D
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what would jordan do?
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How it works
In the human body, the Hypothalamic-Pituitary-Testicular Axis (HPTA) controls testosterone biosynthesis. The HPTA is a tightly regulated system of checks and balances that works to assure the correct level of testosterone is maintained. We can look at this regulating process as having three levels. At the top is the hypothalamic region of the brain, which releases GnRH (Gonadotropin- Releasing Hormone) when it senses a need for more testosterone. GnRH sends a signal to the second level of the axis, the pituitary, to produce Luteinizing Hormone (LH). LH in turn sends a message to the Leydig’s cells in the testes (level three) to secrete testosterone.
However, use of exogenous hormones (like Rad-140) binds to AR receptors (which work like lock and keys), and cause negative feedback to lower the secretion of LH and testosterone, preventing overproduction. This leads to suppression/shutdown.
Recovery
After cessation is that the brain recognizes testosterone levels are low again. This will cause GnRH and LH levels begin correcting fairly quickly. Since Sarms prevent total shutdown and have shorter half lives (in comparison to 19-nors), You can probably "recover" fairly quickly upon stopping. Unaided recovery occurs in around 1-4months from testosterone usage, and is influenced by age, initial testosterone levels, and ethnicity.
Why teenagers shouldnt do sarms
The idea behind SARMS are that they are Selective Androgen Receptor Modulators. They were developed medically with the intention to selectively bind to muscles, and excert no androgenic effects. This is a great breakthrough for bodybuilders who want to build muscle without acne. Androgenicity is what makes you a male. When you take this substance during puberty, you are essentially blocking your puberty. Testosterone acts in so many pathways, for example:
"It also appears that androgens are necessary for the local production and function of IGF-1 in skeletal muscle cells, independent of circulating growth hormone, and IGF-1 levels", DHT is required for maturation,penis growth, bone structure growth, and other pubertal changes. By taking sarms you are replacing Testosterone with Testostelone, and trading maturation and development for more selective muscle growth. You are trading height, bone mass increase, penis growth, brain development for more muscles. Not to mention the detremental effect low estrogen will have on your development.
"Recovery"
When you suppress your LH (by negative feedback loop), your leydig cells in your testies atrophy. They dont develop as they should since your body is using rad140. The effect is underdeveloped testicles. Even if you can bounce back from a cycle or two, long term use will cause permanent underdevelopment of the testicles and impaired abilty for spermatogenesis.
Our investigations reported that prolonged treatment of intact rats with testosterone significantly disturbed steroidogenic machinery and remarkably reduced the capacity of purified Leydig cells to produce testosterone ex vivo"
"Result showed that prolonged in vivo treatment with testosterone decreased the expression of Scarb1 (scavenger receptor class B type 1), Tspo (translocator protein), Star (steroidogenic acute regulatory protein), Cyp11a1 (cholesterol side-chain cleavage enzyme), and Cyp17a1 (17α-hydroxylase/17, 20 lyase) in Leydig cells. Oppositely, the expression of Hsd3b (3-beta-hydroxysteroid dehydrogenase/delta-5-delta-4 isomerase), Ar (androgen receptor), and Pde4a/b (cyclic adenosine monophosphate-dependent phosphodiesterases) was increased. Androgenization for 2 weeks inhibited Cyp19 (aromatase) transcription, whereas 2-month exposure caused the opposite effect. Direct in vitro testosterone treatment also decreased the expression of Cyp11a1, Cyp17a1, and Cyp19a1, whereas Hsd3b was upregulated. The results of expression analysis were supported by declined steroidogenic capacity and activity of Leydig cells, although conversion of pregnenolone to progesterone was stimulated." https://academic.oup.com/toxsci/article/121/2/397/1727752
Reductions of these was the same as old Rats which couldnt produce as much testosterone:
"Defects in aging Brown Norway rat Leydig cells include reductions in each of LH-stimulated cAMP production, STAR, TSPO, CYP11A1, and downstream steroidogenic enzymes"
Recovery (my personal experience)
I aimed to upregulate the steroidogenic enzymes which I had inhibited. I took Cistanche since it contains echinacoside. echinacoside was shown too "significantly increasesmRNA (Genetic) levels of CYP11A1, CYP17A1, HSD3β1/2 and HSD17β, and particularly HSD3β1/2, which are key enzymes responsible for active hormonal conversions ". Same ones which are damaged by sarms and steroids
In the human body, the Hypothalamic-Pituitary-Testicular Axis (HPTA) controls testosterone biosynthesis. The HPTA is a tightly regulated system of checks and balances that works to assure the correct level of testosterone is maintained. We can look at this regulating process as having three levels. At the top is the hypothalamic region of the brain, which releases GnRH (Gonadotropin- Releasing Hormone) when it senses a need for more testosterone. GnRH sends a signal to the second level of the axis, the pituitary, to produce Luteinizing Hormone (LH). LH in turn sends a message to the Leydig’s cells in the testes (level three) to secrete testosterone.
However, use of exogenous hormones (like Rad-140) binds to AR receptors (which work like lock and keys), and cause negative feedback to lower the secretion of LH and testosterone, preventing overproduction. This leads to suppression/shutdown.
Recovery
After cessation is that the brain recognizes testosterone levels are low again. This will cause GnRH and LH levels begin correcting fairly quickly. Since Sarms prevent total shutdown and have shorter half lives (in comparison to 19-nors), You can probably "recover" fairly quickly upon stopping. Unaided recovery occurs in around 1-4months from testosterone usage, and is influenced by age, initial testosterone levels, and ethnicity.
Why teenagers shouldnt do sarms
The idea behind SARMS are that they are Selective Androgen Receptor Modulators. They were developed medically with the intention to selectively bind to muscles, and excert no androgenic effects. This is a great breakthrough for bodybuilders who want to build muscle without acne. Androgenicity is what makes you a male. When you take this substance during puberty, you are essentially blocking your puberty. Testosterone acts in so many pathways, for example:
"It also appears that androgens are necessary for the local production and function of IGF-1 in skeletal muscle cells, independent of circulating growth hormone, and IGF-1 levels", DHT is required for maturation,penis growth, bone structure growth, and other pubertal changes. By taking sarms you are replacing Testosterone with Testostelone, and trading maturation and development for more selective muscle growth. You are trading height, bone mass increase, penis growth, brain development for more muscles. Not to mention the detremental effect low estrogen will have on your development.
"Recovery"
When you suppress your LH (by negative feedback loop), your leydig cells in your testies atrophy. They dont develop as they should since your body is using rad140. The effect is underdeveloped testicles. Even if you can bounce back from a cycle or two, long term use will cause permanent underdevelopment of the testicles and impaired abilty for spermatogenesis.
Our investigations reported that prolonged treatment of intact rats with testosterone significantly disturbed steroidogenic machinery and remarkably reduced the capacity of purified Leydig cells to produce testosterone ex vivo"
"Result showed that prolonged in vivo treatment with testosterone decreased the expression of Scarb1 (scavenger receptor class B type 1), Tspo (translocator protein), Star (steroidogenic acute regulatory protein), Cyp11a1 (cholesterol side-chain cleavage enzyme), and Cyp17a1 (17α-hydroxylase/17, 20 lyase) in Leydig cells. Oppositely, the expression of Hsd3b (3-beta-hydroxysteroid dehydrogenase/delta-5-delta-4 isomerase), Ar (androgen receptor), and Pde4a/b (cyclic adenosine monophosphate-dependent phosphodiesterases) was increased. Androgenization for 2 weeks inhibited Cyp19 (aromatase) transcription, whereas 2-month exposure caused the opposite effect. Direct in vitro testosterone treatment also decreased the expression of Cyp11a1, Cyp17a1, and Cyp19a1, whereas Hsd3b was upregulated. The results of expression analysis were supported by declined steroidogenic capacity and activity of Leydig cells, although conversion of pregnenolone to progesterone was stimulated." https://academic.oup.com/toxsci/article/121/2/397/1727752
Reductions of these was the same as old Rats which couldnt produce as much testosterone:
"Defects in aging Brown Norway rat Leydig cells include reductions in each of LH-stimulated cAMP production, STAR, TSPO, CYP11A1, and downstream steroidogenic enzymes"
Recovery (my personal experience)
I aimed to upregulate the steroidogenic enzymes which I had inhibited. I took Cistanche since it contains echinacoside. echinacoside was shown too "significantly increasesmRNA (Genetic) levels of CYP11A1, CYP17A1, HSD3β1/2 and HSD17β, and particularly HSD3β1/2, which are key enzymes responsible for active hormonal conversions ". Same ones which are damaged by sarms and steroids
