NEW META FOR ROIDS & PUBERTY

[lookingbad]

wait so based on what u know now. can i just run exemestane/letrozole for slower growth plate closure? or do i need a ERD like fulvestrant or maybe other stuff like raloxifene or tamoxifene. comapre that with erdagitnib or infigatnib.

do letro with every day frequency and dont do fulve just nuke ur e2 to oblivion and use s-equol for inflammation/skin mitigation from low e2, then use either erda/infigra for inhibiting fgfr3. Erda is riskier but looks promising on paper

 

[infrainfra]

do letro with every day frequency and dont do fulve just nuke ur e2 to oblivion and use s-equol for inflammation/skin mitigation from low e2, then use either erda/infigra for inhibiting fgfr3. Erda is riskier but looks promising on paper

why not fulve? mice treated with estradiol and fulvestrant still got an increase in body length and delayed gp closure. i mean yeah its expensive tbh. can i do 2.5mg letro daily?
i wont ise raloxifene/tamoxifen/endoxifen bc at certain concentrations it literally activates ERa. yes erda>infig its super powerful. is the skin affects from low e2 really that bad?

btw i was thinking of running actual dht with low dose test and dht gel on penis + face. + halotestin. and something to upregulate cAMP and maybe cGMP.

like 300 test and some dht idk yet. but my problem is i cant do bloods and track my e2

 

[lookingbad]

why not fulve? mice treated with estradiol and fulvestrant still got an increase in body length and delayed gp closure. i mean yeah its expensive tbh. can i do 2.5mg letro daily?
i wont ise raloxifene/tamoxifen/endoxifen bc at certain concentrations it literally activates ERa. yes erda>infig its super powerful. is the skin affects from low e2 really that bad?

btw i was thinking of running actual dht with low dose test and dht gel on penis + face. + halotestin. and something to upregulate cAMP and maybe cGMP.

like 300 test and some dht idk yet. but my problem is i cant do bloods and track my e2

no test base is more beneficial cos fulve degrades ur igf1r as it has been used in trials for this cause and worked as a igf1r antagonist to an extent so i would avoid that. running no test base is meta but no one can understand this concept yet

 

[infrainfra]

no test base is more beneficial cos fulve degrades ur igf1r as it has been used in trials for this cause and worked as a igf1r antagonist to an extent so i would avoid that. running no test base is meta but no one can understand this concept yet

Yessss thats what im talking about. but maybe imma do 5mg test (microdose) just for the cognative maintenance.
what do u think sbout running JUST HALOTESTIN with letro(idk if a ai is worth it if im on nearly 0 test) to get the facial dimo benefits + delaying my plate closure? also some other compunds i dont want to leak on public maybe you can DM me and we discuss this

 

[infrainfra]

Confident but wrong, what is this study going to prove? Yes tren increases trabecular bone in mice after skeletal maturity as stated in the study aswell, but in growing mice it's shown to decrease femur length and cause early epiphyseal closure (1).

Other pathways need e2 to work, but also not high amounts as that will stunt growth. You need low e2 in order for androgens and igf-1 to work properly they all synergise.

Heightmaxxing is mostly cope ngl and most will fuck it up and do it wrong, and this is coming from me

„Other pathways need e2 to work, but also not high amounts as that will stunt growth. You need low e2 in order for androgens and igf-1 to work properly they all synergise.”

can u explain why thatd apply to bone cells? can u go in depth i disagree

 

[Zagro]

„Other pathways need e2 to work, but also not high amounts as that will stunt growth. You need low e2 in order for androgens and igf-1 to work properly they all synergise.”

can u explain why thatd apply to bone cells? can u go in depth i disagree

For longitudinal growth you may rape E2 all you want as long as you have something to inhibit ER partially as your body will make them even more sensitive as a compensatory mechanism + something for IGF-1 as without E2 your serum levels will decrease.

I completely agree with raping E2 to 2-6pg/dL and having low T as even aromatase inhibitors don't work, this take was shitty but still holds some truth for craniofacial growth

 

[infrainfra]

For longitudinal growth you may rape E2 all you want as long as you have something to inhibit ER partially as your body will make them even more sensitive as a compensatory mechanism + something for IGF-1 as without E2 your serum levels will decrease.

I completely agree with raping E2 to 2-6pg/dL and having low T as even aromatase inhibitors don't work, this take was shitty but still holds some truth for craniofacial growth

„Something to inhibit ER” like fulvestrant ?
i cant do hgh itself since i have a trouble hiding refrigerated injectibles in my house.

but heres my take: nuke e2 with letro and nuke test with halo since bones can make their own local e2 not only by aromatase. halo is already the best androgen oat so i wont miss out on any cranofacial growth i would with just nuking e2. what u think about that? 2,5letr 5mg halo. im still wondering do i even use letro if im going to 0ng test on halo anyway

 

[ostanomy]

For longitudinal growth you may rape E2 all you want as long as you have something to inhibit ER partially as your body will make them even more sensitive as a compensatory mechanism + something for IGF-1 as without E2 your serum levels will decrease.

I completely agree with raping E2 to 2-6pg/dL and having low T as even aromatase inhibitors don't work, this take was shitty but still holds some truth for craniofacial growth

so you would switch letro for endoxifen?

 

[Palan]

Why you should run NAAAS only and how?

We know that even low dosage test will induce aromatisation and thus we'll have a minimum intracellular e2 proliferating around the growth plates cartilage binding to the ERα, the estrogen receptor that is more potent for bone effects and has low neurological/brain properties --> risking growth plates closure even at really low E2 levels making it a risk option to run aromatising AAS. Furthermore ERβ signal(estrogen receptor needed for BDNF increase and neuroprotection + sligthly modulating bone effects, but a lot less potent than ERa on bones) will be really low or none at all, making that even riskier by compromising the antioxidant properties of estrogen (really bad for everyone, especislly people running 19-NORs)so the best thing we can run is


Non aromatising AAS (NAAAS) + Raloxifene (SERM acting mildly well only on the ERb making useful and a good neuroprotector when not using any aromatising AAS and furthermore for Raloxifene activates ERα (the actual receptor that signal growth plates to maturate and thus close) much less strongly than estradiol and does not produce the same closure signal
ERβ modulates ; ERα is the main driver
ERα ≈ 80–90% ERβ ≈ 10–20%


Using androgens this way:
(NAAAS + RALOXIFENE as ERb signal for neuroprotection) would slows growth plates closure a lot more compared to when: test dosage is low-high (even 40-80mg/week) even if local/serum e2 are low because ERα signalling is less present in the NAAAS subject than the LOW TEST DOSAGE subject and Neuroprotection would be more valid in the NAAAS subject.

Now, combining what we said we can use Trenbolone IGF-1 affinity in tissue/bones (and mitigating the neurological side effects with raloxifene + drugs that increase dopaminergic and protective seratonergic effects + other ancillaries for health) with high dosage HGH (with maybe insulin for upregulating the receptors even more) with other drugs for height (PTHA's + FGFR3i + HDAC modulation) we can drastically improve Adult Final Height.


STUDIES:

• In the study tamoxifene was compered to raloxifene, tamoxifene was stronger on paper:
  -directly inhibited osteoclast differentiation:
  -directly reduced bone resorption:
  https://pubmed.ncbi.nlm.nih.gov/17420779/
  so by knowing that tamoxifene can be used in teenager for blocking local estrogens in growth plates and raloxifene is weaker, raloxifene could be used for the same context.
  
  
• Neurological-dopaminergic benefits of raloxifene:
  https://pubmed.ncbi.nlm.nih.gov/39799793/
  
  
• TRENBOLONE POTENCY ON IGF-1 RECEPTORS:
  https://pubmed.ncbi.nlm.nih.gov/2707149/
  https://www.sciencedirect.com/science/article/abs/pii/S0739724010001001

Use that information at your own responsibility.

low iq post

 

[ostanomy]

do letro with every day frequency and dont do fulve just nuke ur e2 to oblivion and use s-equol for inflammation/skin mitigation from low e2, then use either erda/infigra for inhibiting fgfr3. Erda is riskier but looks promising on paper

why would you recommend him to take it ed instead of eod?

 

[infrainfra]

so you would switch letro for endoxifen?

endoxifen?? at certain concentrations literally activates ERa. people that promote that haven’t looked into it really.

 

[infrainfra]

For longitudinal growth you may rape E2 all you want as long as you have something to inhibit ER partially as your body will make them even more sensitive as a compensatory mechanism + something for IGF-1 as without E2 your serum levels will decrease.

I completely agree with raping E2 to 2-6pg/dL and having low T as even aromatase inhibitors don't work, this take was shitty but still holds some truth for craniofacial growth

yo can u respond to my message above )

 

[lookingbad]

no test base is more beneficial cos fulve degrades ur igf1r as it has been used in trials for this cause and worked as a igf1r antagonist to an extent so i would avoid that. running no test base is meta but no one can understand this concept yet

low iq post

explain nigga and just put raloxifene out of the thread that was a sitty take but yes if u dont have any aromatase agent is OP for growth the only thing u want is ERb then cos u will rape all ur health indicators and risk brain damage. and u take ERb agonsits

 

[mtn.923]

I'm Iqlet why not run just a slight amount of test tho? or HCG?

 

[mtn.923]

No idea if that's the truth have to look into it but sounds alright

The thing is that abaloparatide still wont work (https://pubmed.ncbi.nlm.nih.gov/9276090/)

so run low test base?

 

[tayolite]

no bhai, niche genie poop.
and also, non aromatising androgens still age the bone, and considering the fact that anavar if dosed too high can age bone twice as fast as you age is pretty bad for more androgenic options

if you use hcg, you're just gonna produce test again and the same residual e2 problem occurs

is taking HCG advisable DURING. a test+HGH cycle though?

 

[birthdefect]

is taking HCG advisable DURING. a test+HGH cycle though?

if test and you want to keep testicles functioning its mandatory

 

[infrainfra]

I'm Iqlet why not run just a slight amount of test tho? or HCG?

because why? why add aromatizable substrates

 

[mtn.923]

because why? why add aromatizable substrates

you need some estrogen for neuroprotection especially whilst in development

 

[tayolite]

if test and you want to keep testicles functioning its mandatory

does it increase chances of recovery post cycle?

 

[infrainfra]

you need some estrogen for neuroprotection especially whilst in development

letrozole has been shown to not cause any problems. just use something like s-equol if u care so much. its a Erß agonist

 

[birthdefect]

does it increase chances of recovery post cycle?

yes

 

[smizz]

dnr

 

[Finncelchud]

What would be a good naaas to utilise?

 

[tayolite]

yes

what about during cycle

 

[birthdefect]

what about during cycle

you take it during cycle so it increases the chance of recovery when doing pct