NEW META FOR ROIDS & PUBERTY

[lookingbad]

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.

 

[birthdefect]

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.

just inhibit the downstream cascade e2 uses to fuse plates and profit

 

[lookingbad]

just inhibit the downstream cascade e2 uses to fuse plates and profit

why would you risk inhibiting aromatase and have even really low local concentration that signal ERα when u can have none at all using NAAAS only and profit without having any less ERα signalling as possible and use something for ERβ?

 

[birthdefect]

why would you risk inhibiting aromatase and have even really low local concentration that signal ERα when u can have none at all using NAAAS only and profit without having any less ERα signalling as possible and use something for ERβ?

first of all how would you even maintain the testicles while using only NAAAS
second of all, i meant downstream signalling cascade, i didnt even mention aromatase

 

[birthdefect]

also, a way to mitigate the (in my opinion fearmongered) risk of brain development, just take 17a estradiol and again, profit

 

[lookingbad]

first of all how would you even maintain the testicles while using only NAAAS
second of all, i meant downstream signalling cascade, i didnt even mention aromatase

the same way you mantain them while ur on on Aromasting compounds? and then how tf you inhibit the downstream cascade e2 uses?? u use fulvestrant?

 

[birthdefect]

the same way you mantain them while ur on on Aromasting compounds? and then how tf you inhibit the downstream cascade e2 uses?? u use fulvestrant?

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

 

[test monster]

first of all how would you even maintain the testicles while using only NAAAS
second of all, i meant downstream signalling cascade, i didnt even mention aromatase

Have you heard of trt

 

[birthdefect]

Have you heard of trt

well obviously nigga
whats the point of using trt if the goal of using naaas is to obliterate any residual e2
if you introduce something aromatisable then the whole thing is pointless now
thus you cant use hcg either, and so i asked how you would maintain the testicles
if im wrong let me know

 

[lookingbad]

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

then just dont use hcg or microdose hcg; it wouldnt make a difference.. btw if ERA signalling (no e2 base) is low the growth plates will mature less compared to when u run aromatising AAS as e2 base (test/deca/ment/dbol)

 

[looks4life]

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.

bazedoxifene is best for this but mirin post

 

[lookingbad]

bazedoxifene is best for this but mirin post

just done a couple of reaserch and seems really promising for the purpose

 

[ccwb]

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.

Price?

 

[lookingbad]

Price?

its pretty cheap;
btw i wouldnt raccomend it as it ould have some ERa agonism after i done a couple of more reaserch...
a SERD like fulverstant degredes ERA and ERB and fs works but could have some bad side effects;
Bazedoxifene could actually be the best but hard to source tho;


or

just run no e2 base cycle and use pharmas to replicate E2 neurobenefits in the brain.

 

[ccwb]

its pretty cheap;
btw i wouldnt raccomend it as it ould have some ERa agonism after i done a couple of more reaserch...
a SERD like fulverstant degredes ERA and ERB and fs works but could have some bad side effects;
Bazedoxifene could actually be the best but hard to source tho;


or

just run no e2 base cycle and use pharmas to replicate E2 neurobenefits in the brain.

Any advice or any think I shouldn’t add/take cuz I’m 14, thinking on test tho only

 

[lookingbad]

Any advice or any think I shouldn’t add/take cuz I’m 14, thinking on test tho only

i wouldnt do test only dont listen to faggots on this forum or others.
doing test only even with an AI wont stop growth plate closure,
btw u gotta a lot of time for implementing pharma. do it asap. dont wait, the younger the better.

if u want to grow the most in height do HGH + AI + Abaloparatide + FGFR3i like vosoritide or infigratinib(this combined with the others would make u certainly grow taller than ur adult final height.

Add NAAAS in ur journey but just start with this and u will see a lot of improvement. use masteron/halotestin/tren for dimorphism and crazy frame growth combined with hgh.

 

[ccwb]

i wouldnt do test only dont listen to faggots on this forum or others.
doing test only even with an AI wont stop growth plate closure,
btw u gotta a lot of time for implementing pharma. do it asap. dont wait, the younger the better.

if u want to grow the most in height do HGH + AI + Abaloparatide + FGFR3i like vosoritide or infigratinib(this combined with the others would make u certainly grow taller than ur adult final height.

Add NAAAS in ur journey but just start with this and u will see a lot of improvement. use masteron/halotestin/tren for dimorphism and crazy frame growth combined with hgh.

Bruh, where can I get this much money, and I I only can run one compound what would it be hgh?

 

[lookingbad]

Bruh, where can I get this much money, and I I only can run one compound what would it be hgh?

HGH + AI + Abaloparatide (bones) ; a lot of way to make money;
Abaloparatide is 140$ for a year, HGH is about 120 $ a month for a pretty good dosage; AI is like 50 $ a year

 

[Zagro]

HGH + AI + Abaloparatide (bones) ; a lot of way to make money;
Abaloparatide is 140$ for a year, HGH is about 120 $ a month for a pretty good dosage; AI is like 50 $ a year

You need E2

Abaloparatide wont even work without ER nor will the others ones be efficient

 

[lookingbad]

You need E2

Abaloparatide wont even work without ER nor will the others ones be efficient

wrong
Both TE and TREN administration suppressed cancellous bone turnover similarly and fully prevented ORX-induced cancellous bone loss. TE− and TREN-treated animals also exhibited greater femoral neck shear strength than ORX animals:

https://pmc.ncbi.nlm.nih.gov/articles/PMC8366408/


having no e2 doesnt mean other pathways dont work, u will potentially have a medium-lower igf 1 sensitivity compared to normal puberty levels but if u use HGH combined with drugs that increases it exponentially (e.g. tren and slin) u wouldnt have to worry;
maybe if u want to have 100% of ur potential bmd u would have a moderate-high amount of e2.
but for height having no e2 is better. change my mind.

 

[Zagro]

wrong
Both TE and TREN administration suppressed cancellous bone turnover similarly and fully prevented ORX-induced cancellous bone loss. TE− and TREN-treated animals also exhibited greater femoral neck shear strength than ORX animals:

https://pmc.ncbi.nlm.nih.gov/articles/PMC8366408/


having no e2 doesnt mean other pathways work, u will potentially have a medium-lower igf 1 sensitivity compared to normal puberty levels but if u use HGH combined with drugs that increases it exponentially (e.g. tren and slin) u wouldnt have to worry;
maybe if u want to have 100% of ur potential bmd u would have a moderate-high amount of e2.
but for height having no e2 is better. change my mind.

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

 

[Wexilarious]

Bump, more gymcels, less competition

 

[lookingbad]

Bump, more gymcels, less competition

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

in growing mice with e2 presence so with normal ERA signalling + strong androgen the ERA is amplified and thus growth plates closes.
LEO AND LONGEVITY

 

[Zagro]

in growing mice with e2 presence so with normal ERA signalling + strong androgen the ERA is amplified and thus growth plates closes.
LEO AND LONGEVITY

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/)

 

[lookingbad]

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/)

this study shows nothing; neither what u mentioned on the ER..

 

[Zagro]

this study shows nothing; neither what u mentioned on the ER..

You obviously have no idea what you're talking about you retard lol

 

[lookingbad]

You obviously have no idea what you're talking about you retard lol

u meant that abaloparatide wont work? or that no ER = abaloparatide doesnt work?

 

[Zagro]

in growing mice with e2 presence so with normal ERA signalling + strong androgen the ERA is amplified and thus growth plates closes.
LEO AND LONGEVITY

Where's the evidence behind this

u meant that abaloparatide wont work? or that no ER = abaloparatide doesnt work?

You wont benefit from PTH

 

[lookingbad]

Where's the evidence behind this


You wont benefit from PTH

keep coping nga

 

[Zagro]

keep coping nga

Yes bro pull shit out your ass and counter-argument with “heheh keep coping nigga”

 

[lookingbad]

Abalo in the context of linear growth --> interaction with chondrocyte maturation and osteoblast activation.

modulating endochondral ossification dynamics --> support a more favorable balance between cartilage formation and bone deposition, potentially preserving or enhancing growth plate activity.

 

[Zagro]

Abalo in the context of linear growth --> interaction with chondrocyte maturation and osteoblast activation.

modulating endochondral ossification dynamics --> support a more favorable balance between cartilage formation and bone deposition, potentially preserving or enhancing growth plate activity.

You can just paste what gpt said bro not as if it isn't obvious

Just telling me random processes which you don't have a clue about

I still see zero evidence? Interesting point bro did you know bac water increases SOX9? Source? Nah i don't have one just trust me

 

[Genio]

DNR, Mirin the Fady Bakry pfp though

 

[lookingbad]

You can just paste what gpt said bro not as if it isn't obvious

Just telling me random processes which you don't have a clue about

I still see zero evidence? Interesting point bro did you know bac water increases SOX9? Source? Nah i don't have one just trust me

smarter people than you raccomend it; fletch raccomend it

 

[Zagro]

smarter people than you raccomend it; fletch raccomend it

Okay bro androgenic told me to smash my pelvic bone for longitudinal growth and he is smarter so he must be right?

Fletch doesn't have extended knowledge in heightmaxxing, he supports compounds such as T3 which directly ossify the epiphyseal growth plates through TRα1 and TRβ1, not so smart innit

 

[lookingbad]

Okay bro androgenic told me to smash my pelvic bone for longitudinal growth and he is smarter so he must be right?

Fletch doesn't have extended knowledge in heightmaxxing, he supports compounds such as T3 which directly ossify the epiphyseal growth plates through TRα1 and TRβ1, not so smart innit

he doesnt raccomend them in puberty nga

 

[Zagro]

he doesnt raccomend them in puberty nga

Oh yeah very obviously bro he does say that, he never said to use it only in puberty and if he did I'm not in some secret circle jerk of his.

He's a retard if he supports nuking E2 and I do not fucking care about what you do lol go believe whatever he says with zero research yourself as you cant even back your own claims here

 

[lookingbad]

Oh yeah very obviously bro he does say that, he never said to use it only in puberty and if he did I'm not in some secret circle jerk of his.

He's a retard if he supports nuking E2 and I do not fucking care about what you do lol go believe whatever he says with zero research yourself as you cant even back your own claims here

he just says to avoid any ERa and use something for ERb agonism
u could use a lot more for neuroprotection but u cant understand that.

 

[Zagro]

he just says to avoid any ERa and use something for ERb agonism
u could use a lot more for neuroprotection but u cant understand that.

The fact that I never talked about neuroprotection but you brought it up and told me I cant understand it

 

[lookingbad]

The fact that I never talked about neuroprotection but you brought it up and told me I cant understand it

i was talking about the neuroprotection effect of the erb; why the fuck u need e2 explain more nga

 

[Swtchrr]

just inhibit the downstream cascade e2 uses to fuse plates and profit

how

 

[birthdefect]

how

bro quiet literally anything but researching

 

[birthdefect]

Oh yeah very obviously bro he does say that, he never said to use it only in puberty and if he did I'm not in some secret circle jerk of his.

He's a retard if he supports nuking E2 and I do not fucking care about what you do lol go believe whatever he says with zero research yourself as you cant even back your own claims here

how do you feel about the idea i had?
nuke e2 to 2-5 pg/ml and use alfatradiol to make up for whats lost with low e2

 

[lookingbad]

how do you feel about the idea i had?
nuke e2 to 2-5 pg/ml and use alfatradiol to make up for whats lost with low e2

or take s equol; better ERb agonism and little to none ERa agonism

 

[birthdefect]

or take s equol; better ERb agonism and little to none ERa agonism

thank you for showing me this
i wonder how this would compare to alfatradiol

 

[pedro218]

the same way you mantain them while ur on on Aromasting compounds? and then how tf you inhibit the downstream cascade e2 uses?? u use fulvestrant?

do you got source of fulvestrant?

 

[lookingbad]

do you got source of fulvestrant?

message me man

 

[pedro218]

message me man

can u send your discord?

 

[lookingbad]

thank you for showing me this
i wonder how this would compare to alfatradiol

i think either using s-equol 15-40mg a day for ERb agonism to fill the E2 absence or using Fluvoxamine for the BDNF Increase & Seratonergic effects at a low dosage (e.g.: 25mg/day) should be the base when u have really low e2 levels..

 

[infrainfra]

i think either using s-equol 15-40mg a day for ERb agonism to fill the E2 absence or using Fluvoxamine for the BDNF Increase & Seratonergic effects at a low dosage (e.g.: 25mg/day) should be the base when u have really low e2 levels..

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.