The Ultimate pubertymaxxing guide, an introduction into androgens and growth factors, and how to apply them.

[Jayjay0001]

That would fuck my Body up right?

 

[AHAHAXDDD]

SAM-e
MSM
Glucosamine Sulphate
Chondroitin
Ecdysterone
Folinic acid
Folic acid
Si-Wu-tang extract
Meclizine
BMP
Hexarelin

So this is your full stack right? I'm gonna add T3, GHRP 2, CJC w/o DAC, DSIP and Astragalus extract mixture HT042, if i don't grow im going ER on 6ft+ lanklets tbh

did it work

 

[gwiz]

why use hgh and igf-1 at the same time when igf-1 causes all the growth anyway wouldn't it be better to spend more money on the igf-1 peptides and remove the expensive hgh and just swap it out with mk-677 for that hgh boost of course the hgh is stronger than mk-677 but why not just use pure igf-1?

 

[PlatinumBoy51]

View attachment 1489229



it is estrogen with no negative side effects of estrogen

I still believe in erdar, I talk with him on WhatsApp ,,he said his formula have improved ,, also he is working on dickmaxxing research and suggested some compound,, he also got scientist of year again , so we can trust him,,
also rapist's growth plate research link,, we all be 6'2 on may 2022

also arent u "bri__" in our private heightmaxxing discord?

Hi, is you private heightmaxxing discord with a capybara/beaver-like profile pic ?

 

[Jayjay0001]

Hi, is you private heightmaxxing discord with a capybara/beaver-like profile pic ?

what discord?

 

[jware]

Same what’s the discord

 

[PlatinumBoy51]

what discord?

He claimed to have a private heightmaxxing discord

 

[Iblamejordan]

Preface:
I've had a lot of questions in my pm's recently regarding growth hormone, IGF-1, and androgens.
specifically, people asking me for sources and stacks, how they work, etc, I'm hoping this guide will be able to answer as many of your questions as possible.

Disclaimer:
this thread is going to be very long, I'm going, to begin with explaining each of these chemicals, their mechanisms, and functions whilst also citing studies,
if you're wanting to learn how to apply these chemicals to your protocol than skip down to where I begin talking about methods.

Introduction:
Okay, so this in this thread I'm going to do my best at explaining how growth factors and androgens
affect facial development, induce sexual dimorphism and vertical growth, I'm going to begin
explaining the biological mechanisms of these hormones and then how you can apply them
cost-effectively.

HGH:
Somatropin, commonly referred to as HGH or GH is a 191 amino acid chain that is produced by the pituitary gland,
this peptide stimulates growth, cell reproduction, and cell regeneration in humans and other animals. It is thus important in human development.
GH also stimulates the production of IGF-1 and increases the concentration of glucose and free fatty acids. It belongs to a family of hormones known as the growth hormone family. This also includes prolactin (PRL) and placental lactogen. Despite the obvious differences in function, these hormones share a very similar structure. Likewise, GH and PRL are the only two non-tropic hormones synthesized and released from the anterior pituitary gland. (So yes if you're taking cabergoline you will inhibit growth hormone as they are from the same family).

Growth hormone itself isn't actually what induces growth, it's the metabolites of somatropin that induce cell proliferation, hyperplasia, and hypertrophy.
this class of growth factors is called insulin-like growth factors, they are molecularly structured similar to that of insulin, somatropin is needed for the creation of IGF's within the liver. IGF-2 is the primary growth factor responsible for fetal development, whereas IGF-1 is the primary growth factor responsible for inducing growth within adolescent children. (more on insulin-like growth factors later).

somatropin is needed for the development of our bodies, the reason us looksmaxxers are obsessed with it is because of dimorphic growth-related effects
that are induced by the insulin-like growth factor family of hormones.

somatropin's effect on craniofacial development within children.




Yes, these children did have GHDD (growth hormone deficiency disorder), but this doesn't disprove that the usage of exogenous somatropin
can induce craniofacial growth. These children would have been administrated growth hormone dosages that would have aligned with normal children's endogenous production. Our goal with growth hormone is to increase the endogenous production of IGF-1 way above super physiological levels in order to affect our craniofacial growth. Keep in mind, in this study the children were dosed 0.5IU daily, that's around 15-fold less than what I suggest you should dose daily, and these children still reap the positive craniofacial benefits.

The abstract of a study based on how the GH/IGF-1 axis influences bone formation, growth, and remodeling.


somatropin's effect on hard tissue, bone formation, and osteoclasts.


somatropin effects on bone formation through osteoblasts.


The GH/IGF-1 axis and it's interaction with androgens when it comes to bone formation.



Insulin-like growth factors, specifically somatomedin-C (IGF-1):
IGF-1 is produced all the way throughout life. The highest rates of IGF-1 production occur during the pubertal growth spurt. The lowest levels occur in infancy and old age. This is why children grow rapidly during puberty, somatropin is at an all-time high, meaning more conversion to IGF-1, typically in healthy children, the baseline IGF-1 scoring is between 250-500ng/dl, although higher IGF-1 scoring is possible with exogenous intervention.

IGF-1 is a primary mediator of the effects of somatropin (GH), growth hormone is released into the bloodstream, and then stimulates the liver to produce insulin-like growth factors, we are specifically focusing on IGF-1. These IGF's then stimulate systemic body growth and has growth-promoting effects on almost every cell in the body, especially skeletal muscle, cartilage, bone, liver, etc... In addition to the insulin-like effects, IGF-1 can also regulate cellular DNA synthesis. IGF-1 is our friend, we want our levels to be sky-high during puberty to reap all of the dimorphic growth and surpass our genetic potential, there are some road blockages though, along with the insulin-like growth factor family comes the IGFBP's (insulin-like growth factor binding proteins) yeah it's a mouth full jfl. These proteins bind to IGF-1 and inhibit it from attaching to the IGF-1R, basically, it renders our IGF-1 useless within the body. These proteins, unfortunately, have a high affinity to bind to IGF's, there are counter measurements to these IGFBP's though, stay tuned.

Protein intake increases IGF-1 levels in humans, independent of total calorie consumption. Factors that are known to cause variation in the levels of growth hormone (GH) and IGF-1 in the circulation include insulin levels, genetic make-up, the time of day, age, sex, exercise status, stress levels, nutrition level and body mass index, disease state, ethnicity, and estrogen status.

I'm not going to be citing studies for IGF-1, as GH and IGF-1 fall in the same category, the GH/IGF-1 axis is what influences growth.

Androgens, androgenic metabolites, and pro-hormones:
despite the common knowledge surrounding testosterone there seems to be less appreciation when it comes to other androgens. Androgens are synthesized from cholesterol and are produced primarily in the gonads (testicles and ovaries) and also in the adrenal glands to a small extent. The testicles produce a much higher quantity than the ovaries in females. Dimorphic growth is heavily dependent on androgens, specifically testosterone, dihydrotestosterone (DHT), and dehydroepiandrosterone (DHEA), I'm going to be underling each androgen, and their biological mechanisms.

View attachment 258656
Testosterone:
testosterone is the primary male sex hormone that is responsible for differentiating a male fetus from a female fetus, In male humans, testosterone plays a key role in the development of reproductive tissues such as testes and prostate, as well as promoting sexual dimorphisms such as increased muscle mass, bone mass and the growth of body hair. The pituitary gland located within the brain produces a signaling chemical called luteinizing hormone (LH), LH signals the Leydig cells within the testes to synthesize testosterone from cholesterol. Production of luteinizing hormone spikes during puberty, sending multiple signals to the Leydig cells to produce more testosterone, in turn, promoting masculinization and dimorphism to occur.

the effect of low dose testosterone on the craniofacial development in children with delayed puberty.


Keep in mind, these children didn't have zero testosterone, they were just experiencing delayed puberty, low dose testosterone was enough to kickstart their craniofacial development.

View attachment 258654
Dihydrotestosterone:
DHT is biologically important for sexual differentiation of the male genitalia during embryogenesis, maturation of the penis and scrotum at puberty, growth of facial, body and pubic hair, and development and maintenance of the prostate gland and seminal vesicles. It is produced from testosterone by an enzyme called 5-alpha-reductase (5AR) in select tissues and is the primary androgen in the genitals, prostate gland, seminal vesicles, skin, and hair follicles. Dihydrotestosterone can have up to 5x the potency of testosterone when it comes to inducing androgenic dimorphism, that isn't to say that testosterone isn't important though.

View attachment 258653
Androsterone:
Androsterone is an androgenic steroid derived via the activity of the enzyme 5-AR and is a downstream metabolite of the more potent androgen DHT. Like all 5-AR derived androgens, androsterone displays anti-estrogenic and anti-glucocorticoid activity and in addition, serves as a pro-hormone for DHT and other potent androgens. In addition, androsterone is a neurosteroid with potent GABA agonist activity and is known to function as a pheromone in many animal species including humans. It has been shown to possess anti-depressant and anti-proliferative effects. Perhaps most importantly, it has been found to act like as a potent thyroid mimetic and as such to increase basal temperature, oxygen consumption and lower lipid levels in humans.

androsterone and its effect on the masculinization of male fetuses.





View attachment 258780
dehydroepiandrosterone
Dehydroepiandrosterone (DHEA), also known as androstenolone, is an endogenous steroid hormone. It is one of the most abundant circulating steroids in humans, in whom it is produced in the adrenal glands, the gonads, and the brain. It functions as a metabolic intermediate in the biosynthesis of the androgen and estrogen sex steroids both in the gonads and in various other tissues. On its own, it's a very weak androgen, but it potently converts to testosterone within certain tissue, it is more abundant within females than males as it also converts to estrogen.

How to apply these hormones to your protocol:

let's begin with the growth hormone/igf1 aspect to our protocol, our main goal is to induce craniofacial growth (specifically maxillary and mandibular growth), vertical growth, and dimorphism, this can be achieved via a multitude of method, here we go.

How to increase IGF-1 levels beyond the super physiological natural range
through the usage of exogenous GH and PEPTIDES:

Method 1:
Recombinant growth hormone:
increasing our IGF-1 levels beyond the super physiological range is simple, although I disagree with some of
@Extra Chromosome's opinions on heightmaxxing, I'm going to do my best to express my opinion as I have experience and knowledge within the field of GH and Peptides.

To begin with, I personally think the usage of recombinant growth hormone (synthetic bioidentical somatropin) is the best and most practical way to increase IGF-1 and induce growth, that's not to say that peptides don't have their place, but they aren't as effective as HGH (I'll go into more detail later). Recombinant growth hormone is expensive, very expensive, but if you source it correctly you can bypass the majority of the cost issues.

I'd suggest dosing HGH at around 5IU-8IU's daily. This will skyrocket your IGF-1, even more so if you're a teenager as the conversion rate from somatropin to IGF-1 is higher, in most growing teenagers this amount of GH will put you into the 700-900ng/dl range for IGF-1 scoring, at this level cell proliferation, hyperplasia and osteoblast/osteoclast activity will increase dramatically. In other words, you'll grow, vertically and horizontally. If your soul usage of HGH is for height gains than either exemestane, letrozole or Arimidex will suffice for aromatase inhibition.

To sum method 1 up:
5-8iu's of HGH ED
(optional) Aromatase inhibitor of your choice.

Method 2:
HGH combined with IGF-1 LR3 and IGF-1 DES.
the combination of both exogenous GH and exogenous IGF-1 is amazing. As I've mentioned above alongside insulin-like growth factors comes IGFBP's (Insulin-like growth factor binding proteins) IGFPB's have a high affinity to bind onto IGF-1 and IGF-2 within the bloodstream rendering them useless and unable to attach to the IGF-1R and IGF-2R, meaning a small portion of the HGH that we inject into ourselves is going to waste as these proteins are rendering the IGF-1 unable to function, there is a way around this.

the polypeptides IGF-LR3 and IGF-DES have a low affinity to bind to the IGFBP's, meaning they are up to 3x more potent than regular endogenous IGF-1. IGF-1LR3 also happens to have a half-life of up to 30 hours. IGF-DES is even more potent than LR3, the only downside is that it has a 30-minute half-life before it is metabolized by the body, DES also happens to be more localized, so we are going to opt for LR3 in this method as it is more systemic than DES. The combination of HGH and exogenous IGF-1 will guarantee growth. (if your plates are open of course).

To sum method 2 up:
5-8iu's of HGH ED
IGF-1 LR3 100mcg ED
(optional) IGF-1 DES 50mcg ED
(optional) Aromatase inhibitor

Method 3
Peptide protocol.
peptides can be great for increasing serum levels of growth hormone and inevitably increasing IGF-1 scoring within the blood, the reason why I prefer synthetic GH is that the pituitary gland can only produce so much GH, meaning there is a limit to the number of signals it can take to produce a certain amount of somatropin. For example, you could inject more exogenous GH than you could make endogenous GH with the help of peptides, I hope that makes sense. Peptides can still boost your IGF-1 scoring beyond the natural range, some peptides even stimulate the Pi3k pathways, which is a bonus.

peptides are split up into 2 categories, GHRH's and GHRP's, our bodies make growth hormone-releasing hormone to signal the somatroph cells to produce somatropin within the pituitary gland, GHRH peptides basically tell the pituitary to release GH, growth hormone-releasing peptides basically amplify the production of growth hormone that is being secreted, stacking both a GHRH and a GHRP is necessary for increasing IGF-1 as they synergize well.

here's the peptide protocol that I recommend, whilst on this stack my IGF-1 came back at over 800ng/dl, in that time period I grew an inch and a half in height within 2 and a half months.



switching back and forth from hexarelin and GHRP-2 is necessary as desensitization will occur whilst using hexarelin at any dosage for longer than 14 days. Having 14 days off and 7 days on allows your body to sensitize to the peptide again. I do not recommend the usage of CJC DAC as it has been proven to cause damage to the pituitary gland with chronic usage.

Okay, that sums up the GH/IGF-1 section, overall I'd say if you're on a budget than peptides is the route you should take, if you have more money to spend than go for HGH if you're really fucking determined than take the HGH/IGF-1LR3 route.

The good thing about working with somatropin and peptides is that exogenous usage won't cause a negative feedback loop to occur, meaning if you discontinue the usage of growth hormone you won't feel like shit as you would with testosterone (unless you do a correct PCT). Your endogenous somatropin will begin producing normally again.

How to increase endogenous androgen activity without causing suppression
or shutdown from occurring:
working with androgens can be tricky and dangerous, you can take two routes with androgens, you can either take metabolites and non-suppressive prohormones or you can take androgens like testosterone and cause a shutdown.

the usage of androgens such as dehydroepiandrosterone and androsterone along with progesterone can be of great benefit to those who are looking
to masculinize themselves without using testosterone. dehydroepiandrosterone (DHEA) is one of the most abundant steroid hormones within the human body, it is produced by the adrenals and can be converted to either testosterone or estrogen. The supplementation of exogenous DHEA alone can lead to both an increase in estrogen and testosterone, combining DHEA with androsterone is a good idea as androsterone is a very powerful anti-aromatase, estrogen isn't the enemy, it's just having high estrogen is a negative, inhibiting the aromatase enzyme from converting testosterone from converting to estrogen allows for the DHEA to convert into testosterone smoothly without a spike in estrogen as your original estrogen will just be replaced.

View attachment 258661
The usage of Delta-sleep-inducing-peptide to increase natural testosterone:
my recent findings suggest that the usage of the delta-sleep inducing peptide (DSIP) can greatly benefit steroid users who are trying to regain their LH production.
DSIP increases the amount of gonadotropin that is being secreted at night time, gonadotropin signals the pituitary gland to produce LH, that LH than signals the Leydig cells to synthesize testosterone from cholesterol. More gonadotropin signaling = more luteinizing hormone signaling meaning more testosterone being made. DSIP also happens to block corticotropin from releasing cortisol, meaning cortisol cannot antagonize testosterone, leaving you with more testosterone to circulate the bloodstream. DSIP also blocks the release of somatostatin (growth hormone inhibiting hormone), somatostatins role is to lower growth hormone if it raises to high, so by blocking the release of this hormone we are preventing our blood serum level of GH dropping.

Delta-sleep inducing peptide is a must for those looking to increase testosterone without the usage of AAS or those who are using peptides and/or Recombinant GH, as it has potent somatostatin inhibiting properties.
check out my thread on DSIP

The usage of HCG
human chorionic gonadotropin is an LH mimic that can be injected subcutaneously, it acts the exact same way that LH does in that it signals the Leydig cells to produce testosterone, HCG will keep your balls from shrinking if you're running testosterone on an AAS cycle. It can increase testosterone but it has a tendency to also increase estrogen, in combination with testosterone it can induce dimorphism greatly, whilst maintaining testicular functions and fertility, it can also be implemented to make your PCT easier.

The usage of exogenous testosterone:
the usage of exogenous testosterone can greatly induce sexual dimorphism, increase bone density, anabolism, protein synthesis, and nitrogen retention. Whilst also saturated the androgen receptors. There are obvious downsides to the usage, but if done effectively there shouldn't be any issues. For teenagers willing to run testosterone, (I don't condone the usage) I'd suggest using testosterone base (no ester attached) dissolved into DMSO applied to the skin, I'd also suggest that you take the best measure to run a safe and sought out PCT.

The usage of exogenous dihydrotestosterone (androstanolone)
dihydrotestosterone can be very beneficial for those who are in the midst of puberty, at the correct dosages it isn't very suppressive and if minimal suppression occurs, then you can easily bounce back. Androstanolone is a synthetic DHT that is bioidentical to DHT. The usage of dihydrotestosterone will have an intense masculinizing effect, if you're in puberty it may affect the size of your penis and frame.

You can make a transdermal concoction with DMSO and androstanolone, with a high absorption rate. Androstanolone is an extremely androgenic steroid hormone, it has highly anti-estrogenic properties so be cautious with the dosages if you don't want to crash your E2 levels.
check out my thread on dihydrotestosterone

conclusion
a combination of both high dosages of either recombinant growth hormone or peptides alongside the optimization or exogenous usage of androgens is synergistic when it comes to craniofacial forward growth, sexual dimorphism and vertical growth.

here's my current stack for perspective.


this took like 3 days to make because I'm a lazy cunt, anyways hoped you gained something from it.

View attachment 258787

hoping that'll answer some questions for you guys.
@JustTrynaGrow @Slyfex8 @draco @Don't Forget to mew @Tom2004 @Crazzen8 @ht-normie-ascending @Dr Shekelberg @forwardgrowth @maxmendietta @PubertyMaxxer @apollothegun @KKK

​

Do very low calories negatively affect this pubertymaxxing? Should consume enough calories?

 

[zipzam]

What would you recommend for a 17 year old?

 

[Jayjay0001]

Do very low calories negatively affect this pubertymaxxing? Should consume enough calories?

ofcourse.. your body need to be at maintain or best at surplus calories. But its another story if you
are above 20%bf, you then should cut down to 12-15% bf

 

[Jayjay0001]

View attachment 1489229



it is estrogen with no negative side effects of estrogen

I still believe in erdar, I talk with him on WhatsApp ,,he said his formula have improved ,, also he is working on dickmaxxing research and suggested some compound,, he also got scientist of year again , so we can trust him,,
also rapist's growth plate research link,, we all be 6'2 on may 2022

also arent u "bri__" in our private heightmaxxing discord?

could you send me an invite to your private discord?

 

[zipzam]

Preface:
I've had a lot of questions in my pm's recently regarding growth hormone, IGF-1, and androgens.
specifically, people asking me for sources and stacks, how they work, etc, I'm hoping this guide will be able to answer as many of your questions as possible.

Disclaimer:
this thread is going to be very long, I'm going, to begin with explaining each of these chemicals, their mechanisms, and functions whilst also citing studies,
if you're wanting to learn how to apply these chemicals to your protocol than skip down to where I begin talking about methods.

Introduction:
Okay, so this in this thread I'm going to do my best at explaining how growth factors and androgens
affect facial development, induce sexual dimorphism and vertical growth, I'm going to begin
explaining the biological mechanisms of these hormones and then how you can apply them
cost-effectively.

HGH:
Somatropin, commonly referred to as HGH or GH is a 191 amino acid chain that is produced by the pituitary gland,
this peptide stimulates growth, cell reproduction, and cell regeneration in humans and other animals. It is thus important in human development.
GH also stimulates the production of IGF-1 and increases the concentration of glucose and free fatty acids. It belongs to a family of hormones known as the growth hormone family. This also includes prolactin (PRL) and placental lactogen. Despite the obvious differences in function, these hormones share a very similar structure. Likewise, GH and PRL are the only two non-tropic hormones synthesized and released from the anterior pituitary gland. (So yes if you're taking cabergoline you will inhibit growth hormone as they are from the same family).

Growth hormone itself isn't actually what induces growth, it's the metabolites of somatropin that induce cell proliferation, hyperplasia, and hypertrophy.
this class of growth factors is called insulin-like growth factors, they are molecularly structured similar to that of insulin, somatropin is needed for the creation of IGF's within the liver. IGF-2 is the primary growth factor responsible for fetal development, whereas IGF-1 is the primary growth factor responsible for inducing growth within adolescent children. (more on insulin-like growth factors later).

somatropin is needed for the development of our bodies, the reason us looksmaxxers are obsessed with it is because of dimorphic growth-related effects
that are induced by the insulin-like growth factor family of hormones.

somatropin's effect on craniofacial development within children.




Yes, these children did have GHDD (growth hormone deficiency disorder), but this doesn't disprove that the usage of exogenous somatropin
can induce craniofacial growth. These children would have been administrated growth hormone dosages that would have aligned with normal children's endogenous production. Our goal with growth hormone is to increase the endogenous production of IGF-1 way above super physiological levels in order to affect our craniofacial growth. Keep in mind, in this study the children were dosed 0.5IU daily, that's around 15-fold less than what I suggest you should dose daily, and these children still reap the positive craniofacial benefits.

The abstract of a study based on how the GH/IGF-1 axis influences bone formation, growth, and remodeling.


somatropin's effect on hard tissue, bone formation, and osteoclasts.


somatropin effects on bone formation through osteoblasts.


The GH/IGF-1 axis and it's interaction with androgens when it comes to bone formation.



Insulin-like growth factors, specifically somatomedin-C (IGF-1):
IGF-1 is produced all the way throughout life. The highest rates of IGF-1 production occur during the pubertal growth spurt. The lowest levels occur in infancy and old age. This is why children grow rapidly during puberty, somatropin is at an all-time high, meaning more conversion to IGF-1, typically in healthy children, the baseline IGF-1 scoring is between 250-500ng/dl, although higher IGF-1 scoring is possible with exogenous intervention.

IGF-1 is a primary mediator of the effects of somatropin (GH), growth hormone is released into the bloodstream, and then stimulates the liver to produce insulin-like growth factors, we are specifically focusing on IGF-1. These IGF's then stimulate systemic body growth and has growth-promoting effects on almost every cell in the body, especially skeletal muscle, cartilage, bone, liver, etc... In addition to the insulin-like effects, IGF-1 can also regulate cellular DNA synthesis. IGF-1 is our friend, we want our levels to be sky-high during puberty to reap all of the dimorphic growth and surpass our genetic potential, there are some road blockages though, along with the insulin-like growth factor family comes the IGFBP's (insulin-like growth factor binding proteins) yeah it's a mouth full jfl. These proteins bind to IGF-1 and inhibit it from attaching to the IGF-1R, basically, it renders our IGF-1 useless within the body. These proteins, unfortunately, have a high affinity to bind to IGF's, there are counter measurements to these IGFBP's though, stay tuned.

Protein intake increases IGF-1 levels in humans, independent of total calorie consumption. Factors that are known to cause variation in the levels of growth hormone (GH) and IGF-1 in the circulation include insulin levels, genetic make-up, the time of day, age, sex, exercise status, stress levels, nutrition level and body mass index, disease state, ethnicity, and estrogen status.

I'm not going to be citing studies for IGF-1, as GH and IGF-1 fall in the same category, the GH/IGF-1 axis is what influences growth.

Androgens, androgenic metabolites, and pro-hormones:
despite the common knowledge surrounding testosterone there seems to be less appreciation when it comes to other androgens. Androgens are synthesized from cholesterol and are produced primarily in the gonads (testicles and ovaries) and also in the adrenal glands to a small extent. The testicles produce a much higher quantity than the ovaries in females. Dimorphic growth is heavily dependent on androgens, specifically testosterone, dihydrotestosterone (DHT), and dehydroepiandrosterone (DHEA), I'm going to be underling each androgen, and their biological mechanisms.

View attachment 258656
Testosterone:
testosterone is the primary male sex hormone that is responsible for differentiating a male fetus from a female fetus, In male humans, testosterone plays a key role in the development of reproductive tissues such as testes and prostate, as well as promoting sexual dimorphisms such as increased muscle mass, bone mass and the growth of body hair. The pituitary gland located within the brain produces a signaling chemical called luteinizing hormone (LH), LH signals the Leydig cells within the testes to synthesize testosterone from cholesterol. Production of luteinizing hormone spikes during puberty, sending multiple signals to the Leydig cells to produce more testosterone, in turn, promoting masculinization and dimorphism to occur.

the effect of low dose testosterone on the craniofacial development in children with delayed puberty.


Keep in mind, these children didn't have zero testosterone, they were just experiencing delayed puberty, low dose testosterone was enough to kickstart their craniofacial development.

View attachment 258654
Dihydrotestosterone:
DHT is biologically important for sexual differentiation of the male genitalia during embryogenesis, maturation of the penis and scrotum at puberty, growth of facial, body and pubic hair, and development and maintenance of the prostate gland and seminal vesicles. It is produced from testosterone by an enzyme called 5-alpha-reductase (5AR) in select tissues and is the primary androgen in the genitals, prostate gland, seminal vesicles, skin, and hair follicles. Dihydrotestosterone can have up to 5x the potency of testosterone when it comes to inducing androgenic dimorphism, that isn't to say that testosterone isn't important though.

View attachment 258653
Androsterone:
Androsterone is an androgenic steroid derived via the activity of the enzyme 5-AR and is a downstream metabolite of the more potent androgen DHT. Like all 5-AR derived androgens, androsterone displays anti-estrogenic and anti-glucocorticoid activity and in addition, serves as a pro-hormone for DHT and other potent androgens. In addition, androsterone is a neurosteroid with potent GABA agonist activity and is known to function as a pheromone in many animal species including humans. It has been shown to possess anti-depressant and anti-proliferative effects. Perhaps most importantly, it has been found to act like as a potent thyroid mimetic and as such to increase basal temperature, oxygen consumption and lower lipid levels in humans.

androsterone and its effect on the masculinization of male fetuses.





View attachment 258780
dehydroepiandrosterone
Dehydroepiandrosterone (DHEA), also known as androstenolone, is an endogenous steroid hormone. It is one of the most abundant circulating steroids in humans, in whom it is produced in the adrenal glands, the gonads, and the brain. It functions as a metabolic intermediate in the biosynthesis of the androgen and estrogen sex steroids both in the gonads and in various other tissues. On its own, it's a very weak androgen, but it potently converts to testosterone within certain tissue, it is more abundant within females than males as it also converts to estrogen.

How to apply these hormones to your protocol:

let's begin with the growth hormone/igf1 aspect to our protocol, our main goal is to induce craniofacial growth (specifically maxillary and mandibular growth), vertical growth, and dimorphism, this can be achieved via a multitude of method, here we go.

How to increase IGF-1 levels beyond the super physiological natural range
through the usage of exogenous GH and PEPTIDES:

Method 1:
Recombinant growth hormone:
increasing our IGF-1 levels beyond the super physiological range is simple, although I disagree with some of
@Extra Chromosome's opinions on heightmaxxing, I'm going to do my best to express my opinion as I have experience and knowledge within the field of GH and Peptides.

To begin with, I personally think the usage of recombinant growth hormone (synthetic bioidentical somatropin) is the best and most practical way to increase IGF-1 and induce growth, that's not to say that peptides don't have their place, but they aren't as effective as HGH (I'll go into more detail later). Recombinant growth hormone is expensive, very expensive, but if you source it correctly you can bypass the majority of the cost issues.

I'd suggest dosing HGH at around 5IU-8IU's daily. This will skyrocket your IGF-1, even more so if you're a teenager as the conversion rate from somatropin to IGF-1 is higher, in most growing teenagers this amount of GH will put you into the 700-900ng/dl range for IGF-1 scoring, at this level cell proliferation, hyperplasia and osteoblast/osteoclast activity will increase dramatically. In other words, you'll grow, vertically and horizontally. If your soul usage of HGH is for height gains than either exemestane, letrozole or Arimidex will suffice for aromatase inhibition.

To sum method 1 up:
5-8iu's of HGH ED
(optional) Aromatase inhibitor of your choice.

Method 2:
HGH combined with IGF-1 LR3 and IGF-1 DES.
the combination of both exogenous GH and exogenous IGF-1 is amazing. As I've mentioned above alongside insulin-like growth factors comes IGFBP's (Insulin-like growth factor binding proteins) IGFPB's have a high affinity to bind onto IGF-1 and IGF-2 within the bloodstream rendering them useless and unable to attach to the IGF-1R and IGF-2R, meaning a small portion of the HGH that we inject into ourselves is going to waste as these proteins are rendering the IGF-1 unable to function, there is a way around this.

the polypeptides IGF-LR3 and IGF-DES have a low affinity to bind to the IGFBP's, meaning they are up to 3x more potent than regular endogenous IGF-1. IGF-1LR3 also happens to have a half-life of up to 30 hours. IGF-DES is even more potent than LR3, the only downside is that it has a 30-minute half-life before it is metabolized by the body, DES also happens to be more localized, so we are going to opt for LR3 in this method as it is more systemic than DES. The combination of HGH and exogenous IGF-1 will guarantee growth. (if your plates are open of course).

To sum method 2 up:
5-8iu's of HGH ED
IGF-1 LR3 100mcg ED
(optional) IGF-1 DES 50mcg ED
(optional) Aromatase inhibitor

Method 3
Peptide protocol.
peptides can be great for increasing serum levels of growth hormone and inevitably increasing IGF-1 scoring within the blood, the reason why I prefer synthetic GH is that the pituitary gland can only produce so much GH, meaning there is a limit to the number of signals it can take to produce a certain amount of somatropin. For example, you could inject more exogenous GH than you could make endogenous GH with the help of peptides, I hope that makes sense. Peptides can still boost your IGF-1 scoring beyond the natural range, some peptides even stimulate the Pi3k pathways, which is a bonus.

peptides are split up into 2 categories, GHRH's and GHRP's, our bodies make growth hormone-releasing hormone to signal the somatroph cells to produce somatropin within the pituitary gland, GHRH peptides basically tell the pituitary to release GH, growth hormone-releasing peptides basically amplify the production of growth hormone that is being secreted, stacking both a GHRH and a GHRP is necessary for increasing IGF-1 as they synergize well.

here's the peptide protocol that I recommend, whilst on this stack my IGF-1 came back at over 800ng/dl, in that time period I grew an inch and a half in height within 2 and a half months.



switching back and forth from hexarelin and GHRP-2 is necessary as desensitization will occur whilst using hexarelin at any dosage for longer than 14 days. Having 14 days off and 7 days on allows your body to sensitize to the peptide again. I do not recommend the usage of CJC DAC as it has been proven to cause damage to the pituitary gland with chronic usage.

Okay, that sums up the GH/IGF-1 section, overall I'd say if you're on a budget than peptides is the route you should take, if you have more money to spend than go for HGH if you're really fucking determined than take the HGH/IGF-1LR3 route.

The good thing about working with somatropin and peptides is that exogenous usage won't cause a negative feedback loop to occur, meaning if you discontinue the usage of growth hormone you won't feel like shit as you would with testosterone (unless you do a correct PCT). Your endogenous somatropin will begin producing normally again.

How to increase endogenous androgen activity without causing suppression
or shutdown from occurring:
working with androgens can be tricky and dangerous, you can take two routes with androgens, you can either take metabolites and non-suppressive prohormones or you can take androgens like testosterone and cause a shutdown.

the usage of androgens such as dehydroepiandrosterone and androsterone along with progesterone can be of great benefit to those who are looking
to masculinize themselves without using testosterone. dehydroepiandrosterone (DHEA) is one of the most abundant steroid hormones within the human body, it is produced by the adrenals and can be converted to either testosterone or estrogen. The supplementation of exogenous DHEA alone can lead to both an increase in estrogen and testosterone, combining DHEA with androsterone is a good idea as androsterone is a very powerful anti-aromatase, estrogen isn't the enemy, it's just having high estrogen is a negative, inhibiting the aromatase enzyme from converting testosterone from converting to estrogen allows for the DHEA to convert into testosterone smoothly without a spike in estrogen as your original estrogen will just be replaced.

View attachment 258661
The usage of Delta-sleep-inducing-peptide to increase natural testosterone:
my recent findings suggest that the usage of the delta-sleep inducing peptide (DSIP) can greatly benefit steroid users who are trying to regain their LH production.
DSIP increases the amount of gonadotropin that is being secreted at night time, gonadotropin signals the pituitary gland to produce LH, that LH than signals the Leydig cells to synthesize testosterone from cholesterol. More gonadotropin signaling = more luteinizing hormone signaling meaning more testosterone being made. DSIP also happens to block corticotropin from releasing cortisol, meaning cortisol cannot antagonize testosterone, leaving you with more testosterone to circulate the bloodstream. DSIP also blocks the release of somatostatin (growth hormone inhibiting hormone), somatostatins role is to lower growth hormone if it raises to high, so by blocking the release of this hormone we are preventing our blood serum level of GH dropping.

Delta-sleep inducing peptide is a must for those looking to increase testosterone without the usage of AAS or those who are using peptides and/or Recombinant GH, as it has potent somatostatin inhibiting properties.
check out my thread on DSIP

The usage of HCG
human chorionic gonadotropin is an LH mimic that can be injected subcutaneously, it acts the exact same way that LH does in that it signals the Leydig cells to produce testosterone, HCG will keep your balls from shrinking if you're running testosterone on an AAS cycle. It can increase testosterone but it has a tendency to also increase estrogen, in combination with testosterone it can induce dimorphism greatly, whilst maintaining testicular functions and fertility, it can also be implemented to make your PCT easier.

The usage of exogenous testosterone:
the usage of exogenous testosterone can greatly induce sexual dimorphism, increase bone density, anabolism, protein synthesis, and nitrogen retention. Whilst also saturated the androgen receptors. There are obvious downsides to the usage, but if done effectively there shouldn't be any issues. For teenagers willing to run testosterone, (I don't condone the usage) I'd suggest using testosterone base (no ester attached) dissolved into DMSO applied to the skin, I'd also suggest that you take the best measure to run a safe and sought out PCT.

The usage of exogenous dihydrotestosterone (androstanolone)
dihydrotestosterone can be very beneficial for those who are in the midst of puberty, at the correct dosages it isn't very suppressive and if minimal suppression occurs, then you can easily bounce back. Androstanolone is a synthetic DHT that is bioidentical to DHT. The usage of dihydrotestosterone will have an intense masculinizing effect, if you're in puberty it may affect the size of your penis and frame.

You can make a transdermal concoction with DMSO and androstanolone, with a high absorption rate. Androstanolone is an extremely androgenic steroid hormone, it has highly anti-estrogenic properties so be cautious with the dosages if you don't want to crash your E2 levels.
check out my thread on dihydrotestosterone

conclusion
a combination of both high dosages of either recombinant growth hormone or peptides alongside the optimization or exogenous usage of androgens is synergistic when it comes to craniofacial forward growth, sexual dimorphism and vertical growth.

here's my current stack for perspective.


this took like 3 days to make because I'm a lazy cunt, anyways hoped you gained something from it.

View attachment 258787

hoping that'll answer some questions for you guys.
@JustTrynaGrow @Slyfex8 @draco @Don't Forget to mew @Tom2004 @Crazzen8 @ht-normie-ascending @Dr Shekelberg @forwardgrowth @maxmendietta @PubertyMaxxer @apollothegun @KKK

​

HGH too expensive

 

[Iblamejordan]

Before pubertymaxxing

After pubertymaxxing

 

[Luxury]

Before pubertymaxxing
View attachment 2127623

After pubertymaxxing
View attachment 2127624

thats just cocainemaxxing

 

[Iblamejordan]

thats just cocainemaxxing

I'm gonna do cocainemaxxing

 

[letsdoit]

i saw a post in a thread in a different form of a guy who's being scouted for major league basketball who takes hgh alongside ghrp2 and cjc1295 no dac. thoughts?

He was on this forum?

 

[Fayg0]

First of all Great Thread! . Currently 16.5 yo and interested in taking the peptides method. I have a few questions :

- What would be the best and most fiable source to get the peptides from (Preferably cost efficient but oh well)
- I still have around 750 mg of liquid mk-677 still brand new and sealed, can i stack it with the peptides?
- Ive never injected hgh so i was wondering if someone who knew better could quickly sum it up in a few steps, nothing too detailed

Thanks for the thread anyways! Good luck to anyone reading this

 

[Deleted member 29225]

First of all Great Thread! . Currently 16.5 yo and interested in taking the peptides method. I have a few questions :

- What would be the best and most fiable source to get the peptides from (Preferably cost efficient but oh well)
- I still have around 750 mg of liquid mk-677 still brand new and sealed, can i stack it with the peptides?
- Ive never injected hgh so i was wondering if someone who knew better could quickly sum it up in a few steps, nothing too detailed

Thanks for the thread anyways! Good luck to anyone reading this

Just know that the use of MK-677 Ibutamoren is illegal for minors and will probably cause gyno. Either way best of luck.

 

[Fayg0]

Just know that the use of MK-677 Ibutamoren is illegal for minors and will probably cause gyno. Either way best of luck.

I've done some research and people say it barely raises prolactin enough to be considered a risk

 

[letsdoit]

Hey strike, Is your method effective even for adults ?
And If a person grows using your method, will it have any side effects on his progeny ?

Thoughts @Osie

 

[letsdoit]

Hey strike, Is your method effective even for adults ?
And If a person grows using your method, will it have any side effects on his progeny ?

Thoughts? @midlatinocel
Is your stack better?

 

[midlatinocel]

Thoughts? @midlatinocel
Is your stack better?

my stack is for height and this is overall puberty maxxing + this stack messes more with the androgenic hormones while mine focuses on growth

2 different things brother

 

[sibience]

lol

 

[lookmaxx28]

What do you recommend for a 15 year old?

 

[futureashtray]

Take a look at this, gives you an explanation on why pituitary tumors (Gigantism) happens, not because of fucking low levels of testosterone or estrogen https://www.cancer.org/cancer/pituitary-tumors/causes-risks-prevention/what-causes.html 'Some genes control when cells grow, divide into new cells, and die. Genes that help cells grow, divide, and stay alive are called oncogenes. Genes that slow down cell division or cause cells to die at the right time are called tumor suppressor genes. Tumors can be caused by DNA changes that turn on oncogenes or turn off tumor suppressor genes.'

Of course there are DNA mutations inherited by their parents but this is very rare for pituitary tumors but this has just shown that DNA hypermethylation being one of the pathways causing one this pituitary tumor, look at this :https://www.sciencedirect.com/science/article/abs/pii/S1357431097010198 oncogenic mechanism mediated by DNA methylation and https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1421942/ 'Methylation within the promoter regions of tumor suppressor genes causes their silencing, and methylation within the gene itself can induce mutational events'

There you go, gigantism induced by hypermethylation as hypermethylation can silence tumor suppressor genes and increase oncogenes meaning uncontrolled cell growth, combined with high levels of HGH secretion, this makes them grow super tall fast. Do I need to explain to you all any further? Gigantism ain't just HGH, it is HGH+a mutation in the DNA (can also be induced by methylation in the gene) and hypermethylation by itself silences tumor suppressor genes and promotes more oncogensis, this is what is meant by all the SAM-e and folic acid I am telling you all to take, crucial balance IS NEEDED or you will induce a tumor to grow, now I know that may sound exciting for all of you desperate people trying to grow taller fast but please don't fucking do it, I won't be held responsible if u do, 2g enteric coated SAM-e and 800 mcg folic acid is the crucial balance needed just enough to grow taller, and pi3k activation from hexarelin will help while meclizine inhbiits the FGFR3 pathway which is a potent inhibitor of longitudinal bone growth, this is the best stack, stop coping with only peptide stacks. This is what I mean by inducing hypermethylation being necessary to grow well over you DNA limit and to grow as long as gigantism patients do (they grow even after age 30), this is why your men with P.H.D's aren't actively trying to induce hypermethylation as a mechanism to make people grow taller @Dyorotic2. If a tumor comes about because of their intervention their reputation is fucked forever.

Also there is evidence that hypermethylation can turn back the epigenetic clock and reactivate your senescent growth plate activity by looking at gigantism studies. One example of this is Adam Rainer, also look how young Robert wadlow looked before he died, height 8ft 11 and still absolutely no facial hair and how much taller he was compared to his father... also look at naturalheightgrowth website on a person age 27,28, got acromegaly and started growing: http://www.naturalheightgrowth.com/...possible-after-epiphyseal-plate-ossification/. http://www.naturalheightgrowth.com/2012/09/02/update-on-tanya-angus-and-her-growth-progression/

Another piece of evidence suggesting that hypermethylation can turn back the epigenetic clock, making senescent changes in the MSC's reversed as well ready for chondrocyte differentiation.

This is period to this, anyone who still doesn't believe or understand how important inducing hypermethylation is for for growing beyond your DNA regulated growth, start off with these two studies: https://joe.bioscientifica.com/view/journals/joe/186/1/1860241.xml https://europepmc.org/article/PMC/4697695

@Alexanderr @PubertyMaxxer @ghkid2019 @BasedSpinelet257 @Seth Walsh @goat2x @fuccccc @Don't Forget to mew @Dope @Chadelite @Chad1212 hope this clears up some shit for y'all

This is what is meant by heightmaxxing is the exact opposite of cancer treatments! Please stick to the recommendations of SAM-e and folic acid y'all, you DO NOT want to end up like Tanya Angus

do you still think this works?

 

[futureashtray]

Wow.... I just keep finding more and more info every day about this do I, you know how y'all said the HMGA2 gene is a very restrictive gene when it comes to your height? Well guess exactly what is upregulated and downregulated in a pituitary tumor? Look at the screenshot below from the study, btw DMNT3B,DMNT3A( specific CpG site methylation (there are CpG sites like this on your growth plate as well)) and DNMT1 (global methylation), are enzymes which control DNA methylation, look exactly what is upregulation in a pituitary tumor. https://www.frontiersin.org/articles/10.3389/fendo.2019.00290/full
'High levels of methylation have been identified in invasive and large pituitary tumors. DNA methyltransferase overexpression has been detected in pituitary tumors, especially in macroadenomas. Methylation differences at CpG sites in promoter regions may distinguish several types of tumors from normal pituitary tissue'

Btw CpG sites are the promoter regions of genes, DNA methylation is what effects the upregulation and downregulation of these CpG sites, but the DMNT1 enzyme is for all over global methylation as it a maintenance methylase for many different things in the body, as for DMNT1 (maintenance methylase) maintaining chondrocyte phenotype that has already been proved through this study:https://europepmc.org/article/PMC/4697695
In terms of the CpG sites related to the chondrocytes and and growth plate senescence, that is already been associated through this study: https://joe.bioscientifica.com/view/journals/joe/186/1/1860241.xml

Damn the evidence is piling up now, and I had found an association between FGFR2 mutation and mass longitudinal bone growth, this is where meclizine comes in as it inhibits FGFR3 signalling, this gives me so much encouragement to get my stack at my house already, if it weren't for the stupid Aus post it'd be here by now.

Also this article: https://www.frontiersin.org/articles/10.3389/fendo.2019.00007/full#B57 explains how crucial FGF-2 is and and VEGF expression through the Pi3k-Akt pathway (potent stimulator is hexarelin) so pi3k-akt activates VEGF and VEGF upregulated Tumor Necrosis Factor a which is a reason why the FDA allowed pi3k inhibitors for cancer treatment

Any questions?

To put it in simple words bois, the best stack which will make you grow and keep you biological age go extremely slow is Hexarelin, Aromasin, SAM-e, Folic Acid, Meclizine, glucosamine chondroitin MSM, everything else your body will take care of,

still think this works?

 

[futureashtray]

Attention everyone, sam-e and all this methylation stuff is a slow ass process. We need to research more into BMP's like BMP-2 and BMP-7 the makers of the BMP formula: https://evolutionarymuse.com/products/bmp are looking at my research now for a more potent formula for increasing height, their BMP formula brings about osteogenesis mainly instead of chondrogenesis, I need either your help or someone else's help to figure out the pathway and transcriptional factors for BMP-7 to bring chondrogenesis, evomuse (https://evolutionarymuse.com/products/bmp) will make an effective height formula.

In terms of BMP-2 I have figured out how this can revert inactive growth plate back into MSC, we need compounds which upregulate BMP-2 but don't use any smad-dependent pathway and transcriptional factors like cbfa1/runx2 (this is for osteosgenesis), we need chondrogenesis and for that you can target a smad-independent pathway, a possible mechanism for this is activating a SMAD-Indepndent pathway like the MAPK pathway by downregulating FGFR3 and upregulating FGFR2 from BMPR-IA, this is most effective way with BMP-2. But for BMP-7 (since BMP is far better for chondrogenesis) it may be a different pathway or protein component, again we are trying to bring about chondrogenesis, not osteogenesis.

That BMP formula by evomuse is only good for people with active plates who are also taking sam-e and shit for methylation, if u took that formula alone if u had closed/inactive plates you would not grow with it as it induces osteogenesis, not chondrogenesis. Russianstarpeptides has a lot to learn from this because apart from using the right pathway for BMP-7, there are intraarticular injections of it that can immediately help, but what we are looking for a systemic effect, the maker of the BMP formula has confirmed it is possible with the right pathway and transcriptional factors (most likely sox9): http://russianstarpeptides.com/bmp-7-height-formula-to-grow-taller/, I will be emailing Russianstar,alkoclar and the creator of the evomuse bmp formula to find a solution for this and make it into a formula that can upregulate endogenous bmp-7 and bmp-2 and receptors while activating the correct pathway and transcriptional factors. Meanwhile you guys can also help by studying the BMP-7 and exactly which pathway and transcriptional factor is used to bring about chondrogenesis NOT osteogenesis. If BMP-7 is used correctly, height growth will resume at full force regardless of your age

P.S for inhibiting noggin we have meclizine and it also helps with one part of activating MAPK, FGFR3 downregulation

what ended up happening

 

[futureashtray]

like i said we are keeping our height increase knowledge, results and advancements to the discord, how about you stop trying to doxx? i may make a thread only to showcase results once a lot more people have done it

discord link bro, i NEED IT

 

[futureashtray]

I found a text document from way back with notes from the days of XCrunner and Hakker. Most of Hakkers work was on his private forum so there's no web archive for that. I don't have much notes but I have old memory that will probably get jogged by reading blogs that documented some of his stacks on naturalheightincrease

In the notes I also have a bunch of studies regarding CNP with many of them involving BMP, FGF2, FGF3, MAPK, Sox9, and more. I will need a few days to go through all of those studies both to relearn and to relate everything mentioned here to it. I won't have any updates for over a week or later when I really get the time to dig in

you have any update? plz im 15

 

[futureashtray]

those walls of texts were made in my stupid, naive 15 year old self

bro u serious my nigga.

 

[futureashtray]

View attachment 1489229



it is estrogen with no negative side effects of estrogen

I still believe in erdar, I talk with him on WhatsApp ,,he said his formula have improved ,, also he is working on dickmaxxing research and suggested some compound,, he also got scientist of year again , so we can trust him,,
also rapist's growth plate research link,, we all be 6'2 on may 2022

also arent u "bri__" in our private heightmaxxing discord?

could you plz give me link to discord server im 5"8 almost 19

 

[futureashtray]

It's obviously a troll bro, how the fuck do you get BREAST CANCER of some methylation supplement? The sam-e at most probably fucked with his brain and made him think the soy he's consuming isn't the cause of his breast cancer

oh nvm my nigga, u reinvited to tha cookout

 

[futureashtray]

I am going to make a thread on aromatase deficient men with open growth plates in their 30s and 3cm(1 inch) per year growth in their 20s,they grew with high androgens but low igf1 levels.

2 had height of 6'9 but were predicted to end at 187.

1 had a height of 190 as an Italian man and was predicted to end at 170 cm.

All had bone ages under 15.

1 guy had no increase in his bone age from his age 31 to 38,that means his bone age stopped increasing at bone age 14.

This proves estrogen is the main reason for senescence/bone aging/chondrocyte proliferation decline.

I will make a full thread about estrogen levels and epiphyseal closure.


Also bone age is pretty much a meme, a high bone age dosent mean all plates are closed.

Androgens aren't bad for growth,but they are good

Thinking of taking butea superba which increases DHT upto 5 times,this coupled with the 200% DHT increase from aromasin will be super helpful.

I also read about 17 hydroexemestane of aromasin, only 10-15% aromasin converts to 17HE and it's quite Androgenic.


The only doubt/query is will such high androgen levels increase my prostate size or result in testicular cancer/prostate cancer,i am 18,what do ya think?

I don't care about balding for 1-2 years,if i get height and gainz.

Will take ru58841 if i see something bad happening on my head.

good info but strike stack moggs

 

[futureashtray]

bolic and has been reported to increase total testosterone by whooping 30%. It's not like tribulus terrestris, tribulus doesn't work at all.
After taking Chrysin my pumps became stronger, fuller and I dropped 2-3% bodyfat instantly in 5 weeks. My strenght increased and I went from 1139ng/dl before sunbathing and taking chrysin back in early July, to 1326ng/dl naturally. Some of you may already saw my July test, I would post December update soon, altought Testosterone peaks in October.

" - Vorman

holy mogger t

 

[Methhead]

Preface:
I've had a lot of questions in my pm's recently regarding growth hormone, IGF-1, and androgens.
specifically, people asking me for sources and stacks, how they work, etc, I'm hoping this guide will be able to answer as many of your questions as possible.

Disclaimer:
this thread is going to be very long, I'm going, to begin with explaining each of these chemicals, their mechanisms, and functions whilst also citing studies,
if you're wanting to learn how to apply these chemicals to your protocol than skip down to where I begin talking about methods.

Introduction:
Okay, so this in this thread I'm going to do my best at explaining how growth factors and androgens
affect facial development, induce sexual dimorphism and vertical growth, I'm going to begin
explaining the biological mechanisms of these hormones and then how you can apply them
cost-effectively.

HGH:
Somatropin, commonly referred to as HGH or GH is a 191 amino acid chain that is produced by the pituitary gland,
this peptide stimulates growth, cell reproduction, and cell regeneration in humans and other animals. It is thus important in human development.
GH also stimulates the production of IGF-1 and increases the concentration of glucose and free fatty acids. It belongs to a family of hormones known as the growth hormone family. This also includes prolactin (PRL) and placental lactogen. Despite the obvious differences in function, these hormones share a very similar structure. Likewise, GH and PRL are the only two non-tropic hormones synthesized and released from the anterior pituitary gland. (So yes if you're taking cabergoline you will inhibit growth hormone as they are from the same family).

Growth hormone itself isn't actually what induces growth, it's the metabolites of somatropin that induce cell proliferation, hyperplasia, and hypertrophy.
this class of growth factors is called insulin-like growth factors, they are molecularly structured similar to that of insulin, somatropin is needed for the creation of IGF's within the liver. IGF-2 is the primary growth factor responsible for fetal development, whereas IGF-1 is the primary growth factor responsible for inducing growth within adolescent children. (more on insulin-like growth factors later).

somatropin is needed for the development of our bodies, the reason us looksmaxxers are obsessed with it is because of dimorphic growth-related effects
that are induced by the insulin-like growth factor family of hormones.

somatropin's effect on craniofacial development within children.




Yes, these children did have GHDD (growth hormone deficiency disorder), but this doesn't disprove that the usage of exogenous somatropin
can induce craniofacial growth. These children would have been administrated growth hormone dosages that would have aligned with normal children's endogenous production. Our goal with growth hormone is to increase the endogenous production of IGF-1 way above super physiological levels in order to affect our craniofacial growth. Keep in mind, in this study the children were dosed 0.5IU daily, that's around 15-fold less than what I suggest you should dose daily, and these children still reap the positive craniofacial benefits.

The abstract of a study based on how the GH/IGF-1 axis influences bone formation, growth, and remodeling.


somatropin's effect on hard tissue, bone formation, and osteoclasts.


somatropin effects on bone formation through osteoblasts.


The GH/IGF-1 axis and it's interaction with androgens when it comes to bone formation.



Insulin-like growth factors, specifically somatomedin-C (IGF-1):
IGF-1 is produced all the way throughout life. The highest rates of IGF-1 production occur during the pubertal growth spurt. The lowest levels occur in infancy and old age. This is why children grow rapidly during puberty, somatropin is at an all-time high, meaning more conversion to IGF-1, typically in healthy children, the baseline IGF-1 scoring is between 250-500ng/dl, although higher IGF-1 scoring is possible with exogenous intervention.

IGF-1 is a primary mediator of the effects of somatropin (GH), growth hormone is released into the bloodstream, and then stimulates the liver to produce insulin-like growth factors, we are specifically focusing on IGF-1. These IGF's then stimulate systemic body growth and has growth-promoting effects on almost every cell in the body, especially skeletal muscle, cartilage, bone, liver, etc... In addition to the insulin-like effects, IGF-1 can also regulate cellular DNA synthesis. IGF-1 is our friend, we want our levels to be sky-high during puberty to reap all of the dimorphic growth and surpass our genetic potential, there are some road blockages though, along with the insulin-like growth factor family comes the IGFBP's (insulin-like growth factor binding proteins) yeah it's a mouth full jfl. These proteins bind to IGF-1 and inhibit it from attaching to the IGF-1R, basically, it renders our IGF-1 useless within the body. These proteins, unfortunately, have a high affinity to bind to IGF's, there are counter measurements to these IGFBP's though, stay tuned.

Protein intake increases IGF-1 levels in humans, independent of total calorie consumption. Factors that are known to cause variation in the levels of growth hormone (GH) and IGF-1 in the circulation include insulin levels, genetic make-up, the time of day, age, sex, exercise status, stress levels, nutrition level and body mass index, disease state, ethnicity, and estrogen status.

I'm not going to be citing studies for IGF-1, as GH and IGF-1 fall in the same category, the GH/IGF-1 axis is what influences growth.

Androgens, androgenic metabolites, and pro-hormones:
despite the common knowledge surrounding testosterone there seems to be less appreciation when it comes to other androgens. Androgens are synthesized from cholesterol and are produced primarily in the gonads (testicles and ovaries) and also in the adrenal glands to a small extent. The testicles produce a much higher quantity than the ovaries in females. Dimorphic growth is heavily dependent on androgens, specifically testosterone, dihydrotestosterone (DHT), and dehydroepiandrosterone (DHEA), I'm going to be underling each androgen, and their biological mechanisms.

View attachment 258656
Testosterone:
testosterone is the primary male sex hormone that is responsible for differentiating a male fetus from a female fetus, In male humans, testosterone plays a key role in the development of reproductive tissues such as testes and prostate, as well as promoting sexual dimorphisms such as increased muscle mass, bone mass and the growth of body hair. The pituitary gland located within the brain produces a signaling chemical called luteinizing hormone (LH), LH signals the Leydig cells within the testes to synthesize testosterone from cholesterol. Production of luteinizing hormone spikes during puberty, sending multiple signals to the Leydig cells to produce more testosterone, in turn, promoting masculinization and dimorphism to occur.

the effect of low dose testosterone on the craniofacial development in children with delayed puberty.


Keep in mind, these children didn't have zero testosterone, they were just experiencing delayed puberty, low dose testosterone was enough to kickstart their craniofacial development.

View attachment 258654
Dihydrotestosterone:
DHT is biologically important for sexual differentiation of the male genitalia during embryogenesis, maturation of the penis and scrotum at puberty, growth of facial, body and pubic hair, and development and maintenance of the prostate gland and seminal vesicles. It is produced from testosterone by an enzyme called 5-alpha-reductase (5AR) in select tissues and is the primary androgen in the genitals, prostate gland, seminal vesicles, skin, and hair follicles. Dihydrotestosterone can have up to 5x the potency of testosterone when it comes to inducing androgenic dimorphism, that isn't to say that testosterone isn't important though.

View attachment 258653
Androsterone:
Androsterone is an androgenic steroid derived via the activity of the enzyme 5-AR and is a downstream metabolite of the more potent androgen DHT. Like all 5-AR derived androgens, androsterone displays anti-estrogenic and anti-glucocorticoid activity and in addition, serves as a pro-hormone for DHT and other potent androgens. In addition, androsterone is a neurosteroid with potent GABA agonist activity and is known to function as a pheromone in many animal species including humans. It has been shown to possess anti-depressant and anti-proliferative effects. Perhaps most importantly, it has been found to act like as a potent thyroid mimetic and as such to increase basal temperature, oxygen consumption and lower lipid levels in humans.

androsterone and its effect on the masculinization of male fetuses.





View attachment 258780
dehydroepiandrosterone
Dehydroepiandrosterone (DHEA), also known as androstenolone, is an endogenous steroid hormone. It is one of the most abundant circulating steroids in humans, in whom it is produced in the adrenal glands, the gonads, and the brain. It functions as a metabolic intermediate in the biosynthesis of the androgen and estrogen sex steroids both in the gonads and in various other tissues. On its own, it's a very weak androgen, but it potently converts to testosterone within certain tissue, it is more abundant within females than males as it also converts to estrogen.

How to apply these hormones to your protocol:

let's begin with the growth hormone/igf1 aspect to our protocol, our main goal is to induce craniofacial growth (specifically maxillary and mandibular growth), vertical growth, and dimorphism, this can be achieved via a multitude of method, here we go.

How to increase IGF-1 levels beyond the super physiological natural range
through the usage of exogenous GH and PEPTIDES:

Method 1:
Recombinant growth hormone:
increasing our IGF-1 levels beyond the super physiological range is simple, although I disagree with some of
@Extra Chromosome's opinions on heightmaxxing, I'm going to do my best to express my opinion as I have experience and knowledge within the field of GH and Peptides.

To begin with, I personally think the usage of recombinant growth hormone (synthetic bioidentical somatropin) is the best and most practical way to increase IGF-1 and induce growth, that's not to say that peptides don't have their place, but they aren't as effective as HGH (I'll go into more detail later). Recombinant growth hormone is expensive, very expensive, but if you source it correctly you can bypass the majority of the cost issues.

I'd suggest dosing HGH at around 5IU-8IU's daily. This will skyrocket your IGF-1, even more so if you're a teenager as the conversion rate from somatropin to IGF-1 is higher, in most growing teenagers this amount of GH will put you into the 700-900ng/dl range for IGF-1 scoring, at this level cell proliferation, hyperplasia and osteoblast/osteoclast activity will increase dramatically. In other words, you'll grow, vertically and horizontally. If your soul usage of HGH is for height gains than either exemestane, letrozole or Arimidex will suffice for aromatase inhibition.

To sum method 1 up:
5-8iu's of HGH ED
(optional) Aromatase inhibitor of your choice.

Method 2:
HGH combined with IGF-1 LR3 and IGF-1 DES.
the combination of both exogenous GH and exogenous IGF-1 is amazing. As I've mentioned above alongside insulin-like growth factors comes IGFBP's (Insulin-like growth factor binding proteins) IGFPB's have a high affinity to bind onto IGF-1 and IGF-2 within the bloodstream rendering them useless and unable to attach to the IGF-1R and IGF-2R, meaning a small portion of the HGH that we inject into ourselves is going to waste as these proteins are rendering the IGF-1 unable to function, there is a way around this.

the polypeptides IGF-LR3 and IGF-DES have a low affinity to bind to the IGFBP's, meaning they are up to 3x more potent than regular endogenous IGF-1. IGF-1LR3 also happens to have a half-life of up to 30 hours. IGF-DES is even more potent than LR3, the only downside is that it has a 30-minute half-life before it is metabolized by the body, DES also happens to be more localized, so we are going to opt for LR3 in this method as it is more systemic than DES. The combination of HGH and exogenous IGF-1 will guarantee growth. (if your plates are open of course).

To sum method 2 up:
5-8iu's of HGH ED
IGF-1 LR3 100mcg ED
(optional) IGF-1 DES 50mcg ED
(optional) Aromatase inhibitor

Method 3
Peptide protocol.
peptides can be great for increasing serum levels of growth hormone and inevitably increasing IGF-1 scoring within the blood, the reason why I prefer synthetic GH is that the pituitary gland can only produce so much GH, meaning there is a limit to the number of signals it can take to produce a certain amount of somatropin. For example, you could inject more exogenous GH than you could make endogenous GH with the help of peptides, I hope that makes sense. Peptides can still boost your IGF-1 scoring beyond the natural range, some peptides even stimulate the Pi3k pathways, which is a bonus.

peptides are split up into 2 categories, GHRH's and GHRP's, our bodies make growth hormone-releasing hormone to signal the somatroph cells to produce somatropin within the pituitary gland, GHRH peptides basically tell the pituitary to release GH, growth hormone-releasing peptides basically amplify the production of growth hormone that is being secreted, stacking both a GHRH and a GHRP is necessary for increasing IGF-1 as they synergize well.

here's the peptide protocol that I recommend, whilst on this stack my IGF-1 came back at over 800ng/dl, in that time period I grew an inch and a half in height within 2 and a half months.



switching back and forth from hexarelin and GHRP-2 is necessary as desensitization will occur whilst using hexarelin at any dosage for longer than 14 days. Having 14 days off and 7 days on allows your body to sensitize to the peptide again. I do not recommend the usage of CJC DAC as it has been proven to cause damage to the pituitary gland with chronic usage.

Okay, that sums up the GH/IGF-1 section, overall I'd say if you're on a budget than peptides is the route you should take, if you have more money to spend than go for HGH if you're really fucking determined than take the HGH/IGF-1LR3 route.

The good thing about working with somatropin and peptides is that exogenous usage won't cause a negative feedback loop to occur, meaning if you discontinue the usage of growth hormone you won't feel like shit as you would with testosterone (unless you do a correct PCT). Your endogenous somatropin will begin producing normally again.

How to increase endogenous androgen activity without causing suppression
or shutdown from occurring:
working with androgens can be tricky and dangerous, you can take two routes with androgens, you can either take metabolites and non-suppressive prohormones or you can take androgens like testosterone and cause a shutdown.

the usage of androgens such as dehydroepiandrosterone and androsterone along with progesterone can be of great benefit to those who are looking
to masculinize themselves without using testosterone. dehydroepiandrosterone (DHEA) is one of the most abundant steroid hormones within the human body, it is produced by the adrenals and can be converted to either testosterone or estrogen. The supplementation of exogenous DHEA alone can lead to both an increase in estrogen and testosterone, combining DHEA with androsterone is a good idea as androsterone is a very powerful anti-aromatase, estrogen isn't the enemy, it's just having high estrogen is a negative, inhibiting the aromatase enzyme from converting testosterone from converting to estrogen allows for the DHEA to convert into testosterone smoothly without a spike in estrogen as your original estrogen will just be replaced.

View attachment 258661
The usage of Delta-sleep-inducing-peptide to increase natural testosterone:
my recent findings suggest that the usage of the delta-sleep inducing peptide (DSIP) can greatly benefit steroid users who are trying to regain their LH production.
DSIP increases the amount of gonadotropin that is being secreted at night time, gonadotropin signals the pituitary gland to produce LH, that LH than signals the Leydig cells to synthesize testosterone from cholesterol. More gonadotropin signaling = more luteinizing hormone signaling meaning more testosterone being made. DSIP also happens to block corticotropin from releasing cortisol, meaning cortisol cannot antagonize testosterone, leaving you with more testosterone to circulate the bloodstream. DSIP also blocks the release of somatostatin (growth hormone inhibiting hormone), somatostatins role is to lower growth hormone if it raises to high, so by blocking the release of this hormone we are preventing our blood serum level of GH dropping.

Delta-sleep inducing peptide is a must for those looking to increase testosterone without the usage of AAS or those who are using peptides and/or Recombinant GH, as it has potent somatostatin inhibiting properties.
check out my thread on DSIP

The usage of HCG
human chorionic gonadotropin is an LH mimic that can be injected subcutaneously, it acts the exact same way that LH does in that it signals the Leydig cells to produce testosterone, HCG will keep your balls from shrinking if you're running testosterone on an AAS cycle. It can increase testosterone but it has a tendency to also increase estrogen, in combination with testosterone it can induce dimorphism greatly, whilst maintaining testicular functions and fertility, it can also be implemented to make your PCT easier.

The usage of exogenous testosterone:
the usage of exogenous testosterone can greatly induce sexual dimorphism, increase bone density, anabolism, protein synthesis, and nitrogen retention. Whilst also saturated the androgen receptors. There are obvious downsides to the usage, but if done effectively there shouldn't be any issues. For teenagers willing to run testosterone, (I don't condone the usage) I'd suggest using testosterone base (no ester attached) dissolved into DMSO applied to the skin, I'd also suggest that you take the best measure to run a safe and sought out PCT.

The usage of exogenous dihydrotestosterone (androstanolone)
dihydrotestosterone can be very beneficial for those who are in the midst of puberty, at the correct dosages it isn't very suppressive and if minimal suppression occurs, then you can easily bounce back. Androstanolone is a synthetic DHT that is bioidentical to DHT. The usage of dihydrotestosterone will have an intense masculinizing effect, if you're in puberty it may affect the size of your penis and frame.

You can make a transdermal concoction with DMSO and androstanolone, with a high absorption rate. Androstanolone is an extremely androgenic steroid hormone, it has highly anti-estrogenic properties so be cautious with the dosages if you don't want to crash your E2 levels.
check out my thread on dihydrotestosterone

conclusion
a combination of both high dosages of either recombinant growth hormone or peptides alongside the optimization or exogenous usage of androgens is synergistic when it comes to craniofacial forward growth, sexual dimorphism and vertical growth.

here's my current stack for perspective.


this took like 3 days to make because I'm a lazy cunt, anyways hoped you gained something from it.

View attachment 258787

hoping that'll answer some questions for you guys.
@JustTrynaGrow @Slyfex8 @draco @Don't Forget to mew @Tom2004 @Crazzen8 @ht-normie-ascending @Dr Shekelberg @forwardgrowth @maxmendietta @PubertyMaxxer @apollothegun @KKK

​

cope for 90% of the forum

 

[krylx]

ive 16 5'9 save me my insta is krylx0 thank you very much

 

[st.hamudi but 6‘5]

here's my current stack for perspective.

how long should i run this cycle and do i need pct after? im 19 btw just looking for more dimorphism and bone growth.

 

[Napoleon1800]

Op's posts are actually cancer to read through. It's almost as if he has a different take every 2 months. One time he says hgh doesn't work the other time he says it's the best drug in the world jtl

 

[st.hamudi but 6‘5]

Op's posts are actually cancer to read through. It's almost as if he has a different take every 2 months. One time he says hgh doesn't work the other time he says it's the best drug in the world jtl

idc i’ll blast hgh and dht for 2 months with hcg for balls and test base for balance

 

[Dyorotic]

Didn't read + inject trestolone

 

[Meganut]

Preface:
I've had a lot of questions in my pm's recently regarding growth hormone, IGF-1, and androgens.
specifically, people asking me for sources and stacks, how they work, etc, I'm hoping this guide will be able to answer as many of your questions as possible.

Disclaimer:
this thread is going to be very long, I'm going, to begin with explaining each of these chemicals, their mechanisms, and functions whilst also citing studies,
if you're wanting to learn how to apply these chemicals to your protocol than skip down to where I begin talking about methods.

Introduction:
Okay, so this in this thread I'm going to do my best at explaining how growth factors and androgens
affect facial development, induce sexual dimorphism and vertical growth, I'm going to begin
explaining the biological mechanisms of these hormones and then how you can apply them
cost-effectively.

HGH:
Somatropin, commonly referred to as HGH or GH is a 191 amino acid chain that is produced by the pituitary gland,
this peptide stimulates growth, cell reproduction, and cell regeneration in humans and other animals. It is thus important in human development.
GH also stimulates the production of IGF-1 and increases the concentration of glucose and free fatty acids. It belongs to a family of hormones known as the growth hormone family. This also includes prolactin (PRL) and placental lactogen. Despite the obvious differences in function, these hormones share a very similar structure. Likewise, GH and PRL are the only two non-tropic hormones synthesized and released from the anterior pituitary gland. (So yes if you're taking cabergoline you will inhibit growth hormone as they are from the same family).

Growth hormone itself isn't actually what induces growth, it's the metabolites of somatropin that induce cell proliferation, hyperplasia, and hypertrophy.
this class of growth factors is called insulin-like growth factors, they are molecularly structured similar to that of insulin, somatropin is needed for the creation of IGF's within the liver. IGF-2 is the primary growth factor responsible for fetal development, whereas IGF-1 is the primary growth factor responsible for inducing growth within adolescent children. (more on insulin-like growth factors later).

somatropin is needed for the development of our bodies, the reason us looksmaxxers are obsessed with it is because of dimorphic growth-related effects
that are induced by the insulin-like growth factor family of hormones.

somatropin's effect on craniofacial development within children.




Yes, these children did have GHDD (growth hormone deficiency disorder), but this doesn't disprove that the usage of exogenous somatropin
can induce craniofacial growth. These children would have been administrated growth hormone dosages that would have aligned with normal children's endogenous production. Our goal with growth hormone is to increase the endogenous production of IGF-1 way above super physiological levels in order to affect our craniofacial growth. Keep in mind, in this study the children were dosed 0.5IU daily, that's around 15-fold less than what I suggest you should dose daily, and these children still reap the positive craniofacial benefits.

The abstract of a study based on how the GH/IGF-1 axis influences bone formation, growth, and remodeling.


somatropin's effect on hard tissue, bone formation, and osteoclasts.


somatropin effects on bone formation through osteoblasts.


The GH/IGF-1 axis and it's interaction with androgens when it comes to bone formation.



Insulin-like growth factors, specifically somatomedin-C (IGF-1):
IGF-1 is produced all the way throughout life. The highest rates of IGF-1 production occur during the pubertal growth spurt. The lowest levels occur in infancy and old age. This is why children grow rapidly during puberty, somatropin is at an all-time high, meaning more conversion to IGF-1, typically in healthy children, the baseline IGF-1 scoring is between 250-500ng/dl, although higher IGF-1 scoring is possible with exogenous intervention.

IGF-1 is a primary mediator of the effects of somatropin (GH), growth hormone is released into the bloodstream, and then stimulates the liver to produce insulin-like growth factors, we are specifically focusing on IGF-1. These IGF's then stimulate systemic body growth and has growth-promoting effects on almost every cell in the body, especially skeletal muscle, cartilage, bone, liver, etc... In addition to the insulin-like effects, IGF-1 can also regulate cellular DNA synthesis. IGF-1 is our friend, we want our levels to be sky-high during puberty to reap all of the dimorphic growth and surpass our genetic potential, there are some road blockages though, along with the insulin-like growth factor family comes the IGFBP's (insulin-like growth factor binding proteins) yeah it's a mouth full jfl. These proteins bind to IGF-1 and inhibit it from attaching to the IGF-1R, basically, it renders our IGF-1 useless within the body. These proteins, unfortunately, have a high affinity to bind to IGF's, there are counter measurements to these IGFBP's though, stay tuned.

Protein intake increases IGF-1 levels in humans, independent of total calorie consumption. Factors that are known to cause variation in the levels of growth hormone (GH) and IGF-1 in the circulation include insulin levels, genetic make-up, the time of day, age, sex, exercise status, stress levels, nutrition level and body mass index, disease state, ethnicity, and estrogen status.

I'm not going to be citing studies for IGF-1, as GH and IGF-1 fall in the same category, the GH/IGF-1 axis is what influences growth.

Androgens, androgenic metabolites, and pro-hormones:
despite the common knowledge surrounding testosterone there seems to be less appreciation when it comes to other androgens. Androgens are synthesized from cholesterol and are produced primarily in the gonads (testicles and ovaries) and also in the adrenal glands to a small extent. The testicles produce a much higher quantity than the ovaries in females. Dimorphic growth is heavily dependent on androgens, specifically testosterone, dihydrotestosterone (DHT), and dehydroepiandrosterone (DHEA), I'm going to be underling each androgen, and their biological mechanisms.

View attachment 258656
Testosterone:
testosterone is the primary male sex hormone that is responsible for differentiating a male fetus from a female fetus, In male humans, testosterone plays a key role in the development of reproductive tissues such as testes and prostate, as well as promoting sexual dimorphisms such as increased muscle mass, bone mass and the growth of body hair. The pituitary gland located within the brain produces a signaling chemical called luteinizing hormone (LH), LH signals the Leydig cells within the testes to synthesize testosterone from cholesterol. Production of luteinizing hormone spikes during puberty, sending multiple signals to the Leydig cells to produce more testosterone, in turn, promoting masculinization and dimorphism to occur.

the effect of low dose testosterone on the craniofacial development in children with delayed puberty.


Keep in mind, these children didn't have zero testosterone, they were just experiencing delayed puberty, low dose testosterone was enough to kickstart their craniofacial development.

View attachment 258654
Dihydrotestosterone:
DHT is biologically important for sexual differentiation of the male genitalia during embryogenesis, maturation of the penis and scrotum at puberty, growth of facial, body and pubic hair, and development and maintenance of the prostate gland and seminal vesicles. It is produced from testosterone by an enzyme called 5-alpha-reductase (5AR) in select tissues and is the primary androgen in the genitals, prostate gland, seminal vesicles, skin, and hair follicles. Dihydrotestosterone can have up to 5x the potency of testosterone when it comes to inducing androgenic dimorphism, that isn't to say that testosterone isn't important though.

View attachment 258653
Androsterone:
Androsterone is an androgenic steroid derived via the activity of the enzyme 5-AR and is a downstream metabolite of the more potent androgen DHT. Like all 5-AR derived androgens, androsterone displays anti-estrogenic and anti-glucocorticoid activity and in addition, serves as a pro-hormone for DHT and other potent androgens. In addition, androsterone is a neurosteroid with potent GABA agonist activity and is known to function as a pheromone in many animal species including humans. It has been shown to possess anti-depressant and anti-proliferative effects. Perhaps most importantly, it has been found to act like as a potent thyroid mimetic and as such to increase basal temperature, oxygen consumption and lower lipid levels in humans.

androsterone and its effect on the masculinization of male fetuses.





View attachment 258780
dehydroepiandrosterone
Dehydroepiandrosterone (DHEA), also known as androstenolone, is an endogenous steroid hormone. It is one of the most abundant circulating steroids in humans, in whom it is produced in the adrenal glands, the gonads, and the brain. It functions as a metabolic intermediate in the biosynthesis of the androgen and estrogen sex steroids both in the gonads and in various other tissues. On its own, it's a very weak androgen, but it potently converts to testosterone within certain tissue, it is more abundant within females than males as it also converts to estrogen.

How to apply these hormones to your protocol:

let's begin with the growth hormone/igf1 aspect to our protocol, our main goal is to induce craniofacial growth (specifically maxillary and mandibular growth), vertical growth, and dimorphism, this can be achieved via a multitude of method, here we go.

How to increase IGF-1 levels beyond the super physiological natural range
through the usage of exogenous GH and PEPTIDES:

Method 1:
Recombinant growth hormone:
increasing our IGF-1 levels beyond the super physiological range is simple, although I disagree with some of
@Extra Chromosome's opinions on heightmaxxing, I'm going to do my best to express my opinion as I have experience and knowledge within the field of GH and Peptides.

To begin with, I personally think the usage of recombinant growth hormone (synthetic bioidentical somatropin) is the best and most practical way to increase IGF-1 and induce growth, that's not to say that peptides don't have their place, but they aren't as effective as HGH (I'll go into more detail later). Recombinant growth hormone is expensive, very expensive, but if you source it correctly you can bypass the majority of the cost issues.

I'd suggest dosing HGH at around 5IU-8IU's daily. This will skyrocket your IGF-1, even more so if you're a teenager as the conversion rate from somatropin to IGF-1 is higher, in most growing teenagers this amount of GH will put you into the 700-900ng/dl range for IGF-1 scoring, at this level cell proliferation, hyperplasia and osteoblast/osteoclast activity will increase dramatically. In other words, you'll grow, vertically and horizontally. If your soul usage of HGH is for height gains than either exemestane, letrozole or Arimidex will suffice for aromatase inhibition.

To sum method 1 up:
5-8iu's of HGH ED
(optional) Aromatase inhibitor of your choice.

Method 2:
HGH combined with IGF-1 LR3 and IGF-1 DES.
the combination of both exogenous GH and exogenous IGF-1 is amazing. As I've mentioned above alongside insulin-like growth factors comes IGFBP's (Insulin-like growth factor binding proteins) IGFPB's have a high affinity to bind onto IGF-1 and IGF-2 within the bloodstream rendering them useless and unable to attach to the IGF-1R and IGF-2R, meaning a small portion of the HGH that we inject into ourselves is going to waste as these proteins are rendering the IGF-1 unable to function, there is a way around this.

the polypeptides IGF-LR3 and IGF-DES have a low affinity to bind to the IGFBP's, meaning they are up to 3x more potent than regular endogenous IGF-1. IGF-1LR3 also happens to have a half-life of up to 30 hours. IGF-DES is even more potent than LR3, the only downside is that it has a 30-minute half-life before it is metabolized by the body, DES also happens to be more localized, so we are going to opt for LR3 in this method as it is more systemic than DES. The combination of HGH and exogenous IGF-1 will guarantee growth. (if your plates are open of course).

To sum method 2 up:
5-8iu's of HGH ED
IGF-1 LR3 100mcg ED
(optional) IGF-1 DES 50mcg ED
(optional) Aromatase inhibitor

Method 3
Peptide protocol.
peptides can be great for increasing serum levels of growth hormone and inevitably increasing IGF-1 scoring within the blood, the reason why I prefer synthetic GH is that the pituitary gland can only produce so much GH, meaning there is a limit to the number of signals it can take to produce a certain amount of somatropin. For example, you could inject more exogenous GH than you could make endogenous GH with the help of peptides, I hope that makes sense. Peptides can still boost your IGF-1 scoring beyond the natural range, some peptides even stimulate the Pi3k pathways, which is a bonus.

peptides are split up into 2 categories, GHRH's and GHRP's, our bodies make growth hormone-releasing hormone to signal the somatroph cells to produce somatropin within the pituitary gland, GHRH peptides basically tell the pituitary to release GH, growth hormone-releasing peptides basically amplify the production of growth hormone that is being secreted, stacking both a GHRH and a GHRP is necessary for increasing IGF-1 as they synergize well.

here's the peptide protocol that I recommend, whilst on this stack my IGF-1 came back at over 800ng/dl, in that time period I grew an inch and a half in height within 2 and a half months.



switching back and forth from hexarelin and GHRP-2 is necessary as desensitization will occur whilst using hexarelin at any dosage for longer than 14 days. Having 14 days off and 7 days on allows your body to sensitize to the peptide again. I do not recommend the usage of CJC DAC as it has been proven to cause damage to the pituitary gland with chronic usage.

Okay, that sums up the GH/IGF-1 section, overall I'd say if you're on a budget than peptides is the route you should take, if you have more money to spend than go for HGH if you're really fucking determined than take the HGH/IGF-1LR3 route.

The good thing about working with somatropin and peptides is that exogenous usage won't cause a negative feedback loop to occur, meaning if you discontinue the usage of growth hormone you won't feel like shit as you would with testosterone (unless you do a correct PCT). Your endogenous somatropin will begin producing normally again.

How to increase endogenous androgen activity without causing suppression
or shutdown from occurring:
working with androgens can be tricky and dangerous, you can take two routes with androgens, you can either take metabolites and non-suppressive prohormones or you can take androgens like testosterone and cause a shutdown.

the usage of androgens such as dehydroepiandrosterone and androsterone along with progesterone can be of great benefit to those who are looking
to masculinize themselves without using testosterone. dehydroepiandrosterone (DHEA) is one of the most abundant steroid hormones within the human body, it is produced by the adrenals and can be converted to either testosterone or estrogen. The supplementation of exogenous DHEA alone can lead to both an increase in estrogen and testosterone, combining DHEA with androsterone is a good idea as androsterone is a very powerful anti-aromatase, estrogen isn't the enemy, it's just having high estrogen is a negative, inhibiting the aromatase enzyme from converting testosterone from converting to estrogen allows for the DHEA to convert into testosterone smoothly without a spike in estrogen as your original estrogen will just be replaced.

View attachment 258661
The usage of Delta-sleep-inducing-peptide to increase natural testosterone:
my recent findings suggest that the usage of the delta-sleep inducing peptide (DSIP) can greatly benefit steroid users who are trying to regain their LH production.
DSIP increases the amount of gonadotropin that is being secreted at night time, gonadotropin signals the pituitary gland to produce LH, that LH than signals the Leydig cells to synthesize testosterone from cholesterol. More gonadotropin signaling = more luteinizing hormone signaling meaning more testosterone being made. DSIP also happens to block corticotropin from releasing cortisol, meaning cortisol cannot antagonize testosterone, leaving you with more testosterone to circulate the bloodstream. DSIP also blocks the release of somatostatin (growth hormone inhibiting hormone), somatostatins role is to lower growth hormone if it raises to high, so by blocking the release of this hormone we are preventing our blood serum level of GH dropping.

Delta-sleep inducing peptide is a must for those looking to increase testosterone without the usage of AAS or those who are using peptides and/or Recombinant GH, as it has potent somatostatin inhibiting properties.
check out my thread on DSIP

The usage of HCG
human chorionic gonadotropin is an LH mimic that can be injected subcutaneously, it acts the exact same way that LH does in that it signals the Leydig cells to produce testosterone, HCG will keep your balls from shrinking if you're running testosterone on an AAS cycle. It can increase testosterone but it has a tendency to also increase estrogen, in combination with testosterone it can induce dimorphism greatly, whilst maintaining testicular functions and fertility, it can also be implemented to make your PCT easier.

The usage of exogenous testosterone:
the usage of exogenous testosterone can greatly induce sexual dimorphism, increase bone density, anabolism, protein synthesis, and nitrogen retention. Whilst also saturated the androgen receptors. There are obvious downsides to the usage, but if done effectively there shouldn't be any issues. For teenagers willing to run testosterone, (I don't condone the usage) I'd suggest using testosterone base (no ester attached) dissolved into DMSO applied to the skin, I'd also suggest that you take the best measure to run a safe and sought out PCT.

The usage of exogenous dihydrotestosterone (androstanolone)
dihydrotestosterone can be very beneficial for those who are in the midst of puberty, at the correct dosages it isn't very suppressive and if minimal suppression occurs, then you can easily bounce back. Androstanolone is a synthetic DHT that is bioidentical to DHT. The usage of dihydrotestosterone will have an intense masculinizing effect, if you're in puberty it may affect the size of your penis and frame.

You can make a transdermal concoction with DMSO and androstanolone, with a high absorption rate. Androstanolone is an extremely androgenic steroid hormone, it has highly anti-estrogenic properties so be cautious with the dosages if you don't want to crash your E2 levels.
check out my thread on dihydrotestosterone

conclusion
a combination of both high dosages of either recombinant growth hormone or peptides alongside the optimization or exogenous usage of androgens is synergistic when it comes to craniofacial forward growth, sexual dimorphism and vertical growth.

here's my current stack for perspective.


this took like 3 days to make because I'm a lazy cunt, anyways hoped you gained something from it.

View attachment 258787

hoping that'll answer some questions for you guys.
@JustTrynaGrow @Slyfex8 @draco @Don't Forget to mew @Tom2004 @Crazzen8 @ht-normie-ascending @Dr Shekelberg @forwardgrowth @maxmendietta @PubertyMaxxer @apollothegun @KKK

​

good thread but how can you regulate facial growth cause i heard hgh can make you look like a ogre and shit. Im considering taking it as i want a bit more growth( im 184cm and 15) and i basically have no midface so i want to increase that and grow my maxilla. Any suggestions?

 

[Data]

I'm 15 i fucking hate the fact that i cant get any of this shit because im 15 but broke and cant hide this stuff from my parents.
And im too fucking retarded to be able to know how to inject this shit. Feelsbadman

 

[pemphigus]

Preface:
I've had a lot of questions in my pm's recently regarding growth hormone, IGF-1, and androgens.
specifically, people asking me for sources and stacks, how they work, etc, I'm hoping this guide will be able to answer as many of your questions as possible.

Disclaimer:
this thread is going to be very long, I'm going, to begin with explaining each of these chemicals, their mechanisms, and functions whilst also citing studies,
if you're wanting to learn how to apply these chemicals to your protocol than skip down to where I begin talking about methods.

Introduction:
Okay, so this in this thread I'm going to do my best at explaining how growth factors and androgens
affect facial development, induce sexual dimorphism and vertical growth, I'm going to begin
explaining the biological mechanisms of these hormones and then how you can apply them
cost-effectively.

HGH:
Somatropin, commonly referred to as HGH or GH is a 191 amino acid chain that is produced by the pituitary gland,
this peptide stimulates growth, cell reproduction, and cell regeneration in humans and other animals. It is thus important in human development.
GH also stimulates the production of IGF-1 and increases the concentration of glucose and free fatty acids. It belongs to a family of hormones known as the growth hormone family. This also includes prolactin (PRL) and placental lactogen. Despite the obvious differences in function, these hormones share a very similar structure. Likewise, GH and PRL are the only two non-tropic hormones synthesized and released from the anterior pituitary gland. (So yes if you're taking cabergoline you will inhibit growth hormone as they are from the same family).

Growth hormone itself isn't actually what induces growth, it's the metabolites of somatropin that induce cell proliferation, hyperplasia, and hypertrophy.
this class of growth factors is called insulin-like growth factors, they are molecularly structured similar to that of insulin, somatropin is needed for the creation of IGF's within the liver. IGF-2 is the primary growth factor responsible for fetal development, whereas IGF-1 is the primary growth factor responsible for inducing growth within adolescent children. (more on insulin-like growth factors later).

somatropin is needed for the development of our bodies, the reason us looksmaxxers are obsessed with it is because of dimorphic growth-related effects
that are induced by the insulin-like growth factor family of hormones.

somatropin's effect on craniofacial development within children.




Yes, these children did have GHDD (growth hormone deficiency disorder), but this doesn't disprove that the usage of exogenous somatropin
can induce craniofacial growth. These children would have been administrated growth hormone dosages that would have aligned with normal children's endogenous production. Our goal with growth hormone is to increase the endogenous production of IGF-1 way above super physiological levels in order to affect our craniofacial growth. Keep in mind, in this study the children were dosed 0.5IU daily, that's around 15-fold less than what I suggest you should dose daily, and these children still reap the positive craniofacial benefits.

The abstract of a study based on how the GH/IGF-1 axis influences bone formation, growth, and remodeling.


somatropin's effect on hard tissue, bone formation, and osteoclasts.


somatropin effects on bone formation through osteoblasts.


The GH/IGF-1 axis and it's interaction with androgens when it comes to bone formation.



Insulin-like growth factors, specifically somatomedin-C (IGF-1):
IGF-1 is produced all the way throughout life. The highest rates of IGF-1 production occur during the pubertal growth spurt. The lowest levels occur in infancy and old age. This is why children grow rapidly during puberty, somatropin is at an all-time high, meaning more conversion to IGF-1, typically in healthy children, the baseline IGF-1 scoring is between 250-500ng/dl, although higher IGF-1 scoring is possible with exogenous intervention.

IGF-1 is a primary mediator of the effects of somatropin (GH), growth hormone is released into the bloodstream, and then stimulates the liver to produce insulin-like growth factors, we are specifically focusing on IGF-1. These IGF's then stimulate systemic body growth and has growth-promoting effects on almost every cell in the body, especially skeletal muscle, cartilage, bone, liver, etc... In addition to the insulin-like effects, IGF-1 can also regulate cellular DNA synthesis. IGF-1 is our friend, we want our levels to be sky-high during puberty to reap all of the dimorphic growth and surpass our genetic potential, there are some road blockages though, along with the insulin-like growth factor family comes the IGFBP's (insulin-like growth factor binding proteins) yeah it's a mouth full jfl. These proteins bind to IGF-1 and inhibit it from attaching to the IGF-1R, basically, it renders our IGF-1 useless within the body. These proteins, unfortunately, have a high affinity to bind to IGF's, there are counter measurements to these IGFBP's though, stay tuned.

Protein intake increases IGF-1 levels in humans, independent of total calorie consumption. Factors that are known to cause variation in the levels of growth hormone (GH) and IGF-1 in the circulation include insulin levels, genetic make-up, the time of day, age, sex, exercise status, stress levels, nutrition level and body mass index, disease state, ethnicity, and estrogen status.

I'm not going to be citing studies for IGF-1, as GH and IGF-1 fall in the same category, the GH/IGF-1 axis is what influences growth.

Androgens, androgenic metabolites, and pro-hormones:
despite the common knowledge surrounding testosterone there seems to be less appreciation when it comes to other androgens. Androgens are synthesized from cholesterol and are produced primarily in the gonads (testicles and ovaries) and also in the adrenal glands to a small extent. The testicles produce a much higher quantity than the ovaries in females. Dimorphic growth is heavily dependent on androgens, specifically testosterone, dihydrotestosterone (DHT), and dehydroepiandrosterone (DHEA), I'm going to be underling each androgen, and their biological mechanisms.

View attachment 258656
Testosterone:
testosterone is the primary male sex hormone that is responsible for differentiating a male fetus from a female fetus, In male humans, testosterone plays a key role in the development of reproductive tissues such as testes and prostate, as well as promoting sexual dimorphisms such as increased muscle mass, bone mass and the growth of body hair. The pituitary gland located within the brain produces a signaling chemical called luteinizing hormone (LH), LH signals the Leydig cells within the testes to synthesize testosterone from cholesterol. Production of luteinizing hormone spikes during puberty, sending multiple signals to the Leydig cells to produce more testosterone, in turn, promoting masculinization and dimorphism to occur.

the effect of low dose testosterone on the craniofacial development in children with delayed puberty.


Keep in mind, these children didn't have zero testosterone, they were just experiencing delayed puberty, low dose testosterone was enough to kickstart their craniofacial development.

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Dihydrotestosterone:
DHT is biologically important for sexual differentiation of the male genitalia during embryogenesis, maturation of the penis and scrotum at puberty, growth of facial, body and pubic hair, and development and maintenance of the prostate gland and seminal vesicles. It is produced from testosterone by an enzyme called 5-alpha-reductase (5AR) in select tissues and is the primary androgen in the genitals, prostate gland, seminal vesicles, skin, and hair follicles. Dihydrotestosterone can have up to 5x the potency of testosterone when it comes to inducing androgenic dimorphism, that isn't to say that testosterone isn't important though.

View attachment 258653
Androsterone:
Androsterone is an androgenic steroid derived via the activity of the enzyme 5-AR and is a downstream metabolite of the more potent androgen DHT. Like all 5-AR derived androgens, androsterone displays anti-estrogenic and anti-glucocorticoid activity and in addition, serves as a pro-hormone for DHT and other potent androgens. In addition, androsterone is a neurosteroid with potent GABA agonist activity and is known to function as a pheromone in many animal species including humans. It has been shown to possess anti-depressant and anti-proliferative effects. Perhaps most importantly, it has been found to act like as a potent thyroid mimetic and as such to increase basal temperature, oxygen consumption and lower lipid levels in humans.

androsterone and its effect on the masculinization of male fetuses.





View attachment 258780
dehydroepiandrosterone
Dehydroepiandrosterone (DHEA), also known as androstenolone, is an endogenous steroid hormone. It is one of the most abundant circulating steroids in humans, in whom it is produced in the adrenal glands, the gonads, and the brain. It functions as a metabolic intermediate in the biosynthesis of the androgen and estrogen sex steroids both in the gonads and in various other tissues. On its own, it's a very weak androgen, but it potently converts to testosterone within certain tissue, it is more abundant within females than males as it also converts to estrogen.

How to apply these hormones to your protocol:

let's begin with the growth hormone/igf1 aspect to our protocol, our main goal is to induce craniofacial growth (specifically maxillary and mandibular growth), vertical growth, and dimorphism, this can be achieved via a multitude of method, here we go.

How to increase IGF-1 levels beyond the super physiological natural range
through the usage of exogenous GH and PEPTIDES:

Method 1:
Recombinant growth hormone:
increasing our IGF-1 levels beyond the super physiological range is simple, although I disagree with some of
@Extra Chromosome's opinions on heightmaxxing, I'm going to do my best to express my opinion as I have experience and knowledge within the field of GH and Peptides.

To begin with, I personally think the usage of recombinant growth hormone (synthetic bioidentical somatropin) is the best and most practical way to increase IGF-1 and induce growth, that's not to say that peptides don't have their place, but they aren't as effective as HGH (I'll go into more detail later). Recombinant growth hormone is expensive, very expensive, but if you source it correctly you can bypass the majority of the cost issues.

I'd suggest dosing HGH at around 5IU-8IU's daily. This will skyrocket your IGF-1, even more so if you're a teenager as the conversion rate from somatropin to IGF-1 is higher, in most growing teenagers this amount of GH will put you into the 700-900ng/dl range for IGF-1 scoring, at this level cell proliferation, hyperplasia and osteoblast/osteoclast activity will increase dramatically. In other words, you'll grow, vertically and horizontally. If your soul usage of HGH is for height gains than either exemestane, letrozole or Arimidex will suffice for aromatase inhibition.

To sum method 1 up:
5-8iu's of HGH ED
(optional) Aromatase inhibitor of your choice.

Method 2:
HGH combined with IGF-1 LR3 and IGF-1 DES.
the combination of both exogenous GH and exogenous IGF-1 is amazing. As I've mentioned above alongside insulin-like growth factors comes IGFBP's (Insulin-like growth factor binding proteins) IGFPB's have a high affinity to bind onto IGF-1 and IGF-2 within the bloodstream rendering them useless and unable to attach to the IGF-1R and IGF-2R, meaning a small portion of the HGH that we inject into ourselves is going to waste as these proteins are rendering the IGF-1 unable to function, there is a way around this.

the polypeptides IGF-LR3 and IGF-DES have a low affinity to bind to the IGFBP's, meaning they are up to 3x more potent than regular endogenous IGF-1. IGF-1LR3 also happens to have a half-life of up to 30 hours. IGF-DES is even more potent than LR3, the only downside is that it has a 30-minute half-life before it is metabolized by the body, DES also happens to be more localized, so we are going to opt for LR3 in this method as it is more systemic than DES. The combination of HGH and exogenous IGF-1 will guarantee growth. (if your plates are open of course).

To sum method 2 up:
5-8iu's of HGH ED
IGF-1 LR3 100mcg ED
(optional) IGF-1 DES 50mcg ED
(optional) Aromatase inhibitor

Method 3
Peptide protocol.
peptides can be great for increasing serum levels of growth hormone and inevitably increasing IGF-1 scoring within the blood, the reason why I prefer synthetic GH is that the pituitary gland can only produce so much GH, meaning there is a limit to the number of signals it can take to produce a certain amount of somatropin. For example, you could inject more exogenous GH than you could make endogenous GH with the help of peptides, I hope that makes sense. Peptides can still boost your IGF-1 scoring beyond the natural range, some peptides even stimulate the Pi3k pathways, which is a bonus.

peptides are split up into 2 categories, GHRH's and GHRP's, our bodies make growth hormone-releasing hormone to signal the somatroph cells to produce somatropin within the pituitary gland, GHRH peptides basically tell the pituitary to release GH, growth hormone-releasing peptides basically amplify the production of growth hormone that is being secreted, stacking both a GHRH and a GHRP is necessary for increasing IGF-1 as they synergize well.

here's the peptide protocol that I recommend, whilst on this stack my IGF-1 came back at over 800ng/dl, in that time period I grew an inch and a half in height within 2 and a half months.



switching back and forth from hexarelin and GHRP-2 is necessary as desensitization will occur whilst using hexarelin at any dosage for longer than 14 days. Having 14 days off and 7 days on allows your body to sensitize to the peptide again. I do not recommend the usage of CJC DAC as it has been proven to cause damage to the pituitary gland with chronic usage.

Okay, that sums up the GH/IGF-1 section, overall I'd say if you're on a budget than peptides is the route you should take, if you have more money to spend than go for HGH if you're really fucking determined than take the HGH/IGF-1LR3 route.

The good thing about working with somatropin and peptides is that exogenous usage won't cause a negative feedback loop to occur, meaning if you discontinue the usage of growth hormone you won't feel like shit as you would with testosterone (unless you do a correct PCT). Your endogenous somatropin will begin producing normally again.

How to increase endogenous androgen activity without causing suppression
or shutdown from occurring:
working with androgens can be tricky and dangerous, you can take two routes with androgens, you can either take metabolites and non-suppressive prohormones or you can take androgens like testosterone and cause a shutdown.

the usage of androgens such as dehydroepiandrosterone and androsterone along with progesterone can be of great benefit to those who are looking
to masculinize themselves without using testosterone. dehydroepiandrosterone (DHEA) is one of the most abundant steroid hormones within the human body, it is produced by the adrenals and can be converted to either testosterone or estrogen. The supplementation of exogenous DHEA alone can lead to both an increase in estrogen and testosterone, combining DHEA with androsterone is a good idea as androsterone is a very powerful anti-aromatase, estrogen isn't the enemy, it's just having high estrogen is a negative, inhibiting the aromatase enzyme from converting testosterone from converting to estrogen allows for the DHEA to convert into testosterone smoothly without a spike in estrogen as your original estrogen will just be replaced.

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The usage of Delta-sleep-inducing-peptide to increase natural testosterone:
my recent findings suggest that the usage of the delta-sleep inducing peptide (DSIP) can greatly benefit steroid users who are trying to regain their LH production.
DSIP increases the amount of gonadotropin that is being secreted at night time, gonadotropin signals the pituitary gland to produce LH, that LH than signals the Leydig cells to synthesize testosterone from cholesterol. More gonadotropin signaling = more luteinizing hormone signaling meaning more testosterone being made. DSIP also happens to block corticotropin from releasing cortisol, meaning cortisol cannot antagonize testosterone, leaving you with more testosterone to circulate the bloodstream. DSIP also blocks the release of somatostatin (growth hormone inhibiting hormone), somatostatins role is to lower growth hormone if it raises to high, so by blocking the release of this hormone we are preventing our blood serum level of GH dropping.

Delta-sleep inducing peptide is a must for those looking to increase testosterone without the usage of AAS or those who are using peptides and/or Recombinant GH, as it has potent somatostatin inhibiting properties.
check out my thread on DSIP

The usage of HCG
human chorionic gonadotropin is an LH mimic that can be injected subcutaneously, it acts the exact same way that LH does in that it signals the Leydig cells to produce testosterone, HCG will keep your balls from shrinking if you're running testosterone on an AAS cycle. It can increase testosterone but it has a tendency to also increase estrogen, in combination with testosterone it can induce dimorphism greatly, whilst maintaining testicular functions and fertility, it can also be implemented to make your PCT easier.

The usage of exogenous testosterone:
the usage of exogenous testosterone can greatly induce sexual dimorphism, increase bone density, anabolism, protein synthesis, and nitrogen retention. Whilst also saturated the androgen receptors. There are obvious downsides to the usage, but if done effectively there shouldn't be any issues. For teenagers willing to run testosterone, (I don't condone the usage) I'd suggest using testosterone base (no ester attached) dissolved into DMSO applied to the skin, I'd also suggest that you take the best measure to run a safe and sought out PCT.

The usage of exogenous dihydrotestosterone (androstanolone)
dihydrotestosterone can be very beneficial for those who are in the midst of puberty, at the correct dosages it isn't very suppressive and if minimal suppression occurs, then you can easily bounce back. Androstanolone is a synthetic DHT that is bioidentical to DHT. The usage of dihydrotestosterone will have an intense masculinizing effect, if you're in puberty it may affect the size of your penis and frame.

You can make a transdermal concoction with DMSO and androstanolone, with a high absorption rate. Androstanolone is an extremely androgenic steroid hormone, it has highly anti-estrogenic properties so be cautious with the dosages if you don't want to crash your E2 levels.
check out my thread on dihydrotestosterone

conclusion
a combination of both high dosages of either recombinant growth hormone or peptides alongside the optimization or exogenous usage of androgens is synergistic when it comes to craniofacial forward growth, sexual dimorphism and vertical growth.

here's my current stack for perspective.


this took like 3 days to make because I'm a lazy cunt, anyways hoped you gained something from it.

View attachment 258787

hoping that'll answer some questions for you guys.
@JustTrynaGrow @Slyfex8 @draco @Don't Forget to mew @Tom2004 @Crazzen8 @ht-normie-ascending @Dr Shekelberg @forwardgrowth @maxmendietta @PubertyMaxxer @apollothegun @KKK

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Havent read all of it but from what ive seen its mostly drugs and illegal peptides. Even if i tried i dont think there would be any way for me to safely get my hands on these "supplements". Tips?

 

[Geneticsislife]

Hello can you tag me in your documents? thanks.

 

[v0zifyy]

If you haven't realized it yet, HORMONES ARE EVERYTHING

Im 14 rn. What should I do.

 

[v0zifyy]

I'm hoping someone actually reads this shit, somebody needs to continue my legacy.

i've learnt everything that there is to learn, i'm injecting HGH and taking dht, I'm ascending so fucking hard this year boyo

What will happen if you do that?

 

[CurryCelHater]

@dsheppa

 

[mathis]

op is an autistic monkey dont listen to him. f you do that you will ruin your body forever

 

[Bundinkalegend]

7.5iu's of HGH daily (puretropin)
25-50mg of androstanolone daily (made transdermal from raw stanolone powder)
10mg of androsterone for the neurological benefits and basal temperature increase, along with metabolism stimulation
HCG to keep balls going and to make PCT easier, 250i-400u weekly, (this dosage avoids Leydig cell desensitization)
contemplating adding a small testosterone base to avoid a crash in E2 from high dose dihydrotestosterone.

Do you take all the HGH in one injection?

 

[melon6329]

i want to take mk and I read that the creator of this post recommended to take it along with cjc no dac or modgrf, why cant I take mk alone, what would the difference between cjc and modgrf be, and how much should I take of each, how long and any other important detail I could possibly ask since I'm playing around with my body its important to factor in everything