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

AscendingHero

AscendingHero

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those walls of texts were made in my stupid, naive 15 year old self
jfl how old are u now?

alot of the stuff u wrote idk man, so basically disregard them?

give us an update on this stuff btw pls man
 
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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

I'm 17 do I still have time?
 
AscendingHero

AscendingHero

Opportunities dont happen, you create them
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yes, disregard anything I said before this year
ok lol

if u wish to share to the community and fellow pubertycels out there, what do you recommend them to do to become chads?
 
MrIncrelex

MrIncrelex

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excelent thread my friend , just a reminder to not forget proper nutrition and to take vitamin k2 mk4 form and vitamin D, preferably from the sun instead of supplements
 
D

Deleted member 9446

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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

T3/t4, progesterone, pregenelone, and dhea should all be considered for pubertymaxers
 
AscendingHero

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I took sam e and now I have breast cancer :feelswhy::feelswhy::feelswhy:
holy shit, wtf .

@Henry_Gandy if he isn't trolling omg, i don't even know what to say, holy fucking christ. Last yr when i read thru this cascade of pages i knew someting didn't sit right and just disregarded it. JFL at taking so many uber dangerous compounds for more height or muh dimorphism. So stupid.

Like dyro said all this just to castrate yourself. Extremely irresponsible of your 15/16 y/o self when you worte this. Rectify this man.

@dyro (OP) was soo fucking right, wow. Im dumfounded rn.
 
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AscendingHero

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T3/t4, progesterone, pregenelone, and dhea should all be considered for pubertymaxers
Blacpill me on the progersterone, pregenelone, and dhea.

Will they cause a supression of my natty hormones? what dosages do u recommend?

Again unles you have some thyorid issues, gone to a doctor and have done thorough research, thyroid is the last thing one wants to be fucking around with. Healthmaxx for it ffs.
 
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AscendingHero

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@Alexanderr close the BOTB again we can't be having thousands of outsiders getting such prestine info like from OP. Put the rep/post requirements up again.

Thoughts? @Pendejo @PapiMew @Kingkellz @Gargantuan
 
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AscendingHero

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@Henry_Gandy What are your current views on pubertymaxxing?
 
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thyroid is the last thing one wants to be fucking around with
1641926847351



progersterone
it is estrogen with no negative side effects of estrogen
do YOU even believe in heightmaxxing anymore
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:p:p

also arent u "bri__" in our private heightmaxxing discord?
 
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Blacpill me on the progersterone, pregenelone, and dhea.

Will they cause a supression of my natty hormones? what dosages do u recommend?

Again unles you have some thyorid issues, gone to a doctor and have done thorough research, thyroid is the last thing one wants to be fucking around with. Healthmaxx for it ffs.
Oral T3 and T4 are very easy to come off of, they are longevity based drugs that have been quit cold turkey after 40 years of use, and thyroid iodine production had restarted fully in the fuckin grandpas in 2 weeks, full thyroid function back in 8 weeks found in study. You take them at high physiological doses and your fucking fine and your fucking bones grow like a fucking motherfucker. Anybody with even moderate or above depression always gets found to be hypo or borderline hypothyroid so basically every mentally fucked fucking motherfcueker on this forum can use it anyway
 
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T4 don't cross 60mcg
lol I'm popping 150mcg every morning, and feel amazing,, I want to add T3 but can't find pharma grade ,,
I think my t4-t3 conversion is high ,so i don't really need t3,, but still I'm looking for a legit cytom e l source
 
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lol I'm popping 150mcg every morning, and feel amazing,, I want to add T3 but can't find pharma grade ,,
I think my t4-t3 conversion is high ,so i don't really need t3,, but still I'm looking for a legit cytom e l source
Oh well its different if ur taking t4 by itself lmfao. The key is to be almost hyperthyroid, but not quite, same story for testosterone
 
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Oh well its different if ur taking t4 by itself lmfao. The key is to be almost hyperthyroid, but not quite, same story for testosterone
Actually, my fucking trt dose is essentially replicating hypergonadal conditions JFL. 250mg of test every week
 
AscendingHero

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Jfl disprove me then, don't just say cope and then leave it at that.
also arent u "bri__" in our private heightmaxxing discord?
lol....... he is....:sneaky::sneaky:

lol I'm popping 150mcg every morning, and feel amazing,, I want to add T3 but can't find pharma grade ,,
good luck man.


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:p:p
still be better careful, what has he said on dht gel+carnintine?

any legit methods besides this he's propsed so far?
 
AscendingHero

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it is estrogen with no negative side effects of estrogen
why should we take it then?

what abt dhea?

@189 @6foot2_17y0
 
AscendingHero

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Oh well its different if ur taking t4 by itself lmfao. The key is to be almost hyperthyroid, but not quite, same story for testosterone
From a looksmaxx perspective why should one be hyperthyroid?
 
TeenAscender

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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:p:p

also arent u "bri__" in our private heightmaxxing discord?
You still talk to dyoro? Lifefuel
 
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You still talk to dyoro? Lifefuel
Where tf did u get from what all he said, that he still talks to dyro? and judging from the way dyro left what makes u think he's still into this autistic shit?:lul::lul::lul:
 
189

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what abt dhea?
increase estrogen +

looksmaxxing benefit of hyperthyroid?
it gives bug eyes

1641936366249
1641936388076
1641936516283
 
TeenAscender

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Where tf did u get from what all he said, that he still talks to dyro? and judging from the way dyro left what makes u think he's still into this autistic shit?:lul::lul::lul:
Oh nvm he talks to a guy named erdo.
Can you tell me the history of dyro
 
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increase estrogen +


it gives bug eyes

View attachment 1489458 View attachment 1489460 View attachment 1489465
Ik, @RecessedPrettyboy has talked extensively about this. If it causes bug eyes then why tf is @6foot2_17y0 proposed to be hyperthyroid?:lul:

increase estrogen +
and testosterone u could take it with high dose aromasin to combat it being converted into estradiol or use it in combination with androsterone, which im planning to do.

Dht maxx any way u can if ur in puberty and know what good for you+balloning (redirects the dht to cock instead of prostate) easy mega cock.

I'm more interested in the mental benefits+stimulating facial growth +frame with this shit.
 
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Ik, @RecessedPrettyboy has talked extensively about this. If it causes bug eyes then why tf is @6foot2_17y0 proposed to be hyperthyroid?:lul:
increase estrogen +


it gives bug eyes

View attachment 1489458 View attachment 1489460 View attachment 1489465
Bulging eyes actually happen in hypothyroidism. In reality it seems hyperthyroidism could simply be called hypothyroidism in most cases, since 99% of those diagnosed with hyper are actually hypo.

So basically even if hyperthyroidism might be able to cause bulging eyes, true hyperthyroidism is so rare that we can probably assume that it doent even cause bulging eyes. So pretty much everyone you see with bug eyes is actually hypothyroid.

TSH, temperature, pulse rate, and other indicators in hypothyroidism
Because the actions of T3 can be inhibited by many factors, including polyunsaturated fatty acids, reverse T3, and excess thyroxine, the absolute level of T3 can't be used by itself for diagnosis. “Free T3” or “free T4” is a laboratory concept, and the biological activity of T3 doesn't necessarily correspond to its “freedom” in the test.

An Interview With Dr. Raymond Peat who offers his thoughts about Thyroid Disease | TPAUK
Dr. Ray Peat: Graves’ disease and exophthalmos can occur with hypothyroidism or euthyroidism, as well as with hyperthyroidism. Pregnenolone regulates brain chemistry in a way that prevents excessive production of ACTH and cortisol, and it helps to stabilize mitochondrial metabolism. It apparently acts directly on a variety of tissues to reduce their retention of water. In the last several years, all of the people I have seen who had been diagnosed as “hyperthyroid” have actually been hypothyroid, and benefitted from increasing their thyroid function; some of these people had also been told that they had Graves’ disease.


Here is the cause of bulging eyes:
"It's been known most of this century that in areas where they eat beans as a staple of the diet, such as in China, many types of beans, including soybeans, but in the Andes region, just ordinary beans are the major cause of hypothyroidism, because of various anti-thyroid factors in beans, lentils, and certain nuts -- peanuts, for example.

In eastern Europe, the cabbage and turnip staple diets were major causes of cretinism and chronic goiter and myxedema. Myxedema is the name for one type of hypothyroidism that develops in adults, in which mucousy material forms in the tissues, makes the tongue thicken, the skin gets coarse and inelastic -- but variations of myxedema can cause a lot of strange diseases that are put down to genetic causes more often than hypothyroidism, but you can cure them, in sometimes a week or two, with the right dose of thyroid.

For example, certain types of mitral valve prolapses are just from an accumulation of a mucous-like material in the valve, making it thick and inefficient. Glaucoma in low thyroid involves a swelling and overproduction and increased thickness of the fluids in the eyeball. Some types of Graves' disease, which most doctors think of as hyperthyroidism -- but hypothyroidism, which causes the pituitary to become overactive -- hypothyroidism very predictably tends to cause bulging eyes, because the thyroid stimulating hormone from the pituitary causes a mucousy material to form in the area behind the eyeball, causing a protrusion of the eyeball.

The mucousy materials that are overproduced can also cause blood vessel inefficiency and rigidity, and contributes to things like varicose veins. When this material gets in the joints, it causes cartilage deformities. The old textbooks used to show teenagers with deformed joints that caused the same deviation of the bones -- at the elbow joint especially, and the knee joint especially, with knock knees for example -- but in old people you see the fingers deviating to one side, because the cartilage is getting deformed.

The right balance of thyroid and the youth associated hormones -- progesterone and pregnenolone, and to some extent, DHEA -- will rebalance the production of these mucous-like molecules -- the glycoproteins and mucopolysaccharides, they're called -- and in just a week or two, you can often correct the deformity in a permanent way, so that the joint functions without pain or distortion." - Ray Peat
 
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puppymaxer

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could following this shit do anything about downward growth
 
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Because the actions of T3 can be inhibited by many factors, including excess thyroxine
so u r saying by taking 150mcg of thyroxine ,I'm inhibiting action of T3:lul:
all of the people I have seen who had been diagnosed as “hyperthyroid” have actually been hypothyroid,
source- RAYPEAT.COM
1641972913199

hypothyroidism very predictably tends to cause bulging eyes, because the thyroid stimulating hormone from the pituitary causes a mucousy material to form in the area behind the eyeball, causing a protrusion of the eyeball.
BULLSHIT,, IT BECAUSE MUSCLE ENLARGE AND CONTRACT BEHIND EYES
1641973030938



can't blame u tho,, U r a high IQ user, I have seen ur post about injecting ice slurry,,
but I think ray peat is bullshit
 
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Ik, @RecessedPrettyboy has talked extensively about this. If it causes bug eyes then why tf is @6foot2_17y0 proposed to be hyperthyroid?:lul:


and testosterone u could take it with high dose aromasin to combat it being converted into estradiol or use it in combination with androsterone, which im planning to do.

Dht maxx any way u can if ur in puberty and know what good for you+balloning (redirects the dht to cock instead of prostate) easy mega cock.

I'm more interested in the mental benefits+stimulating facial growth +frame with this shit.
I take it to be ALMOST hyperthyroid, but still in physiological boundaries. My eyes are fine and sexy still
 
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Bulging eyes actually happen in hypothyroidism. In reality it seems hyperthyroidism could simply be called hypothyroidism in most cases, since 99% of those diagnosed with hyper are actually hypo.

So basically even if hyperthyroidism might be able to cause bulging eyes, true hyperthyroidism is so rare that we can probably assume that it doent even cause bulging eyes. So pretty much everyone you see with bug eyes is actually hypothyroid.

TSH, temperature, pulse rate, and other indicators in hypothyroidism
Because the actions of T3 can be inhibited by many factors, including polyunsaturated fatty acids, reverse T3, and excess thyroxine, the absolute level of T3 can't be used by itself for diagnosis. “Free T3” or “free T4” is a laboratory concept, and the biological activity of T3 doesn't necessarily correspond to its “freedom” in the test.

An Interview With Dr. Raymond Peat who offers his thoughts about Thyroid Disease | TPAUK
Dr. Ray Peat: Graves’ disease and exophthalmos can occur with hypothyroidism or euthyroidism, as well as with hyperthyroidism. Pregnenolone regulates brain chemistry in a way that prevents excessive production of ACTH and cortisol, and it helps to stabilize mitochondrial metabolism. It apparently acts directly on a variety of tissues to reduce their retention of water. In the last several years, all of the people I have seen who had been diagnosed as “hyperthyroid” have actually been hypothyroid, and benefitted from increasing their thyroid function; some of these people had also been told that they had Graves’ disease.


Here is the cause of bulging eyes:
"It's been known most of this century that in areas where they eat beans as a staple of the diet, such as in China, many types of beans, including soybeans, but in the Andes region, just ordinary beans are the major cause of hypothyroidism, because of various anti-thyroid factors in beans, lentils, and certain nuts -- peanuts, for example.

In eastern Europe, the cabbage and turnip staple diets were major causes of cretinism and chronic goiter and myxedema. Myxedema is the name for one type of hypothyroidism that develops in adults, in which mucousy material forms in the tissues, makes the tongue thicken, the skin gets coarse and inelastic -- but variations of myxedema can cause a lot of strange diseases that are put down to genetic causes more often than hypothyroidism, but you can cure them, in sometimes a week or two, with the right dose of thyroid.

For example, certain types of mitral valve prolapses are just from an accumulation of a mucous-like material in the valve, making it thick and inefficient. Glaucoma in low thyroid involves a swelling and overproduction and increased thickness of the fluids in the eyeball. Some types of Graves' disease, which most doctors think of as hyperthyroidism -- but hypothyroidism, which causes the pituitary to become overactive -- hypothyroidism very predictably tends to cause bulging eyes, because the thyroid stimulating hormone from the pituitary causes a mucousy material to form in the area behind the eyeball, causing a protrusion of the eyeball.

The mucousy materials that are overproduced can also cause blood vessel inefficiency and rigidity, and contributes to things like varicose veins. When this material gets in the joints, it causes cartilage deformities. The old textbooks used to show teenagers with deformed joints that caused the same deviation of the bones -- at the elbow joint especially, and the knee joint especially, with knock knees for example -- but in old people you see the fingers deviating to one side, because the cartilage is getting deformed.

The right balance of thyroid and the youth associated hormones -- progesterone and pregnenolone, and to some extent, DHEA -- will rebalance the production of these mucous-like molecules -- the glycoproteins and mucopolysaccharides, they're called -- and in just a week or two, you can often correct the deformity in a permanent way, so that the joint functions without pain or distortion." - Ray Peat
I had no idea this ray peat guy also talked about progesterone pregenelone and dhea, i just heard him as the guy who has a weird diet to help thyroid and serotonin/dopamine balance
 
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so u r saying by taking 150mcg of thyroxine ,I'm inhibiting action of T3:lul:
He says that it CAN not that it WILL. I dont know who you are or why/if youre taking T4. I was answering to your hyperthyroidism will cause bulging eyes comment. But if you are taking just T4 just check your reverse T3 with a blood test to see if your body is converting the T4 to t3 efficiently. If it is then reverse T3 will be low. That would mean the T4 youre taking is fine.
Most people will feel better combining T4 with T3 btw.
source- RAYPEAT.COM
I see so you prefer a main$tream $cience $ource?

thats exactly why its credible and correct information. I recommend you take your time and read his articles. Before calling bullshit on a topic you dont comprehend. Anyone with a brain that reads his articles will quickly figure out that he is right about what he talks about.

Everyone in this site would benefit a lot if he was mentioned more.

If you scroll to the bottom of the articles there are plenty of references.

BULLSHIT,, IT BECAUSE MUSCLE ENLARGE AND CONTRACT BEHIND EYES
View attachment 1490166


can't blame u tho,, U r a high IQ user, I have seen ur post about injecting ice slurry,,
but I think ray peat is bullshit

Anyway I dont think you understood anything about what I posted.

Why can the muscle become enlarged?? Here just connect the dots with my last post.

The typical hypothyroid person loses salt rapidly in the urine (and probably in the sweat, too, though that is usually diagnosed as cystic fibrosis), and retains water, diluting the urine less than normal. The reduced production of carbon dioxide, with increased susceptibility to producing lactate and ammonium, causes the cells to be more alkaline than normal, increasing their affinity for water. The rise of estrogen that usually accompanies hypothyroidism also increases intracellular pH, loss of sodium, and over-hydration of the blood.


Hypothyroid muscles typically retain excess water, and fatigue easily, taking up more water than normal during exertion. In childhood, mild hypothyroidism often causes the leg muscles to swell and ache in the evenings, with what have been called "growing pains." When the problem is more extreme, all the skeletal muscles can become very large (Hoffman syndrome), because of the anabolic effect of over-hydration. Enlargement of any muscle can result from the excessive hydration produced by thyroid deficiency, but when it happens to the muscles behind the eyes (Itabashi, et al., 1988), it often leads to a diagnosis of hyperthyroidism, rather than hypothyroidism.


The little kids with the Hoffman syndrome don't have the bloated myxedematous appearance that's often associated with hypothyroidism. They look athletic to a ridiculous degree, like miniature body-builders. But after a few weeks of treatment with thyroid, they regain the slender appearance that's normal for their age. The swollen state actually supports enlargement of the muscle, and the cellular processes are probably closely related to the muscle swelling and growth produced by exercise. The growth of the muscle cell during swelling seems to be the result of normal repair processes, in a context of reduced turnover of cellular proteins.​

 
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holy shit, wtf .

@Henry_Gandy if he isn't trolling omg, i don't even know what to say, holy fucking christ. Last yr when i read thru this cascade of pages i knew someting didn't sit right and just disregarded it. JFL at taking so many uber dangerous compounds for more height or muh dimorphism. So stupid.

Like dyro said all this just to castrate yourself. Extremely irresponsible of your 15/16 y/o self when you worte this. Rectify this man.

@dyro (OP) was soo fucking right, wow. Im dumfounded rn.
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 :forcedsmile::forcedsmile:
 
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AscendingHero

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anavar+Test E+ HGH+ AI and the other secret shit I told you is enough.
this alone is enough to gigachad someone tbh. But too high inhib for taking test and anavar do u recommend any pro metabolites or ideal androgens dose dependant non supressive to take? My natty test is too precious...
 
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Good thread but simply all you need is HGH, IGF-1, DHT cream, HCG and Dsip
@Henry_Gandy

why the jfl that is a godly stack tbh w/o fucking up your body too much
 
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@Henry_Gandy

why the jfl that is a godly stack tbh w/o fucking up your body too much
I don’t think there is much evidence for dht growing bone so it might not work? Testosterone seems to have more backing.
 
AscendingHero

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I don’t think there is much evidence for dht growing bone so it might not work? Testosterone seems to have more backing.
this, but more so natural testosterone grows bone, exogenously has been show to more in growing children.

dht is very androgenic and can affect sketal muscle mass/density. DHT will also grow the skull and thicken it.
 
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Before

it was me at 15-16 yo
Hey

17 yo
 
AscendingHero

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what did u do to ascend? any looksmaxxes? ur midface and ratios in general+cuck coloring fucks u over hard.

JFL if you're on a looksmaxx site and aren't actively neckmaxxing+ trying to fix your skin + beter nt hairstyle tbh
normie to htn with good eye shape, lots lots of failos
 
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what did u do to ascend? any looksmaxxes? ur midface and ratios in general+cuck coloring fucks u over hard.

JFL if you're on a looksmaxx site and aren't actively neckmaxxing+ trying to fix your skin + beter nt hairstyle tbh

normie to htn with good eye shape, lots lots of failos
lol most people have told i got a good midface, i think is the lower what i need to improve, im improving my skin i got lots of acne
 
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Arminius

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what did u do to ascend? any looksmaxxes? ur midface and ratios in general+cuck coloring fucks u over hard.

JFL if you're on a looksmaxx site and aren't actively neckmaxxing+ trying to fix your skin + beter nt hairstyle tbh

normie to htn with good eye shape, lots lots of failos
Bulkedup3

me before
Copia de IMG 1170 2
 
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Arminius

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what did u do? take me thru ur routine
it was weird i never expected going into hormones and bodybuiding topics, i was anorexyc and i got sick of that so i started growing muscles with calisthenics, now i train gym and calisthenics
 

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