Halotestin’s effect on height [Manlets GTFIH]

[N4rco]

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:

• 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

View attachment 4752601

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”.

Link: https://pubmed.ncbi.nlm.nih.gov/8464656/

• Stanhope 1985 study on the - “Constitutional delay of growth and puberty in boys: the effect of a short course of treatment with fluoxymesterone”

Link: https://pubmed.ncbi.nlm.nih.gov/4003064/

View attachment 4752591
View attachment 4752596

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.
View attachment 4752618
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.

View attachment 4752699View attachment 4752700

• 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.

View attachment 4752713

• 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.

Has absolutely anyone tried this yet?

 

[vi24v_]

Has absolutely anyone tried this yet?

I’m not the first person to write this so probably

 

[HumbleMTNN]

There are more but still not that much - stopped using it medically due to its side effects which I’ve mentioned, it’s like how there are no studies on humans with Tren but we know it works

Bunch of kids on chemotherapy fucking roid raging and fighting eachother

 

[awesomesauce75]

I started taking it today but with var and accutane so my liver might give up

Nah ur chilling var gets processed in kidneys

 

[foidslayer92910]

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:

• 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

View attachment 4752601

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”.

Link: https://pubmed.ncbi.nlm.nih.gov/8464656/

• Stanhope 1985 study on the - “Constitutional delay of growth and puberty in boys: the effect of a short course of treatment with fluoxymesterone”

Link: https://pubmed.ncbi.nlm.nih.gov/4003064/

View attachment 4752591
View attachment 4752596

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.
View attachment 4752618
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.

View attachment 4752699View attachment 4752700

• 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.

View attachment 4752713

• 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.

mirin thread

 

[infrainfra]

And this paper on fluoxy also doesn’t mean shit for height if that’s what you wanna hear

Tren is 10-fold better

tren increases estrogen receptor sensitivity via its progesterone interactions. and its metabolites literally activate the ER directly. half the time the only reason tren is in a cycle is because it’s been hyped up as the poster child of steroids.

@sherry12

 

[Zagro]

tren increases estrogen receptor sensitivity via its progesterone interactions. and its metabolites literally activate the ER directly. half the time the only reason tren is in a cycle is because it’s been hyped up as the poster child of steroids.

@sherry12

Bro do you wanna do this thing again where I put you down in your place like the last few times you’ve done this, your fucking gpt research doesn’t compare

 

[infrainfra]

Bro do you wanna do this thing again where I put you down in your place like the last few times you’ve done this, your fucking gpt research doesn’t compare

bro you didnt put me back u just put me on ignore and constantly backed ur nonsense up by in vitro studies. why did u put a laughing emoji up there after i named some facts? halo has the same igf-1 mRNA increase as tren does.ALL ANDROGENS DO TO SOME EXTENT. maybe tren is stronger but the sides outweigh the pros any day. i dont want to debunk your knowledge just argue? why not halo? why tren

 

[Zagro]

bro you didnt put me back u just put me on ignore and constantly backed ur nonsense up by in vitro studies. why did u put a laughing emoji up there after i named some facts? halo has the same igf-1 mRNA increase as tren does.ALL ANDROGENS DO TO SOME EXTENT. maybe tren is stronger but the sides outweigh the pros any day. i dont want to debunk your knowledge just argue? why not halo? why tren

Oh mate sorry they don’t fucking give kids research compounds to see how they respond, it’s not like i do it on purpose idiot that’s the evidence we have so far

You didn’t name any facts tren doesn’t bind ER directly or in any way at all, only to the PR which is technically downstream of estrogen, do you know what that means? Rape estrogen

Tell me how long you can run halo at high doses till your liver just gives up

 

[aimar12913en]

good thread

 

[infrainfra]

Oh mate sorry they don’t fucking give kids research compounds to see how they respond, it’s not like i do it on purpose idiot that’s the evidence we have so far

You didn’t name any facts tren doesn’t bind ER directly or in any way at all, only to the PR which is technically downstream of estrogen, do you know what that means? Rape estrogen

Tell me how long you can run halo at high doses till your liver just gives up

i had a stroke reading the 1st part i dont understand what you wanted to say by that.


tren doesnt directly bind ER its metabolites do. i said it increases estrogen RECEPTOR sensitivity via its progesterone interactions. and you yourself said to use something to inhibit ER partially while nuking e2 since ur body makes them more sensitive as a compensatory mechanism ( i think u where talking about SERDs). so why use tren which makes it even worse? plus again its metabolites directly activate it.

for the halo part no u shouldn't run “high doses” tell me what a high dose u think is.
in height growth studies 5mg works really well and 9 year olds take it. it has only been replaced by var for safety reasons.
and since u care so much about health then why rape ur teenage neurotransmitters with tren?

the main reason why im defending halo so much is bc its actually been used for height in the past. and it has a better receptor affinity and dimorphic gene transcription

 

[zkss]

5 minutes and 0 reps

Could you please dm me a legit fgfr3 source. Looking for infig(lost over 1000aud to a fake telegram source recently.)

 

[Matt_r7x]

seems legit, will look into it. ( i read the whole thing brah)

 

[needsomessris]

is taking this with abalo, infig and some other chems safe or no

 

[guts000]

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:

• 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

View attachment 4752601

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”.

Link: https://pubmed.ncbi.nlm.nih.gov/8464656/

• Stanhope 1985 study on the - “Constitutional delay of growth and puberty in boys: the effect of a short course of treatment with fluoxymesterone”

Link: https://pubmed.ncbi.nlm.nih.gov/4003064/

View attachment 4752591
View attachment 4752596

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.
View attachment 4752618
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.

View attachment 4752699View attachment 4752700

• 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.

View attachment 4752713

• 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.

very nice bump

 

[guts000]

is taking this with abalo, infig and some other chems safe or no

with halo dont take ANY OTHER LIVER DAMAGING COMPOUNDS

 

[guts000]

I started taking it today but with var and accutane so my liver might give up

why var tho.thats like adding cjc while having hgh in cycle

 

[Folasade]

Nice post, although is the suppression of the HPT axis permanent? I’m pretty sure that if you stop taking Halo, the side effects become transient.

 

[WilhelmThyWizard]

DR + THANKS

 

[vi24v_]

Nice post, although is the suppression of the HPT axis permanent? I’m pretty sure that if you stop taking Halo, the side effects become transient.

almost all the time it isint permanent - use a test base while running halo but your hpt axis will recover post usage

 

[iblameniceguy]

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:

• 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

View attachment 4752601

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”.

Link: https://pubmed.ncbi.nlm.nih.gov/8464656/

• Stanhope 1985 study on the - “Constitutional delay of growth and puberty in boys: the effect of a short course of treatment with fluoxymesterone”

Link: https://pubmed.ncbi.nlm.nih.gov/4003064/

View attachment 4752591
View attachment 4752596

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.
View attachment 4752618
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.

View attachment 4752699View attachment 4752700

• 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.

View attachment 4752713

• 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.

Is it even worth to hop on Halo + Test for maybe 5-8 Weeks and then do a TRT to save my puperty and natural testosterone production?

 

[vi24v_]

Is it even worth to hop on Halo + Test for maybe 5-8 Weeks and then do a TRT to save my puperty and natural testosterone production?

What is 5 weeks of test even going to do bro

 

[theonlyrealrage]

how much shit u gotta take for height? hgh + ai + androgens + peptides + fgfr3 inhibitros + halotestin + etc

Well definetly not copetides

 

[theonlyrealrage]

What is 5 weeks of test even going to do bro

How long youd run this?

This is ai, but it does seem tren is better. Trenbolone outperforms Halotestin for height because its ~3× higher AR binding affinity plus direct IGF-1 upregulation in growth-plate chondrocytes drives greater chondrocyte proliferation and longitudinal expansion. Cattle implant trials show dose-dependent hip-height and frame-size gains; rat bone models confirm stronger AR-mediated skeletal protection without aromatization. Halotestin delivers proven 5.4–6.1 cm net adult height in delayed boys, but lacks Tren’s amplified IGF-1 signal and therefore caps out lower before senescence.

so theoretically, if youre really desperate, why not take both, halo and tren?
Also thinking about throwing in some test cyp, boldenone and occasionally andadrol for masculineisation

Id cruise tren and pretty much all of these pharmas but I dont know anything about ancillery or side mitigation

 

[sherry12]

How long youd run this?

so theoretically, if youre really desperate, why not take both, halo and tren?
Also thinking about throwing in some test cyp, boldenone and occasionally andadrol for masculineisation

Id cruise tren and pretty much all of these pharmas but I dont know anything about ancillery or side mitigation

do u think it’s a good idea to run halo and tren with no test lmfao

 

[theonlyrealrage]

Mirin, On test rn should i experiment for everyone?

Im on test awell rn.

Im looking to try halo with tren but im not sure how to propely manage the sides, especially the hair shedding..
But also just general ancillary and sides like bp, inflamation or liver toxicity management im currently still learning about.

Not quite sure if the money that i currently have is going to be enough for both the gear, and the side mitigation stack..

So i might as well just study the side mitigation part whilst already blasting, which ofc is more dangerous, but im so insanely tired of being little bitch that gets zero pussy, has no friends, and gets treated like shit by everyone everyday.

I need the gear to make me become lower inhib and actually do shit with my life that i otherwise wouldnt be able to do.(reading this again got me thinking fuck the sides)

I kinda digressed but Yea.. side mitigation, realistically speaking cant be neglected

 

[omicr0n]

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:

• 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

View attachment 4752601

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”.

Link: https://pubmed.ncbi.nlm.nih.gov/8464656/

• Stanhope 1985 study on the - “Constitutional delay of growth and puberty in boys: the effect of a short course of treatment with fluoxymesterone”

Link: https://pubmed.ncbi.nlm.nih.gov/4003064/

View attachment 4752591
View attachment 4752596

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.
View attachment 4752618
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.

View attachment 4752699View attachment 4752700

• 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.

View attachment 4752713

• 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.

Wdyt of other orals like var,stana,etc

 

[stigmaboy]

@0 bone mass mtn take

 

[vi24v_]

@0 bone mass mtn take

Posted months ago I’m not even on halo no more

 

[mouldychicken172]

Literally zero unique properties its just strong get some test or tren and it'll be much better although with tren you have a lot more things to watch out for, nice non-aromatising androgen though

thoughts on hgh and test during puberty for height?

 

[ltnheII]

bump