingolimod[/TD]
[TD]1.75–2 mg days 1/4/8/11, then ten days off; fingolimod 0.25–0.5 mg daily[/TD]
[/TR]
[TR]
[TD]IL-6 / DKK1[/TD]
[TD]Tocilizumab[/TD]
[TD]100–150 mg subcutaneously every other week[/TD]
[/TR]
[TR]
[TD]GSK-3β[/TD]
[TD]Lithium carbonate[/TD]
[TD]800 mg daily[/TD]
[/TR]
[TR]
[TD]HIF / VEGF[/TD]
[TD]Roxadustat + DFO + sildenafil[/TD]
[TD]0.5 mg/kg EOD; 5–7 mg/kg on matching days; 50–100 mg daily[/TD]
[/TR]
[TR]
[TD]Cathepsin K[/TD]
[TD]Odanacatib[/TD]
[TD]50 mg weekly, or 50 mg twice weekly[/TD]
[/TR]
[TR]
[TD]GH / IGF-1[/TD]
[TD]HGH + insulin glargine[/TD]
[TD]At least 12 IU HGH + 25–30 IU insulin daily[/TD]
[/TR]
[TR]
[TD]PPAR-α/β[/TD]
[TD]Linoleic acid[/TD]
[TD]0.05 mg/kg split across three to five daily injections[/TD]
[/TR]
[TR]
[TD]PGE2[/TD]
[TD]Flurbiprofen[/TD]
[TD]8.5 mg EOD with CYP3A4 inhibition, otherwise 5–7 doses weekly[/TD]
[/TR]
[/TABLE]
[/SPOILER]

[HR][/HR]

[SPOILER="10. Studies and figures — REQUIRED BEFORE POSTING"]
[LIST=1]
[*]T3 effects on BMP2, BMP4, IGF-1, FGF1/2, ERK1/2, PTHR1 and CXCL12 — [B][COLOR=rgb(184, 49, 47)]INSERT LINKS[/COLOR][/B]
[*]Hyperthyroid-mouse sclerostin-antibody model — [B][COLOR=rgb(184, 49, 47)]INSERT LINK + FIGURE[/COLOR][/B]
[*]DKK1 increase after sclerostin inhibition — [B][COLOR=rgb(184, 49, 47)]INSERT LINK + FIGURE[/COLOR][/B]
[*]PTH / abaloparatide effect on DKK1 mRNA — [B][COLOR=rgb(184, 49, 47)]INSERT LINK[/COLOR][/B]
[*]Bortezomib effects on SOST, DKK1, RUNX2, SP7, HIF-1 and RANKL/OPG — [B][COLOR=rgb(184, 49, 47)]INSERT LINKS[/COLOR][/B]
[*]Tocilizumab effect on systemic DKK1 — [B][COLOR=rgb(184, 49, 47)]INSERT LINK[/COLOR][/B]
[*]Roxadustat + DFO HIF/VEGF rationale — [B][COLOR=rgb(184, 49, 47)]INSERT LINKS[/COLOR][/B]
[*]Odanacatib adult-monkey cortical/periosteal data — [B][COLOR=rgb(184, 49, 47)]INSERT LINK + FIGURE[/COLOR][/B]
[*]Linoleic-acid periosteal-apposition study — [B][COLOR=rgb(184, 49, 47)]INSERT LINK + FIGURE[/COLOR][/B]
[*]Flurbiprofen periosteal-bone-formation study — [B][COLOR=rgb(184, 49, 47)]INSERT LINK + FIGURE[/COLOR][/B]
[/LIST]
[/SPOILER]

[HR][/HR]

[CENTER]
[SIZE=18px][B][COLOR=rgb(84, 172, 210)]THE ENTIRE IDEA IN ONE SENTENCE[/COLOR][/B][/SIZE]

[B]Use thyroid hormone to create extreme bone turnover; suppress SOST and DKK1; preserve osteoclast coupling while blocking matrix degradation; then exploit HIF/VEGF, GH/IGF-1, PPAR and PGE2 signalling to bias that turnover toward appositional growth.[/B]

[SIZE=15px]Thanks for reading.[/SIZE]
[SIZE=15px]TikTok: [B]@androgen_reap3r[/B] — formerly [B]@19nor_abuse[/B][/SIZE]
[/CENTER]