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

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.
Fifty-seven patients (33 boys and 24 girls; age range 4.5 to 16.7 years) with GHD were investigated and categorized into three groups according to the duration of GH therapy: the untreated group, the short-term therapy group, and the long-term therapy group. Their lateral cephalometric radiographs were studied, and craniofacial measurements were assessed by age and sex by using matched standard deviation scores.
In the untreated group, the anterior cranial base, total facial height, maxillary length, mandibular total length, mandibular body length, and ramus height were smaller than the standard values. In comparison with the untreated group, the long-term therapy group had a significantly larger upper facial height (P < .05), maxillary length (P < .01), and ramus height (P < .01) measurements.
Children who received long-term GH replacement therapy showed increased growth of the craniofacial skeleton, especially the maxilla and ramus. These findings suggest that GH accelerates craniofacial development, which improves occlusion and the facial profile.

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.
Growth hormone is an important regulator of bone homeostasis. In childhood, it determines the longitudinal bone growth, skeletal maturation, and acquisition of bone mass. In adulthood, it is necessary to maintain bone mass throughout life. Although an association between craniofacial and somatic development has been clearly established, craniofacial growth involves complex interactions of genes, hormones, and the environment.

somatropin's effect on hard tissue, bone formation, and osteoclasts.
The development of the dentition is an integral part of craniofacial growth, even though it is not closely related to general growth. At the cellular level, the differentiation of odontoblasts from the neural crest cells is a long process comparable with the process of osteoblast differentiation. GH is known to increase the formation of bone and hard tissues of the tooth (dentine, cementum, and enamel)

somatropin effects on bone formation through osteoblasts.
GH and IGF-I are anabolic hormones and have the potential to regulate bone modeling and remodeling. Growth factors that regulate local bone metabolism include growth hormone (GH), insulin-like growth factor-I (IGF-I), epidermal growth factor (EGF) and interleukin-1 alpha (IL-1alpha). GH stimulates the proliferation in a number of osteoblastic cell lines and primary isolated cells of various origins including human cells

The GH/IGF-1 axis and it's interaction with androgens when it comes to bone formation.
GH/IGF-I axis influences the loading-related bone formation modulating the responsiveness of bone tissue to mechanical stimuli by changing thresholds for bone formation. Cortical bone formation rate and cancellous bone volume increase when bone is reloaded and IGF-I is added. GH/IGF-I axis interacts with sex steroids in periosteal apposition challenging the traditional concept of androgen- stimulatory and estrogen-inhibitory effects on periosteal expansion
GH affects muscle tissues too, which regulate cortical bone geometry. Muscle enlargement is accompanied by increasing muscle strength leading to secondary adaptive bone gain. Growth of the facial bones such as maxilla and mandible occurs partly from direct remodeling of the surfaces of the bone.

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.

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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.
Craniofacial growth was investigated in boys treated with low-dose testosterone for delayed puberty (> 14 years old; testicular volume < 4 ml; n = 7) and compared with controls (12-14 years; n = 37). Cephalometric radiographs, statural height and pubertal stage were recorded at the start of the study and after 1 year. Craniofacial growth was assessed by nine linear measurements. At the beginning of the study, statural height, mandibular ramus length, upper anterior face height, and total cranial base length were significantly shorter in the delayed puberty boys than in the controls. After 1 year, the growth rate of the statural height, total mandibular length, ramus length, and upper and total anterior face height was significantly higher in the treated boys than in the untreated height-matched controls (n = 7). The craniofacial measurements were similar in the treated boys as compared with the controls. These results show that statural height and craniofacial dimensions are low in boys with delayed puberty. Low doses of testosterone accelerate statural and craniofacial growth, particularly in the delayed components, thus leading towards a normalization of facial dimensions.

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.

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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.
androsterone significantly affects masculinization within mammalian fetuses. Masculinization of the external genitalia in humans is subject to dihydrotestosterone (DHT) derived via the recognized androgenic pathway and also via a backdoor pathway. Spectrometric studies identify androsterone as the main backdoor androgen in the human male fetus. Circulating levels are sex-dependent, DHT being essentially absent in the female, in which titers of backdoor intermediates also are very low.

In males, backdoor intermediates occur mainly in the liver and adrenal of the fetus, and in the placenta — hardly at all in the testis. Instead, progesterone in the placenta is the main backdoor substrate for androgen synthesis. This also is consistent with the observation that placental insufficiency has been associated with disruptions of the development of fetal genitalia.


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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.

week A:

morning: ghrp-2 100mcg + mod-grf(1-29) 100mcg.

mid-day: ghrp-2 100mcg + mod-grf(1-29) 100mcg.

night: ghrp-2 100mcg + mod-grf(1-29) 100mcg.

week B-C

morning: hexarelin 100mcg + mod-grf(1-29) 100mcg.

mid-day: hexarelin100mcg + mod-grf(1-29) 100mcg.

night: hexarelin 100mcg + mod-grf(1-29) 100mcg.

(optional) an aromatase inhibitor of your choice.

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.
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.

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

Text 1


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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then dint take this shit my nigga
it increases dht by 148%
i know but he's an anomaly, no other men in my family have gotten bald that early on, at least when i take aromasin i'll know if my hair is sensitive to it and i could avoid it, my dad has to take lots of medication just to lower his DHT, even though he's not bald and only started balding at 40 so i could be fine
 
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i know but he's an anomaly, no other men in my family have gotten bald that early on, at least when i take aromasin i'll know if my hair is sensitive to it and i could avoid it, my dad has to take lots of medication just to lower his DHT, even though he's not bald and only started balding at 40 so i could be fine
YOU NEED DHT FOR PENIS
 
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imagine thinking you can survive 25mg of exemestane.. jfl
 
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imagine thinking you can survive 25mg of exemestane.. jfl
Ai's will stunt your growth since you'll kill yourself before 18 on them
 
  • JFL
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You've been at this for half a year now, when are you gonna show us some results?
 
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You've been at this for half a year now, when are you gonna show us some results?
OP doesn't think heightmaxxing works anymore.
 
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imagine thinking you can survive 25mg of exemestane.. jfl
what do you think is a good dosage of aromasin is to be high T and low E?
 
Cope. I took 25mg aromasin ed for 1 month and nothing happened.
everyone reacts differently to aromatase inhibitors. Completely dependent on your genetic makeup.

-dependent on the expression of CYP19A1 (if it's under-expressed you're more likely to need less exemestane)
-dependent on the expression of CYP3A4 (this is the enzyme that metabolizes exemestane into its inactive metabolite)
-dependent on whether you consumed fat with it.
 
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everyone reacts differently to aromatase inhibitors. Completely dependent on your genetic makeup.

-dependent on the expression of CYP19A1 (if it's under-expressed you're more likely to need less exemestane)
-dependent on the expression of CYP3A4 (this is the enzyme that metabolizes exemestane into its inactive metabolite)
-dependent on whether you consumed fat with it.
Damn seems interesting. What else does my (non existent) reaction to Aromasin tell (about muscle building/fat burning etc) ?
 
Damn seems interesting. What else does my (non existent) reaction to Aromasin tell (about muscle building/fat burning etc) ?
You felt nothing, even at the start?

When I first jumped on Aromasin I felt weaker joints, slight aches and slightly weaker erections with a bit less energy. Nothing crazy though and only lasted for a few weeks of when I first used it.
 
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When I first jumped on Aromasin I felt weaker joints, slight aches and slightly weaker erections with a bit less energy. Nothing crazy though and only lasted for a few weeks of when I first used it.
It's completely genetic related. If you don't take it with fat than you're losing a lot of the potential drug.
 
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You felt nothing, even at the start?

When I first jumped on Aromasin I felt weaker joints, slight aches and slightly weaker erections with a bit less energy. Nothing crazy though and only lasted for a few weeks of when I first used it.
Slightly loosened joints and I went to bath little more often only in first week. But I was clearly taking it after I eat something so I was definitly consumin it with fat
 
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Slightly loosened joints and I went to bath little more often only in first week. But I was clearly taking it after I eat something so I was definitly consumin it with fat
yeah i has the exact same side effect of going toilet more..

i’m not on anything anymore but what do you take and what are your goals? heightmax?
 
yeah i has the exact same side effect of going toilet more..

i’m not on anything anymore but what do you take and what are your goals? heightmax?
I only used it for 1 month. And I will try heightmaxxing with Poseidons stack if I have money in the future. I might add aromasin to it you know, higher dht might be a good for dick size in long term.
 
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Age and for how long did u run this
20 and for 3 months also lifted weights and would like to add put liquid dht on my mandible and i should have also added liquid k2
 
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they never use glucosamine, which 39 or 48 year old have u seen GROWING half an inch

Most likely a measurement error. Or they measured it in the morning. Everybody is half inch taller in the morning from spinal decompression. If it was like at least 2 inches, it would be something worthy to look at.
 
Strikes motto is 'ascend or die' and he takes it completely literally.
him and his lab rats are willing to die in order to grow, it's truly quite pathetic.

I'm willing to die for this. If I can be a matyr for height increase experiment and leave my name in history, it would be an ultimate honorable way to die.
 
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If I can be a matyr for height increase experiment and leave my name in history, it would be an ultimate honorable way to die.
I respect the passion, but no one will care about this in 100 years. There's no benefit in everyone being taller, it just requires more natural resource use. This is one of the few examples where selfishness is a better reason than helping society on a macro level.
 
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I respect the passion, but no one will care about this in 100 years. There's no benefit in everyone being taller, it just requires more natural resource use. This is one of the few examples where selfishness is a better reason than helping society on a macro level.
fuck helping society in all cases, help yourself noone else will
 
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Yeah that’s what I’m gonna do. Hoping to get some frame/height gains from this. Not expecting that much since im 18.
Did you have some results?
 
I only used it for 1 month. And I will try heightmaxxing with Poseidons stack if I have money in the future. I might add aromasin to it you know, higher dht might be a good for dick size in long term.
you ever get back to it?
 
I stumbled onto EvoMuse BMP in a different post and that reinvigorated interest in adult heightmaxxing for me. Going through this thread there really isn't much I can contribute that hasn't already been mentioned but I got a few things


Icariin increases BMP2 and BMP7. Icariin is found in horny goat weed. I don't know if we need to increase BMPs further then EvoMuse BMP does.

Forskolin inhibits FGF3. FGF3 inhibits chondrogenesis

Calcium-D Glucarate reduces estrogen receptor density and helps the liver flush out excess estrogens


Also this blog belongs to Tyler who is one of the founding authors on naturalheightincrease. The search on here pulls up results both from this ol blog of his and naturalheightincrease, which doesn't have a built in search. http://www.heightquest.com/


Some studies on Icariin. There's a lot of moving parts so this might not fit in with everything else. It does increase Runx2 which is something Strike was looking to avoid
 
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@Strike_Poseidon I was looking back to share this post from Mr_Wax but I see you was already in the thread

"FGF2 inhibited CNP dependent GC-B activity"

I'm of the train of thought that we don't know exactly how much FGF2 is increased from EvoMuse BMP. It does concern me that stacking other FGF2 agonist alongside EvoMuse BMP might push the FGF2 too high


If I try this stack I'm going to do it with either puerarin or wu tang + MK677 instead of hexarelin, whichever has lesser FGF2. Instead of 2g of SAM-e I'm going to do either 800mg or the depression dose. Everything else will be done with no corners cut unless I discover some interaction in the coming weeks
 
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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
 
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I turn 16 in 3 months worth to get on peptide stack?
 
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
Lets boil it down. Theoretically, is it absolutely and unequivocally possible to increase adult height? and if so, by how many inces
 
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Lets boil it down. Theoretically, is it absolutely and unequivocally possible to increase adult height? and if so, by how many inces
Yes, with leg lengthening lol

but aside from that, without the growth plate you're almost doomed. The only redeeming thing is Wolff's law. Bones have mechanical receptors and will grow and adapt to mechanical forces acted on it. This is unequivocally proven. The only problem is that it takes a lot of force, and it needs to be constant in order to cause bone remodeling. Theoretically you could change your skeleton's dimensions.
 
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Yes, with leg lengthening lol

but aside from that, without the growth plate you're almost doomed. The only redeeming thing is Wolf's law. Bones have mechanical receptors and will grow and adapt to mechanical forces acted on it. This is unequivocally proven. The only problem is that it takes a lot of force, and it needs to be constant in order to cause bone remodeling. Theoretically you could change your skeleton's dimensions.
I get that, but strike talks about how growth plate ossification is not a final process, they just get smaller and smaller until they stop being receptive to GH. I mean purely theoretically, wasn't there the story of that Adam Rainer guy who was a midget but then became a giant AFTER puberty. I know he had a tumor in his pituirary, but I feel as though him and others who get tumors in their pituitary prove that bone growth is possible at a theoretical level even after puberty. OFC it is not a safe process at all and so is moot, but just for proving that there are alternative ways of thinking about growth it still stands. I am not really looking for crazy dramatic growth, just a few inches and I don't want to risk something completely mechanical like LL.
 
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I get that, but strike talks about how growth plate ossification is not a final process, they just get smaller and smaller until they stop being receptive to GH. I mean purely theoretically, wasn't there the story of that Adam Rainer guy who was a midget but then became a giant AFTER puberty. I know he had a tumor in his pituirary, but I feel as though him and others who get tumors in their pituitary prove that bone growth is possible at a theoretical level even after puberty. OFC it is not a safe process at all and so is moot, but just for proving that there are alternative ways of thinking about growth it still stands. I am not really looking for crazy dramatic growth, just a few inches and I don't want to risk something completely mechanical like LL.
just get a pituitary tumor to escape manletism theory
 
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I get that, but strike talks about how growth plate ossification is not a final process, they just get smaller and smaller until they stop being receptive to GH. I mean purely theoretically, wasn't there the story of that Adam Rainer guy who was a midget but then became a giant AFTER puberty. I know he had a tumor in his pituirary, but I feel as though him and others who get tumors in their pituitary prove that bone growth is possible at a theoretical level even after puberty. OFC it is not a safe process at all and so is moot, but just for proving that there are alternative ways of thinking about growth it still stands. I am not really looking for crazy dramatic growth, just a few inches and I don't want to risk something completely mechanical like LL.
Be optimistic for the future, for there may very well be a significantly safer and less invasive method of LL. There is a very real medical demand to develop the technology further to help people with bone disorders and leg length discrepancies.

For the Adam Rainer story, my theory is that he was lucky to have a delayed bone age. This is evident by his giant hands and feet for his height combined with growth retardation (which is correlated with premature bone age). The pituitary tumor then blasted HGH into his system and he grew an insane amount, due to his underdeveloped skeleton. Without the tumor I'm pretty positive he would have still had a growth spurt that pushed him into the 5 foot+ range easily.

With modern cases of acromegaly there does seem to be a minor height increase, but that only happens at the point where the person has severe acromegalic features to the point of deteriorating their facial features. The growth happens but it is not coming from the growth plate cartilage.
 
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Be optimistic for the future, for there may very well be a significantly safer and less invasive method of LL. There is a very real medical demand to develop the technology further to help people with bone disorders and leg length discrepancies.

For the Adam Rainer story, my theory is that he was lucky to have a delayed bone age. This is evident by his giant hands and feet for his height combined with growth retardation (which is correlated with premature bone age). The pituitary tumor then blasted HGH into his system and he grew an insane amount, due to his underdeveloped skeleton. Without the tumor I'm pretty positive he would have still had a growth spurt that pushed him into the 5 foot+ range easily.

With modern cases of acromegaly there does seem to be a minor height increase, but that only happens at the point where the person has severe acromegalic features to the point of deteriorating their facial features. The growth happens but it is not coming from the growth plate cartilage.
Could you elaborate on what the future of LL would look like? Would it be possible to do it for things like wrists or fingers or feet etc, whatever bone safely without fucking with the ligaments?

I have a theory on LL, usually it is thought that bone grown from LL is not as strong as natural bone thats why people say that it'll fuck you up in the later stages of your life. But what if you start strengtheining your bones by blasting whatever, HGH BMP k2 anything to the point where they just become very strong regardless and you also do conditioning training. Or perhaps some new medicine comes along for people to deal with osteoarthritis or whatever in their old age and we take it. My mother has arthritis and she takes a bunch of bone health stuff because the doctors recommend it.
 
Lets boil it down. Theoretically, is it absolutely and unequivocally possible to increase adult height? and if so, by how many inces

theoretically, it's possible since the mechanisms appear to exist. The problem is if it's realistically achievable. Personally I don't think any of this is possible with supplements and peptides because there's always some negative feedback where increasing one thing increases or decreases something else in the direction we don't want. All of these supplements have multiple effects beyond just the point of interest we're looking at. If we can acquire these growth factors exogenously we can cheat the bodies homeostasis mechanisms by having the right combination of factors elevated together that we otherwise never would have while using supplements to suppress others. I'm more optimistic about LSJL or LIPUS with the aid of a stack to enable it for height. Both LSJL and LIPUS raise and lower some of these factors locally where they are applied to so an LSJL or LIPUS stack would have to be design differently from a 100% systemic stack where you take a cocktail and just grow. Another consideration is what's the goal of these systemic stacks. Are we trying to chemically reactivate growth plates for longitudinal growth of the long bones or are we trying to make the articular cartilage grow to elongate the spine?

In the notes with a bunch of studies on CNP that I had saved from 8 or 9 years ago the notes I had were vague about CNP and FGF2 conflicting. I read through only 3 of them to re learn it and I was planning to make a quality post breaking it down but I found out that someone else @BasedSpinelet257 already did that work in this post https://looksmax.org/threads/erdal-can-alkoclar-on-height-increase.74486/page-2#post-2485318

Read all of his replies in that thread. It's exactly what I would have said but better organized then I would have wrote it up. I have other things I'm going to write up with some free time. Factors not mentioned in this thread, and a breakdown of all the ingredients in EvoMuse BMP. BMP is being used mainly because of 2 ingredients but it still has about 6 more ingredients that all do things too. They may happen to all elevate either BMP 2 or 7, but they do other things and not a single person here took the time to see what they all do because it might not even be worth using once we put it under the microscope.
 
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theoretically, it's possible since the mechanisms appear to exist. The problem is if it's realistically achievable. Personally I don't think any of this is possible with supplements and peptides because there's always some negative feedback where increasing one thing increases or decreases something else in the direction we don't want. All of these supplements have multiple effects beyond just the point of interest we're looking at. If we can acquire these growth factors exogenously we can cheat the bodies homeostasis mechanisms by having the right combination of factors elevated together that we otherwise never would have while using supplements to suppress others. I'm more optimistic about LSJL or LIPUS with the aid of a stack to enable it for height. Both LSJL and LIPUS raise and lower some of these factors locally where they are applied to so an LSJL or LIPUS stack would have to be design differently from a 100% systemic stack where you take a cocktail and just grow. Another consideration is what's the goal of these systemic stacks. Are we trying to chemically reactivate growth plates for longitudinal growth of the long bones or are we trying to make the articular cartilage grow to elongate the spine?

In the notes with a bunch of studies on CNP that I had saved from 8 or 9 years ago the notes I had were vague about CNP and FGF2 conflicting. I read through only 3 of them to re learn it and I was planning to make a quality post breaking it down but I found out that someone else @BasedSpinelet257 already did that work in this post https://looksmax.org/threads/erdal-can-alkoclar-on-height-increase.74486/page-2#post-2485318

Read all of his replies in that thread. It's exactly what I would have said but better organized then I would have wrote it up. I have other things I'm going to write up with some free time. Factors not mentioned in this thread, and a breakdown of all the ingredients in EvoMuse BMP. BMP is being used mainly because of 2 ingredients but it still has about 6 more ingredients that all do things too. They may happen to all elevate either BMP 2 or 7, but they do other things and not a single person here took the time to see what they all do because it might not even be worth using once we put it under the microscope.
Interesting, Where can I find out more about LSJL and LIPUS
 
I look forward to any further insight. At this point further research for me has reached the point of mental masturbation without release. Godspeed. ❤️ @Mad Science
 
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Interesting, Where can I find out more about LSJL and LIPUS


The first site is the blog of Tyler (MiniGolfer). He stopped posting to that when he decided to join the second site with multiple authors. The last one is his forum for LSJL. You can also look up LSJL or Lateral Synovial Joint Loading. LIPUS stands for Low Intensity Pulsed Ultrasound.

Since the 2nd one is missing a search, use the 1st one since the search on there searches both sites. The last one the forum is basically the most active height forum around now excluding leg lengthening surgery forums. Hardly active compared to the old forums 9 years ago.

I look forward to any further insight. At this point further research for me has reached the point of mental masturbation without release. Godspeed. ❤ @Mad Science

Do it in increments. When I make my post maybe you will see something interesting to expand on. CNP is a dead end, eiher because nothing we can take will increase it or we just lack studies where CNP was measured.
 
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heightquest.com
naturalheightgrowth.com

The first site is the blog of Tyler (MiniGolfer). He stopped posting to that when he decided to join the second site with multiple authors. The last one is his forum for LSJL. You can also look up LSJL or Lateral Synovial Joint Loading. LIPUS stands for Low Intensity Pulsed Ultrasound.



Do it in increments. When I make my post maybe you will see something interesting to expand on. CNP is a dead end.

Do you honestly believe there is a way to meaningfully increase height proportionally past epiphyseal fusion? If so, with compounds and molecules available to the public? If not, what about the future?

Also, here is a link to a write up of the BMP formula that may give you some further info. I hope it is of benefit.

 

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