Framemaxxing(high effort) trust me gtfih


before starting lets get the copes out of the way
only for the bone/clavicle


▸ WHY 95% OF FRAMEMAXXING ADVICE IS COPE

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i went through actual medical papers on pubmed, every major framemaxxing thread on here, and im gonna break down whats real and whats pure cope. most of you (dumbasses) arent gonna like hearing that your main coping mechanism isnt gonna work (looking at you greys)

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❖ who is this guide for

if your growth plates are CLOSED (25+, or confirmed fused on imaging) then the pharma section is irrelevant to you. your only real option is surgery. if your plates are still OPEN (under 23-25, specifically the medial clavicular physis) then the compounds section is where the theoretical possibilities live. i will make it clear which sections apply to which situation.


▸ THE ONE THING NOBODY HERE UNDERSTANDS (SHOULD BE WATER)

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❖ LONGER BONE vs THICKER BONE

LONGER BONE (Longitudinal Growth): This ONLY happens through growth plates (physes). Inside the growth plate you have chondrocytes arranged in zones. Resting zone cells get activated and drop into the proliferative zone where they divide and stack into columns like coins, physically pushing the bone longer. Then they enter the hypertrophic zone where they swell to 5-10x their size which actually contributes MORE to length than the division itself. Then they die, leave behind a calcified scaffold, blood vessels invade, osteoblasts replace it with real bone. This conveyor belt is endochondral ossification. Every millimeter of LENGTH comes from this. When the growth plate fuses its over permanently.

For the clavicle: 80% of clavicular LENGTH comes from the medial physis at the sternal end through endochondral ossification. The medial clavicular epiphysis is one of the LAST growth plates in the entire human body to fuse, not completing until age 23 to 25. A LONGER clavicle is what actually makes your shoulders wider. This is what most people actually want.

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THICKER BONE (Appositional Growth): Completely different process. The periosteum (membrane wrapping the bone) contains osteoprogenitor cells that become osteoblasts and deposit new bone matrix directly onto the outer surface. No cartilage, no growth plate, no conveyor belt. This is intramembranous ossification and it can happen at ANY age even in fully grown adults. This is how bones respond to exercise and how osteoporosis drugs work in elderly patients. This IS modeling (new bone where there wasnt any) but it adds to bone diameter not length.

For the clavicle: diameter increase comes from intramembranous ossification of the periosteum. Makes it THICKER and DENSER but NOT meaningfully LONGER. You would need absurd amounts of periosteal deposition to get even a few millimeters of visible width from thickness alone.

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❖ why this matters

when a compound "increases bone formation" or causes "periosteal apposition" that is making bone THICKER. When a compound "increases growth velocity" or "stimulates chondrocyte proliferation at the growth plate" that is making bone LONGER. Completely different mechanisms. Most drugs discussed in bone growth communities primarily do the first one. Very few actually do the second one.


▸ EXERCISE CLAIMS (PLATES OPEN OR CLOSED)

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❖ "reeves deadlifts / dead hangs widen your clavicles 1-2 inches"

nope. not happening.

every guide on here cites wolff's law like its some cheat code. wolff's law actually says bones adapt their STRUCTURE and GEOMETRY to mechanical load, which includes cortical thickening (periosteal apposition). so technically it does predict that loaded bones can get slightly thicker in diameter. but it does NOT predict that bones get LONGER when you pull on them. length requires growth plate activity and no amount of hanging stimulates chondrocyte proliferation at the medial clavicular physis.

the "1-2 inches" thing comes from a steve reeves anecdote. no measurements were ever taken. its literally a myth that gets copypasted from thread to thread and nobody ever questions it.

what actually happens: scapular retraction + bigger delts = you LOOK wider. your skeleton is functionally the same. its a softmaxx not a bonemaxx. easy to mistake for bone growth when its just muscle and posture.

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❖ "heavy compound lifts thicken bones"

technically yes. studies show about 1-3% cortical thickening at loaded sites over 6-12 months. thats sub-millimeter. you will never see this in a mirror or measure it with a tape. it shows up on medical imaging only. this is real periosteal modeling but the magnitude is tiny without pharmaceutical amplification.

still the best thing you can do for bone health though. just dont cope yourself into thinking squats are gonna give you a wider frame. squats load your spine and legs not your clavicles.

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❖ "pullovers expand the ribcage"

no. myth from the 60s. zero clinical evidence. arnold lied to you (or more likely he just had a massive ribcage genetically).

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❖ "swimming widens shoulders"

mostly selection bias. swimmers have wide shoulders because wide-shouldered people are good at swimming and get selected for competitive programs. swimming also builds insane delts and lats which is muscle not bone.


▸ PURE COPE

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❖ "bonesmashing"

i hate talking about this. wolff's law requires controlled cyclic loading like running or lifting. smashing yourself with a hammer causes microfractures, inflammation, and scar tissue. not controlled adaptation. not growth. just damage.

besides, for microfractures to actually stimulate meaningful bone remodeling the load needs to be structured and repetitive, not random blunt trauma. a hammer impact creates disorganized damage and inflammatory scar tissue, not the controlled strain signals that osteocytes interpret as "build more bone here."

and the funniest shit is even if it worked it wouldnt change your frame by a mm.

now we got the copes out of the way lets check the pharmas. if you have open growth plates these are the theoretical possibilities. if your plates are closed (your clavicles are fused) skip to the surgery section at the bottom.


▸ TIER SYSTEM

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the + and - system: if a compound has extra flaws, grey ground, availability, or the effective dose is not known it gets a (-). if it is well known and people have actually tried it with some documentation it gets a (+). the more the minuses or the pluses THE WORSE OR BETTER IT IS

in comparison to surgery all these are D tier at most

"Absolute Shit" and "Questionable" are used when something is a grey ground where we dont know much and/or the evidence is so contradictory and just extremely speculative.


▸ THE NON-WATER COMPOUNDS

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❖ ROMOSOZUMAB (Evenity) - Sclerostin Inhibitor [Tier --A]

What it is: Humanized monoclonal antibody that blocks sclerostin, a protein that suppresses bone formation. By blocking it, you simultaneously STIMULATE osteoblast activity AND reduce osteoclast resorption.

to evaluate the effects we can see what people with sclerostin deficiency look like. they have tall stature and WIDE FRAME because in young individuals the clavicles are a key site of bone deposition. in people with sclerostin deficiency the clavicles become broad and dense. so we can logically deduce if you have open growth plates it is POSSIBLE that inhibiting sclerostin leads to a wider frame.

BUT there are equally brutal points against it. first it may cause unwanted bone growth at other sites like the skull and mandible (not a main side effect at short durations but a real concern from sclerosteosis data). it is extremely expensive (roughly $1,800 to $2,000 per monthly injection). it is going to be hard to determine your dose because it is grey ground and very hard to get. the approved dose is 210mg monthly in postmenopausal women and nobody has studied dosing in young males. though it is probably fear mongering it is said that it could close plates prematurely but there is no study data for this. sclerosteosis patients who have had ZERO sclerostin their entire lives are actually TALL meaning lifelong sclerostin absence does NOT close growth plates early. people are just assuming short term inhibition will cause problems that lifelong deficiency does not.

and PERSONALLY aside from the health risks the main downside is that you are going to take it for a very short amount of time which MAY NOT REPLICATE the skeletal phenotype of someone who has had zero sclerostin their entire life from birth. thats a lifetime of enhanced bone formation vs maybe 12 months. the difference in total bone deposited is massive.

note on denosumab: some people discuss sequencing romosozumab with denosumab (a RANKL inhibitor that blocks bone resorption). the idea is romosozumab builds new bone then denosumab prevents that new bone from being resorbed after you stop romosozumab. this is used in osteoporosis treatment but has never been studied for frame enhancement. denosumab is a completely different drug with a completely different mechanism. it does not build bone, it just prevents bone loss.

Risks: cardiovascular events (heart attack, stroke) from clinical trial data (FDA black box warning). NOT approved for young healthy males. zero safety data in this population.

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❖ TERIPARATIDE (Forteo) / ABALOPARATIDE (Tymlos) - PTH Analogues [Absolute Shit / DO NOT USE]

What it is: Teriparatide = recombinant PTH(1-34). Abaloparatide = PTHrP analogue. Both stimulate osteoblasts when administered INTERMITTENTLY (pulsatile dosing = anabolic, continuous = catabolic).

it has similar bone building effects to romosozumab on paper. why would it not work and why is it actually dangerous? because this drug directly messes with PTHrP signaling. in people with open growth plates there is a critical feedback loop between PTHrP and Indian Hedgehog (Ihh) that controls how fast chondrocytes mature. normally PTHrP DELAYS chondrocyte maturation, keeping them in the proliferative zone longer so they divide more before transitioning to hypertrophy. Indian Hedgehog is what stimulates PTHrP production. this back and forth between Ihh and PTHrP is what keeps the growth plate running at the right speed.

if you flood the system with exogenous PTH or PTHrP analogue you are directly disrupting this finely tuned feedback loop. the balance between "keep dividing" and "start maturing" gets thrown off. the growth plate could either accelerate through its entire program too fast and exhaust itself, or the signaling could get so scrambled that orderly endochondral ossification breaks down entirely. either way you are gambling with a system that needs to be precisely calibrated. and for what? teriparatide primarily drives bone MODELING and periosteal THICKENING in adults, not longitudinal growth.

also: FDA black box warning for osteosarcoma (bone cancer) based on rat studies with long term exposure.

DO NOT USE

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❖ LGD-3303 and Other Osteoblast-Activating SARMs [Tier -B]

What it is: A non-steroidal selective androgen receptor modulator with particularly strong effects on bone tissue. Unlike LGD-4033, LGD-3303 shows specific osteoblast activation and periosteal apposition in preclinical (rat) data.

this got a minus because its again grey area and not much human clinical trial data exists especially not on younger people. some people claim "bone growth" from SARMs but we can never verify those claims. the way this would theoretically work is since it acts like androgens on bone tissue it could cause wider frame like any other androgen can do but with less effects on your hair and your balls than straight testosterone.

and like other androgens it carries the risk of premature growth plate fusion. SARMs still have androgenic activity that can accelerate growth plate senescence.

there is no actual proof that exogenous androgens cause wider frame in healthy individuals who already have normal androgen levels. it is logically justifiable based on the puberty data (males get wider frames during testosterone rise) but that is not definitive proof. puberty is a developmental window not a dose-response you can recreate by adding more androgen on top.

Risks: Suppressive to natural testosterone. Very limited human safety data. Oral bioavailability issues. Most available sources are research chemical grade with no purity verification.

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❖ OXANDROLONE (Anavar) - Periosteal Apposition Steroid [Questionable Tier] has decent effects for height

What it is: An oral anabolic steroid (17-alpha-alkylated DHT derivative) with uniquely strong effects on BONE specifically.

at LOW doses (around 0.25mg/kg/day) oxandrolone increases height velocity without proportionally advancing bone age in some clinical studies on children with growth disorders. but this is dose-dependent and the picture is NOT clean. at higher doses studies showed it actually DECREASED predicted adult height because bone age advanced faster than linear growth. so the "does not advance bone age" claim only holds at specific low doses in specific populations. do not take it as a blanket statement.

the reason i included this is because people report height growth which is longitudinal growth. this is extremely questionable and most of what i am saying here is theoretical with little proof because its hard to get data about steroids in teens. but this is even worse because it is assuming that if it causes longitudinal growth in the legs and spine etc for height then it may be able to do the same for the clavicles too. AGAIN THIS IS SUPER PSEUDOSCIENTIFIC. the growth plates at different anatomical sites can respond differently to hormonal stimuli. what happens at the knee does not automatically happen at the sternal end of the clavicle.

anecdotal claim (do not blindly trust this): https://looksmax.org/threads/i-grew-5cm-with-a-oxandrolone-6-week-cycle.642431/(idk if i can link this but since it would be beneficial for the user i will and i will comply to remove this)

Dosing (from the 0.25mg/kg): 10-20mg/day for bone effects (much lower than bodybuilding doses of 40-80mg). higher doses dramatically accelerate bone age which defeats the purpose.

Risks: Liver toxicity (17-alpha-alkylated). Lipid destruction (HDL crashes dramatically, oxandrolone is one of the worst steroids for lipids even at low doses). Testosterone suppression. At higher doses, bone age advancement that EXCEEDS height gain meaning you actually LOSE predicted adult height.

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❖ FGFR3 INHIBITORS (Infigratinib, TYRA-300) - Growth Plate Brake Removers [Tier -S]

What they are: Drugs that block fibroblast growth factor receptor 3 (FGFR3), a receptor that acts as a BRAKE on longitudinal bone growth. Infigratinib is an oral FGFR1-3 tyrosine kinase inhibitor. TYRA-300 is a newer FGFR3-selective inhibitor.

this is one of the more interesting ones because unlike most compounds on this list FGFR3 inhibitors target a mechanism that directly controls LONGITUDINAL growth not just thickness. here is why.

FGFR3 is a negative regulator of growth plate activity. it is expressed on growth plate chondrocytes and when it signals through the MAPK/ERK pathway it SUPPRESSES chondrocyte proliferation and differentiation. it literally slows down the conveyor belt i described earlier. this is proven by the fact that gain-of-function mutations in FGFR3 (where the receptor is overactive) cause achondroplasia, the most common form of dwarfism. too much FGFR3 signaling = shorter bones. the opposite is also proven. FGFR3 knockout mice (where the receptor is completely absent) have skeletal OVERGROWTH with significantly longer bones everywhere. femurs, tibias, vertebrae, skull, all longer than normal. deleting the brake makes the conveyor belt run faster and longer.

the key finding for this discussion: FGFR3 inhibitors work in WILD TYPE mice too, not just achondroplasia models. TYRA-300 was tested in normal mice with normal FGFR3 and it still increased nasoanal length and long bone length. this means even at baseline signaling levels FGFR3 is actively holding back some growth and removing that restraint causes additional longitudinal growth. this is not just "restoring broken growth to normal." this is pushing normal growth beyond its natural limit.

the mechanism is clean. block FGFR3 on growth plate chondrocytes, less MAPK/ERK suppression, more chondrocyte proliferation in the proliferative zone AND more differentiation into the hypertrophic zone. both phases of the conveyor belt get enhanced. histological analysis confirmed this, treated mice had expanded proliferative and hypertrophic zones in the growth plate. this is real endochondral ossification not periosteal thickening. this makes bone LONGER.

for the clavicle: FGFR3 is expressed on chondrocytes at every growth plate. there is no reason the medial clavicular physis would be exempt. if FGFR3 inhibition increases longitudinal growth at the knee and spine it should theoretically do the same at the sternal end of the clavicle. same receptor, same signaling, same conveyor belt.

though the reason some people are skeptical is because most of the testing was done on children who have over active FGFR3 though its thought to that in healthy teens and adolescents it could still could lead to decent growth and unlike all of these fucking drugs only this (with the sole exception of Satoru gojo[AI]) is the one with no - good effect on growth plate closure

Risks: Off-target FGFR1/FGFR2 inhibition with non-selective inhibitors (wound healing issues, potential vascular effects). Theoretical tumor suppressor disruption from chronic FGFR3 blockade. Unknown safety profile in healthy young adults. Essentially unavailable outside clinical trials or oncology prescriptions. No dosing data for skeletal enhancement in normal individuals.

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▸ WATER COMPOUNDS

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❖ HGH (Human Growth Hormone) [Tier S]

What it is: Recombinant human growth hormone, a 191 amino acid protein identical to what your pituitary gland produces naturally. This is the single most studied compound for bone growth in existence.

GH is the ONLY compound on this entire list with a real mechanism for driving LONGITUDINAL bone growth not just thickness. When GH hits the growth plate it binds to GH receptors on the resting zone chondrocytes and activates JAK2-STAT5 signaling which does two things: it recruits dormant cells into the proliferative zone increasing the supply of cells entering the conveyor belt AND it tells those cells to produce IGF-1 locally right at the growth plate (paracrine IGF-1). This local IGF-1 then binds to IGF-1 receptors on proliferating chondrocytes and activates PI3K/Akt (cell survival, keeps them dividing longer) and MAPK/ERK (direct proliferation, faster division rate). More cells entering, faster division, and IGF-1 also enhances hypertrophic expansion so each cell swells more. The effect on length is multiplicative.

On top of that GH stimulates the liver to produce systemic IGF-1 which reaches every growth plate in the body providing baseline stimulation bodywide, while the locally produced IGF-1 at each growth plate provides the concentrated targeted effect. Systemic IGF-1 also hits periosteal osteoblasts stimulating cortical thickening. So GH gives you BOTH: longer bones through growth plate stimulation AND thicker cortical bone through periosteal IGF-1 activity. Nothing else does both.

For the clavicle: the medial clavicular physis has the exact same zonal architecture and receptor machinery as any other growth plate. Same GH receptors, same IGF-1 receptors, same downstream signaling. There is no biological reason it would respond differently. The only difference is timing since it stays open until 23 to 25 while most other growth plates close by 16 to 18. So theoretically GH could drive clavicular longitudinal growth at ages where it can no longer drive height growth.

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The limitation: GH does accelerate bone age. it makes growth plates more active but it also advances them toward fusion. the reason it is still Tier S is because the NET effect is positive. GH grows you MORE length than the amount of closure time it costs you. the ratio of growth gained to growth window lost is favorable, unlike testosterone where the ratio is terrible (barely any extra length but massive closure acceleration through aromatization). with GH the extra growth outpaces the accelerated closure in most cases. but it does mean the final result on your frame is hard to predict. some people gain extra, some people end up neutral, some might even lose depending on their individual response to bone age advancement. it is not a guaranteed win, just the best odds on this list.

Risks: Insulin resistance (GH directly opposes insulin signaling). Joint pain and edema from IGF-1 mediated fluid retention. Potential acceleration of existing malignancies (IGF-1 is a growth factor that does not distinguish cell types). Carpal tunnel. Cost is extreme.

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❖ MK-677 (Ibutamoren) [Tier C+]

What it is: An oral ghrelin receptor agonist (growth hormone secretagogue). NOT a hormone. It binds to ghrelin receptors (GHSR1a) in the pituitary and hypothalamus and tricks your body into producing more of its OWN growth hormone.

When you take MK-677 it activates GHSR1a on somatotroph cells in the pituitary causing calcium influx which triggers them to dump their stored GH granules into the bloodstream. It also activates GHSR1a on hypothalamic neurons that produce GHRH giving additional pituitary stimulation AND it suppresses somatostatin which is the hormone that normally inhibits GH release. So its pushing the gas in two ways and releasing the brake simultaneously.

Unlike injected GH, MK-677 preserves the natural pulsatile pattern of GH release. Your body releases GH in pulses not a constant stream and MK-677 makes each pulse bigger rather than creating one artificial spike. This might matter because growth plate GH receptors can desensitize with continuous exposure but stay responsive to pulses. So the pulsatile pattern from MK-677 might theoretically be more efficient per unit of GH at stimulating the growth plate.

Once the extra GH is in the bloodstream everything downstream is identical to what i described in the GH section. Same JAK2-STAT5, same local IGF-1, same PI3K/Akt and MAPK/ERK, same liver IGF-1, same periosteal effects. The pathway is not different. The magnitude is.

And that is the honest problem. Your pituitary has a ceiling. Finite somatotroph cells, finite stored GH granules. No matter how hard you stimulate them they can only produce so much. Exogenous GH injections bypass this completely. A therapeutic GH dose might produce peak serum GH levels 3 to 5x higher than what MK-677 can achieve through endogenous stimulation. Since the downstream growth plate effects are dose-dependent, MK-677 produces a proportionally weaker longitudinal growth effect.

lets be real this shit may not even give you a sliver of bone or frame growth. it increases your GH by such levels that for most people it probably does not matter. i REPEAT most people. but it could cause some gain for people who have naturally low GH production where even a small increase might push them into a range where growth plate effects occur. for someone with already normal GH production the additional bump from MK-677 is probably below the threshold for any meaningful skeletal effect.

i dropped this from B+ to C+ because the mechanism is theoretically correct (it works through the right pathway) but the magnitude is so weak that calling it B-tier was generous. there is zero evidence of frame growth from MK-677 in any human at any age. it is theoretical and the theoretical effect size is small.

Why some people stack it with GH: exogenous GH gives you a high baseline, MK-677 amplifies natural pulsatile release to fill in the gaps between injections since GH has a short half-life. whether this additive approach actually translates to more growth plate stimulation than GH alone has never been tested but the logic is consistent.

Risks: Significant appetite increase (ghrelin receptor activation, this is not subtle). Water retention. Potential insulin resistance with chronic use. Elevated cortisol. Numbness and tingling. Long term safety data does not exist. Not approved for human use. Most available sources are research chemical grade.

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❖ AROMATASE INHIBITORS [Tier S for Combo with GH, Tier A for Monotherapy]

What they are: Drugs that block aromatase (CYP19A1) which converts testosterone to estrogen. Third generation AIs include letrozole and anastrozole.

The entire logic of AIs for bone growth is based on one fact: ESTROGEN is what closes growth plates, not testosterone. This is proven by males with aromatase deficiency or estrogen receptor mutations who have normal testosterone but their growth plates NEVER close and they keep growing into their 20s and 30s.

How estrogen closes growth plates: growth plate chondrocytes express both estrogen receptors (ERalpha and ERbeta) AND the aromatase enzyme itself so they can convert local testosterone to estrogen right at the growth plate. When estrogen binds ERalpha on proliferative chondrocytes it initiates growth plate senescence, a gradual program where each chondrocyte's replicative capacity gets reduced. The proliferative zone gets thinner over time as fewer cells are actively dividing. The hypertrophic zone gets compressed. The whole growth plate thins until blood vessels penetrate through it, osteoblasts follow, and the cartilage gets completely replaced by bone. That is fusion and it is permanent. This is CUMULATIVE over years of estrogen exposure which is why girls close earlier (more estrogen earlier) and the medial clavicular epiphysis closes last (inherent resistance to the senescence program).

AIs block aromatase so less testosterone gets converted to estrogen. Less estrogen means the senescence program runs slower and fusion gets delayed.

Why monotherapy is lower is because it cant make you grow taller your plates are open doesn't mean longitudinal growth you need gh local igf-1 release etc, it isn't bad but i would rather not take it alone if i haven't grown for a long time.

Why combo with GH is completely different: GH provides the active growth stimulus (recruiting chondrocytes, driving proliferation, enhancing hypertrophy). AI extends the window over which GH has active growth plate tissue to work on. GH increases rate. AI increases time. Total growth = rate x time. Both variables boosted simultaneously, multiplicative effect.

For the clavicle: if the medial physis is still open, GH + AI should theoretically accelerate endochondral ossification while simultaneously delaying fusion.

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Letrozole blocks ~99% of aromatase, anastrozole ~97%. That 2% matters because estrogen's effects on senescence are cumulative. More complete suppression preserves more growth plate longevity but also more side effects.

Risks: Estrogen is critical for bone MINERALIZATION (ironic), lipid metabolism, glucose metabolism, joint health, mood, cardiovascular function. Crushing it to near zero is not free even in males. Potential vertebral deformities with long term use.

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❖ TESTOSTERONE [Tier D for Frame Width]

What it is: The primary male androgen. Produced naturally by the testes ~5-10mg/day. Available exogenously as injectable esters (enanthate, cypionate), transdermal gels, or oral formulations.

Testosterone affects bone through two pathways that work in OPPOSITE directions for frame growth and most people only know about one.

Pathway 1 makes bone THICKER (works for you). Testosterone and DHT bind to androgen receptors on periosteal osteoblasts activating transcription of differentiation genes, pushing osteoprogenitor cells to mature and deposit new bone matrix on the outer cortical surface. Simultaneously testosterone increases muscle mass through AR activation in myocytes, bigger muscles exert more mechanical force on bone, osteocytes detect this through fluid flow in the canalicular network, they reduce sclerostin production and increase Wnt signaling to periosteal osteoblasts which deposit more bone where stress is highest. Testosterone also upregulates local IGF-1 in bone tissue further stimulating periosteal osteoblasts. Three forces converging on cortical thickening: direct AR, mechanical loading, and local IGF-1. This is why males have thicker bones than females. For the clavicle this means thicker more robust shaft, more cortical density, the "definition" people talk about. But thicker cortex does not change the LENGTH which is what determines frame width.

Pathway 2 closes your growth plates (works against you). Aromatase converts testosterone to estradiol. Growth plate chondrocytes express aromatase so they convert local testosterone to estrogen right at the growth plate. Higher testosterone = more substrate = more estrogen = faster accumulation of the closure signal = earlier fusion. At supraphysiological levels (2-5x normal) you proportionally increase aromatization. The growth plate gets hit with estrogen it would not naturally see for years. The senescence program accelerates. Fusion happens earlier. For the medial clavicular epiphysis that could mean closing at 20 instead of 24, permanently losing years of length growth.

Testosterone does have SOME direct growth plate stimulating effects through AR on chondrocytes. This is part of the pubertal growth spurt where rising testosterone stimulates growth while cumulative estrogen is still below the fusion threshold. But if you already have normal testosterone your growth plate ARs are already occupied at physiological maximum. Extra testosterone does not meaningfully increase direct growth plate stimulation because the receptors are saturated. What it DOES do is massively increase aromatization because aromatase scales linearly with substrate. Almost zero extra length growth but a lot of extra estrogen production. Terrible ratio.

During normal male puberty the clavicle gains ~20mm of length between 13 and 18 (vs ~10mm in females). This is from RISING testosterone during a developmental window, not from supraphysiological levels. Adding more on top of already normal levels does not recreate this window.

The trade is bad. You get somewhat thicker cortical bone (maybe a couple mm of diameter over years) while potentially losing centimeters of length from premature growth plate closure. Not even close. "Not ideal alone for bone growth but helps with thickness and definition" is a fair summary.

the reason i included SARMS and gave them better rating is because they don't aromatize though they actively increase bone age and accelerates bone maturation

Risks: HPG axis shutdown (suppresses natural production). Accelerated growth plate closure via aromatization (irreversible). Erythrocytosis. Acne. Hair loss if genetically predisposed. Cardiovascular effects with long term supraphysiological use. Testicular atrophy. In young males with open growth plates the closure risk is the primary concern because it is permanent.

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▸ WHAT ACTUALLY CHANGES ADULT BONE DIMENSIONS

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if your plates are closed here is the complete list of proven methods:

❖ Clavicle lengthening surgery

surprise surprise the only shit that is proven and not some "if" and "what if" distraction osteogenesis. the surgeon cuts the bone, attaches an external fixator, and slowly separates the two ends over weeks. new bone fills the gap as it widens. adds 1-3cm per side. this is real, documented, and works. no overcomplicated paragraph needed.

costs 15-50k, 3-6 month recovery, real risks (non-union, infection, nerve damage, hardware complications). see how i dont have to write a paragraphs on how it works, it fucking feels like a breath of fresh air, no coping with extra steps

that is the list. there is no second item.

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❖ note on IGF-1 and its derivatives (AI summary)

The IGF-1 that drives growth plate elongation is primarily LOCAL/PARACRINE IGF-1 produced by chondrocytes themselves in response to GH signaling - NOT circulating IGF-1 from the liver or injections. This is why GH works (it tells growth plate cells to make their own IGF-1) and why injecting IGF-1 variants doesnt (it never reaches where it needs to be).

Also covered IGF-1 LR3 (same problem, slightly longer half life but still gets eaten by muscle), mecasermin/Increlex (works in severely deficient kids but nonexistent in normal people), and the cartilage-targeted IGF-1 fusion protein research (the only approach that might actually work but is years from being a drug).

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and final note these pharmas are unfalsifiable and unprovable if it works it natural since your plates should be opened for this to be possible if it, it could just be that it worked, if it didnt work its just that you didnt take enough of your hyo reactive


▸ TL;DR

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this is mostly water but from what i read the only decent pharmas are GH, AI, FGFR3 inhibitors, Anavar and maybe in the future ROMOSOZUMAB thats about it and most of these are expensive af and this is a break down of what i think about them i am not acting these are absolute facts or claiming to be a professional

if your plates are closed (25+): your frame was set by genetics and your growth years. no exercise, no supplement, no injectable reopens fused growth plates. you can get surgery (clavicle lengthening, distraction osteogenesis) or you can accept your frame and optimize what you have with muscle.

if your plates are still open (under 23-25): there is a theoretical window where certain compounds (primarily GH, possibly GH + AI combo) could drive additional clavicular longitudinal growth through the medial physis. none of this is proven for clavicle-specific frame widening. most other compounds discussed in this space primarily make bone thicker not longer which does not meaningfully change frame width. the theoretical possibilities exist but they are exactly that, theoretical.

the honest truth for everyone: you can cope with bonesmashing. you can cope even harder with roids and peptides (theoretical mechanism does not mean it works in practice). or you can save the money and actually get a clavicle lengthening surgery if frame width matters that much to you. surgery is the only method with guaranteed measurable results.


this thread took a lot of fucking time pls rep it took a lot more that you think and since this topic is quite weak i tried to add the non water section but sadly not much to cover and even this is highly debatable since this wasnt that great my next thread will be the best thread in the Forum A 2 part thread about attraction not the rigid mathematical ones but actually evaluating every study comparing ethnic groups and what surgery path you should take etc and the surgery course how to avoid being botched etc trust me it is going to be godly will not be able to write it soon since i will be going on vacation for the next week and after that i have a big test rigth after