Looksmax DONT USE SERMS FOR HEIGHMAXXING. The reformatted ones any mods looking please delete the old one(reupload) (1 Viewer)

[Circadex]

dont hop on serms rn is my reccomendation hop on a year later as serms supress IGF-1 so yeah deal with gyno later as you can always deal with that https://pubmed.ncbi.nlm.nih.gov/2924327/
And rn is the peak growth period if im not wrong hop on them at 15
(how deep are you into being 14 fresh or like nearing 15)
But then again do as you wish they still do retain bone age pretty effectivly too but just the supression might be terrible.

Blah blah blah

Pin whatever you can get your hands on + AI and don't look back. Or, the enlightened method

 

[Mirin]

Fair but damn your lucky to discover all this shit at this young of a age

Yeh over for old fags muh

 

[Fram3Let]

Now, firstly, why did I make this thread?Because too many people don't know wtf they are hopping on.



Yet dont know how these work exactly.So I'll go over it today.

---

Firstly: MECHANISMS OF ACTION(skip this if you already know)

For both SERMs and AIs...(btw I hope EVERYONE here knows est is the thing that ages and closes your plates and bones, if not please do like 2 Google searches and comeback)

Aromatase Inhibitors (AIs) competitively bind to the cytochrome P450 enzyme aromatase (CYP19A1). This enzyme is responsible for the rate-limitingstep in estrogen biosynthesis: the conversion of androgens (like testosterone) into estrogens. By inhibiting this enzyme, AIs reduce the body'sactual estrogen production [Source 2].

SERMs - The "Receptor Blockers": SERMs, however, dont stop the body from producing estrogen; they bind directly to ERs (ERα and ERβ) at thecellular level because they are “selective.” Their shape changes depending on the tissue they bind to. And they can recruit corepressors to act as anestrogen antagonist in some tissues, or recruit coactivators to act as an est agonist in others. Systemic levels remain normal or even becomeelevated when on a SERM, but the target tissues can't “see” est [Source 3].

---

We all know why and how AIs affect height: less conversion to est ➔ less est ➔ less bone aging, and plate fusion. If interested, go to [Source4].

But what about SERMs and, in certain scenarios, tamoxifen?

While yes, tamoxifen can delay bone age, however, its pharmacological profile severely harms the rate of growth. Clinical studies show thattamoxifen acts systemically to suppress IGF-1. Additionally, tamoxifen is TOXIC to your growth plate, inducing apoptosis(programmed cell death) in the resting zone chondrocytes [Source 6].

Therefore, tamoxifen is basically negligible when it comes to heighmaxxing... save that shit for your gyno boyo.

Additionally, Raloxifene in mammalian animal models (rabbits/rats) actually stunted height due to the body thinking that there was a surge inestrogen and therefore accelerating bone age. This has not been proven to be the case with humans, however, why the fuck would you still take this??Just hop on AIs.

---

TLDR for all those dnr spammers:DONT USE SERMS FOR HEIGHMAXXING​

---

Sources:

1. Estrogen's Role in Epiphyseal Fusion (Baseline):Grumbach, M. M. (2000). Estrogen, bone, growth, and sex: a sea change in conventional wisdom. Journal of Pediatric Endocrinology and Metabolism,13(Suppl 6), 1439-1455. [PMID: 11154000]
2. Aromatase Inhibitors - Mechanism and Predicted Height Gains (Hero et al.):Hero, M., Norjavaara, E., & Dunkel, L. (2005). Inhibition of estrogen biosynthesis with a potent aromatase inhibitor increases predicted adult height inboys with idiopathic short stature: a randomized controlled trial. The Journal of Clinical Endocrinology & Metabolism, 90(12), 6396–6402. [PMID:16189252]
3. SERMs - Molecular Mechanism of Action:Riggs, B. L., & Hartmann, L. C. (2003). Selective estrogen-receptor modulators — mechanisms of action and application to clinical practice. New EnglandJournal of Medicine, 348(7), 618-629. [PMID: 12584371]
4. Aromatase Inhibitors - Maintenance of Growth Velocity via Androgens:Hero, M., et al. (2005). Letrozole treatment and pubertal growth in boys. Acta Paediatrica, 94(1), 108-110. [PMID: 15858969]
5. Tamoxifen - Pediatric Dosing and Predicted Height Claims:Kreher, N. C., Eugster, E. A., & Shankar, R. R. (2005). The use of tamoxifen to improve height potential in short pubertal boys. Pediatrics, 116(6),1513-1515. [PMID: 16322179]
6. The SERM Flaw - IGF-1 Suppression and Chondrocyte Apoptosis:Karimian, E., et al. (2008). Tamoxifen and raloxifene differ in their effects on longitudinal bone growth and growth plate chondrocytes. Journal ofEndocrinology, 198(2), 293-300. [PMID: 18492803] (This is the critical study proving why Tamoxifen stunts growth velocity despitedelaying bone age).

---

DisclaimerThis is all hypothetical and satire, and the beliefs of the people in this community do not reflect my own.​

What if you just take a bunch of gh with tamoxifen?
Mandy

 

[oyopth31]

What if you just take a bunch of gh with tamoxifen?

Then it completly overrides the small amoutn of igf-1 supression still would be worried on apoptosis though

 

[Mandy]

It’s a nice thread overall,I just don’t like it. Saying “Don’t use SERMs for height” is simply too broad and retarded,you even said tamoxifen itself dosen’t have negligible effects and it’s most raloxifene that has been shown to accelerate fusion. Also you’re stating obvious knowledge I myself made a thread on tamoxifen today

https://looksmax.gg/threads/i-slowed-down-my-bone-age-dramatically-via-tamoxifen.23646/

And I would like to say the IGF-1 argument with the tamoxifen is negligible,that’s the total serum and CIRCULATORY amount. In fact,the slight reduction in IGF-1 could be a factor in slowing down bone maturation and causing the first layer of chondrocytes in the epiphyseal plate to be resting for a longer period of time ,of course SLIGHT.

Also yeah AI is cope,it’s water and barely to use. I already made a thread about this too.

https://looksmax.gg/threads/water-f...al-aromatase-activity-wont-save-fusion.23397/

 

[Mandy]

And by the way, Apoptosis is one of the main benefits of tamoxifen in gynecomastia,literally the way it kills glandular breast tissue. It’s selective for a reason,it’s a partial agonist for bone yet an antagonist in breast tissue. SELECTIVE.

 

[Mandy]

Mandy Isn't it only toxic or proven to stunt growth in mice

It’s not toxic,how many times do I need to repeat.

 

[Mandy]

dont hop on serms rn is my reccomendation hop on a year later as serms supress IGF-1 so yeah deal with gyno later as you can always deal with that h

You’re massively exaggerating the “suppressed IGF-1”,also after 2-3 years of gynecomastia development the tissue is not active enough for regression. Either now or later,you can’t just get rid of gyno with tamoxifen at any time and if it was possible then gyno surgery wouldn’t be a thing today.

 

[Mandy]

What if you just take a bunch of gh with tamoxifen?
Mandy

Good synergy,this is water and something you could have thought of yourself.

 

[oyopth31]

https://looksmax.gg/threads/water-f...al-aromatase-activity-wont-save-fusion.23397/

I answered that one in the replys idk if you saw it

Don’t use SERMs for height” is simply too broad and retarded,

Ofc yeah should make my titles more nuanced I made it pretty clickbaity

the only other side now really that we cant bypass or is not neglisable is apoptosis https://pubmed.ncbi.nlm.nih.gov/17293177/
Truthfully hope this one gets debunked cus i really do want to hop on serms

 

[Mandy]

I answered that one in the replys idk if you saw it


Ofc yeah should make my titles more nuanced I made it pretty clickbaity

the only other side now really that we cant bypass or is not neglisable is apoptosis https://pubmed.ncbi.nlm.nih.gov/17293177/
Truthfully hope this one gets debunked cus i really do want to hop on serms

Out of all the things that are similar in mice to humans,chondrocytes,growth and bones are often inaccurate and don’t behave the human way. Check this out:
https://pubmed.ncbi.nlm.nih.gov/16322179/

 

[Mirin]

It’s not toxic,how many times do I need to repeat.

Sorry bro

 

[Mandy]

Sorry bro

All it does it upregulate enzymes ALT and AST in the liver,not enough to a point where it actually stresses your liver in any way.

 

[oyopth31]

Out of all the things that are similar in mice to humans,chondrocytes,growth and bones are often inaccurate and don’t behave the human way. Check this out:
https://pubmed.ncbi.nlm.nih.gov/16322179/

alright this has given me reason to consider serms again learning expereince for me today
thanks for the enlightement

 

[Mandy]

alright this has given me reason to consider serms again learning expereince for me today
thanks for the enlightement

Also check my most recent thread,the first one I linked on the first post. I dramatically slowed down my bone age and I grew 3cm in the past 2 months without GH or anything else. (16 years old right now)

 

[Mirin]

Also check my most recent thread,the first one I linked on the first post. I dramatically slowed down my bone age and I grew 3cm in the past 2 months without GH or anything else. (16 years old right now)

Alright thats it im hoping on for 6 months

 

[Biomaxx]

Now, firstly, why did I make this thread?Because too many people don't know wtf they are hopping on.



Yet dont know how these work exactly.So I'll go over it today.

---

Firstly: MECHANISMS OF ACTION(skip this if you already know)

For both SERMs and AIs...(btw I hope EVERYONE here knows est is the thing that ages and closes your plates and bones, if not please do like 2 Google searches and comeback)

Aromatase Inhibitors (AIs) competitively bind to the cytochrome P450 enzyme aromatase (CYP19A1). This enzyme is responsible for the rate-limitingstep in estrogen biosynthesis: the conversion of androgens (like testosterone) into estrogens. By inhibiting this enzyme, AIs reduce the body'sactual estrogen production [Source 2].

SERMs - The "Receptor Blockers": SERMs, however, dont stop the body from producing estrogen; they bind directly to ERs (ERα and ERβ) at thecellular level because they are “selective.” Their shape changes depending on the tissue they bind to. And they can recruit corepressors to act as anestrogen antagonist in some tissues, or recruit coactivators to act as an est agonist in others. Systemic levels remain normal or even becomeelevated when on a SERM, but the target tissues can't “see” est [Source 3].

---

We all know why and how AIs affect height: less conversion to est ➔ less est ➔ less bone aging, and plate fusion. If interested, go to [Source4].

But what about SERMs and, in certain scenarios, tamoxifen?

While yes, tamoxifen can delay bone age, however, its pharmacological profile severely harms the rate of growth. Clinical studies show thattamoxifen acts systemically to suppress IGF-1. Additionally, tamoxifen is TOXIC to your growth plate, inducing apoptosis(programmed cell death) in the resting zone chondrocytes [Source 6].

Therefore, tamoxifen is basically negligible when it comes to heighmaxxing... save that shit for your gyno boyo.

Additionally, Raloxifene in mammalian animal models (rabbits/rats) actually stunted height due to the body thinking that there was a surge inestrogen and therefore accelerating bone age. This has not been proven to be the case with humans, however, why the fuck would you still take this??Just hop on AIs.

---

TLDR for all those dnr spammers:DONT USE SERMS FOR HEIGHMAXXING​

---

Sources:

1. Estrogen's Role in Epiphyseal Fusion (Baseline):Grumbach, M. M. (2000). Estrogen, bone, growth, and sex: a sea change in conventional wisdom. Journal of Pediatric Endocrinology and Metabolism,13(Suppl 6), 1439-1455. [PMID: 11154000]
2. Aromatase Inhibitors - Mechanism and Predicted Height Gains (Hero et al.):Hero, M., Norjavaara, E., & Dunkel, L. (2005). Inhibition of estrogen biosynthesis with a potent aromatase inhibitor increases predicted adult height inboys with idiopathic short stature: a randomized controlled trial. The Journal of Clinical Endocrinology & Metabolism, 90(12), 6396–6402. [PMID:16189252]
3. SERMs - Molecular Mechanism of Action:Riggs, B. L., & Hartmann, L. C. (2003). Selective estrogen-receptor modulators — mechanisms of action and application to clinical practice. New EnglandJournal of Medicine, 348(7), 618-629. [PMID: 12584371]
4. Aromatase Inhibitors - Maintenance of Growth Velocity via Androgens:Hero, M., et al. (2005). Letrozole treatment and pubertal growth in boys. Acta Paediatrica, 94(1), 108-110. [PMID: 15858969]
5. Tamoxifen - Pediatric Dosing and Predicted Height Claims:Kreher, N. C., Eugster, E. A., & Shankar, R. R. (2005). The use of tamoxifen to improve height potential in short pubertal boys. Pediatrics, 116(6),1513-1515. [PMID: 16322179]
6. The SERM Flaw - IGF-1 Suppression and Chondrocyte Apoptosis:Karimian, E., et al. (2008). Tamoxifen and raloxifene differ in their effects on longitudinal bone growth and growth plate chondrocytes. Journal ofEndocrinology, 198(2), 293-300. [PMID: 18492803] (This is the critical study proving why Tamoxifen stunts growth velocity despitedelaying bone age).

---

DisclaimerThis is all hypothetical and satire, and the beliefs of the people in this community do not reflect my own.​

Bm. Will read later