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.
Sources:
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:
- 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]
- 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]
- 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]
- 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]
- 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]
- 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.
