vi24v_
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In this thread I will be talking about how halotestin (aka Fluoxymestorone) can be used to increase final adult height and increase linear growth velocity as long as growth plates aren’t closed.
In this guide I will:
Introduction to Halotestin:
- Halotestin is an oral 17-alpha-alkylated AAS which means that it can survive metabolism, allowing it to reach the bloodstream in an active form without being destroyed by the liver.
- 17x more potent that testosterone
- Halotestin is a DHT derivative which means not aromatize to an amount that is considered significant if any at all
Studies that i am using:
What the studies show:
View attachment 4752604
In the Strickland 1993 study we can see that during treatment of boys with CDGP + GSS (Constitutional delay of growth + genetic short stature) we can see that each patient had 1.7-2.5x increase in linear growth velocity whilst on treatment and that the treatment group had a final height of 6.1-5.4cm.
In the Stanhope 1985 we can see that the mean increment of growth velocity went up to 4.5cm/year on treatment whilst the change in SDS to bone age was not significant. This is shows that Halotestin can be used safely to induce a growth acceleration in adolescent boys.
What does this mean for us:
This study shows that when bone age is around 14 - final height and growth velocity can be increased. This leads me to belive that when bone age is closer to 16 - results are still visible however slowed to an extent. We can also see through the study that androgens can Interact with growth plate chondrocyte, which may increase chondrocyte proliferation and enhance responsiveness to igf-1 which can temporarily increase growth velocity during adolescence.
We also know that the activation of the androgen receptors in bone tissue can stimulate osteoblast activity activity along the periosteum, increasing cortical bone deposition which can lead to thicker craniofacial bones along with the increases in growth.
This means that through the running halotestin at 2.5-10mg we can increase linear growth, increase thickness of craniofacial bones and increase final adult height.
However when bone age is closer to 16 than 14 - epiphyseal fusion is causing the body towards stopping vertical growth. This means to maximise growth output we have to keep our growth plates open for as long as possible through inhibiting aromatase and fgfr3 with drugs such as Anastrozole (arimidex) and Vosoritide.
What are the side effects of Halotestin and how can we use ancillaries to support use:
Halotestin has many sides so we will go through the 1 by 1 to explain how they can be supported:
This is my second post so my formatting is not that good but if u found the post helpful then please rep. If u did not read the post its must appreciated if u just bump the post with a DNR.
In this guide I will:
- Introduce what Halotestin is
- What studies I am using in this thread
- What the studies show
- What this means for us
- Side affects and ancillaries to support use of Halotestin
Introduction to Halotestin:
- Halotestin is an oral 17-alpha-alkylated AAS which means that it can survive metabolism, allowing it to reach the bloodstream in an active form without being destroyed by the liver.
- 17x more potent that testosterone
- Halotestin is a DHT derivative which means not aromatize to an amount that is considered significant if any at all
Studies that i am using:
- Strickland 1993 study on the - “Long-term results of treatment with low-dose fluoxymesterone in constitutional delay of growth and puberty and in genetic short stature”.
- Stanhope 1985 study on the - “Constitutional delay of growth and puberty in boys: the effect of a short course of treatment with fluoxymesterone”
What the studies show:
View attachment 4752604
In the Strickland 1993 study we can see that during treatment of boys with CDGP + GSS (Constitutional delay of growth + genetic short stature) we can see that each patient had 1.7-2.5x increase in linear growth velocity whilst on treatment and that the treatment group had a final height of 6.1-5.4cm.
In the Stanhope 1985 we can see that the mean increment of growth velocity went up to 4.5cm/year on treatment whilst the change in SDS to bone age was not significant. This is shows that Halotestin can be used safely to induce a growth acceleration in adolescent boys.
What does this mean for us:
This study shows that when bone age is around 14 - final height and growth velocity can be increased. This leads me to belive that when bone age is closer to 16 - results are still visible however slowed to an extent. We can also see through the study that androgens can Interact with growth plate chondrocyte, which may increase chondrocyte proliferation and enhance responsiveness to igf-1 which can temporarily increase growth velocity during adolescence.
We also know that the activation of the androgen receptors in bone tissue can stimulate osteoblast activity activity along the periosteum, increasing cortical bone deposition which can lead to thicker craniofacial bones along with the increases in growth.
This means that through the running halotestin at 2.5-10mg we can increase linear growth, increase thickness of craniofacial bones and increase final adult height.
However when bone age is closer to 16 than 14 - epiphyseal fusion is causing the body towards stopping vertical growth. This means to maximise growth output we have to keep our growth plates open for as long as possible through inhibiting aromatase and fgfr3 with drugs such as Anastrozole (arimidex) and Vosoritide.
What are the side effects of Halotestin and how can we use ancillaries to support use:
Halotestin has many sides so we will go through the 1 by 1 to explain how they can be supported:
- Suppression of the HPT axis: This means that the body wont produce its own natural testosterone. To counteract this you must use testosterone while on cycle and use HCG and enclomiphine during PCT to increase LH and FSH signalling and mitigate hormonal imbalances.
- Liver hepatotoxicity: Don’t use other liver toxic drugs such as accutane, tren or other oral AASs. Use drugs and supplements such as glutathione, N-Acetyl, TUDCA and UDCA to support your liver.
- Lipid profile: Since your lipid profile and cholestrol will be under heavy strain. Use drugs such as Ezetimibe and Rosuvastatin to lower LDL and support your lipid profile
This is my second post so my formatting is not that good but if u found the post helpful then please rep. If u did not read the post its must appreciated if u just bump the post with a DNR.
