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.

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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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hwats your stack and the supplemtents your taking
Boron , calclium , keto dht , k2m4 , d3 3,000 iu , eating in a caloric surplus to boost igf1 also 500mgs of test perweek i am now done with this cycle and saw good gains + facial changes will now do MSE + facepulling
 
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Boron , calclium , keto dht , k2m4 , d3 3,000 iu , eating in a caloric surplus to boost igf1 also 500mgs of test perweek i am now done with this cycle and saw good gains + facial changes will now do MSE + facepulling
why 3000 d3 and not one thousand? and where did you get the test
 
bro im legit praying for u rn, plz follow correct dosage and timings, hope u do well brother!
where are the correct dossages and timings for this

folic acid,folinic acid, sam-e, ecdysterone, meclizine, BMP formula, hexarelin, si wu tang and glucosamine chondroitin msm
 
why 3000 d3 and not one thousand? and where did you get the test
test from a friend , 3000 because you need a higher dosage for quick bone gains it works synchronously with the 12-15mg of k2m4 i was taking daily
 
https://www.dailymail.co.uk/health/article-18138/I-stop-growing.html Like I said, increasing methylation too much will make sure you never stop growing, like this article says there is no cure to stop him from growing he will just keep growing till he dies, stick to my dosages and timings and you should be fine, moreover this article says that he can't stop growing but he doesn't have any tumor which is where the hypermethylation part ALSO comes in https://www.healthdirect.gov.au/gigantism#:~:text=There are also rare genetic,as acromegaly, can affect adults.

'There are also rare genetic conditions that can cause gigantism without the child having an adenoma. Examples include Sotos syndrome, Beckwith-Wiedemann syndrome, and Weaver syndrome' all well known epigenetic defects there is also DMNT3A overgrowth syndrome which can contribute for this anyway.

Both sotos and weaver syndrome linked to inactivation of NSD1 gene: https://www.pnas.org/content/106/51/21830
'NSD1 Promoter CpG Island Hypermethylation Leads to Gene Inactivation'

I have experienced sides when taking that sam-e or folic and folinic acid that involve major cramps at times, just something to keep in mind
what does meclinze do?
 
what does meclinize do agian ive read the thread but still dont understand
 
d
bro it's alright man... that was the dosage recommended to me by a guy on the old grow tall forum named xcrunner who studied biochemistry at the med university of antigua and my friend haruda michinoku who also studied biochemistry back in Japan, it's a safe dosage and it is the right dosage, it won't give you a pituitary tumor but it is close enough to make it happen, sensence is the biological process of in many regions of the body, the loss of DNA methylation and growth plate senescence has already been established and so has it's importance in maintaining chondrocyte phenotype for the MSC's in the hyaline cartilage to differentiate into chondrocytes, SAM dependent methylation especially hypermethylation of that pathway has been shown to delay senscent changes pretty quickly and even reverse some senscent changes like bone age and other parts of biological aging, folic acid is used for increasing DNA methylation with another enzyme and to give protection from DNA damage, lowering the dose won't benefit you that much. Look at me, only taken it for 2 days, I have got more red spots, more acne and now more growth pains. This WORKS! read this for a guide on it: https://web.archive.org/web/2011031...NLIMITED-HEIGHT-GROWTH-t-8783-1.html#pid76187 having hight amount of methionine nhibit the enzyme B-Galactosidase, and increase telomerase activity, and high folate intake will all contribute greatly. In terms of reviews there was this guy on the forum named anonymousguy, started taking the folic acid alone for 2 months with a weaker form of hexarelin and he gained 1.5 inches in 2 months when he had not grown at all for a year.

Also Tyler from heightquest.com who now also runs naturalheightgrowth.com understands it's importance, tricking your body that it is in an earlier chondrocyte differentiation state which can be done easily by hypermethylation may be the key to unlimited height growth

Also other than pituitary tumors to watch out for you also gotta watch out for leukemia: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4208652/
'Loss of the deleted in lymphocytic leukemia 7 (DLEU7) gene is frequently observed in chronic lymphocytic leukemia, due to hypermethylation of the DLEU7 promoter (Hammarsund et al. 2004).'
'Hypermethylation of MOS is associated with the development of acute lymphoblastic leukemia (Scholz et al. 2005).'

'Consistent with this, DNA hypermethylation modules were detected in 42 height‐associated genes'

This is going deep deep deep into epigenetics, which is why people have a maximum genetic potential, regulated by switching on or off epigenetic factors. Which is why in some family's even identical twins separated at birth to poorer countries, one turning out table than the other, epigenetics at it's finest...

'Remarkably, 72 of 87 height‐associated genes (82.8%) were found to contain at least one CpG island in the 2,000 bp upstream of the transcription start site (TSS) (99 CpG islands overall) (Table 1).'
o you have nay idea what the weaker form of hexalerin was called?
 
d

o you have nay idea what the weaker form of hexalerin was called?
puerarin, it was effective to give even adults with closed/inactive plates 1-2 inches, and teens with active plates 3-5 inches despite whatever their genetic potential was
 
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what does meclinize do agian ive read the thread but still dont understand
meclizine targets the ERK node in the CNP pathway, basically it acts just like CNP does for growth
 
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puerarin, it was effective to give even adults with closed/inactive plates 1-2 inches, and teens with active plates 3-5 inches despite whatever their genetic potential was
whats an alternative to hexalerin that i can buy from a store thats not as expensive?
 
Where am I supposed to get 2g of SAMe daily in enteric tablets? Is there anywhere that actually sells it in doses of 1000mg+?
 
Do you actually need the stuff like the BMP formula and ecdysterone? I know the basic stack needs hexarelin, meclizine, si wu tang, folic acid, and the SAMe
 
Do you actually need the stuff like the BMP formula and ecdysterone? I know the basic stack needs hexarelin, meclizine, si wu tang, folic acid, and the SAMe
Did I stutter anywhere? I did say you need EVERYTHING, you also need turmeric too as it will have good synergy when used with the bmp formula and u need folinic acid
 
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Did I stutter anywhere? I did say you need EVERYTHING, you also need turmeric too as it will have good synergy when used with the bmp formula and u need folinic acid

On Amazon you can get Glucosamine Chondroitin Turmeric and MSM all in one pill... FYI
 
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Good thread but simply all you need is HGH, IGF-1, DHT cream, HCG and Dsip
 
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Good thread but simply all you need is HGH, IGF-1, DHT cream, HCG and Dsip
Did you read anything past the first post? Not a single person in this thread believes that HGH will do anything except a few of us retarded graycels. Also HCG w/o an AI and proper pct is an accident waiting to happen.
 
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Did you read anything past the first post? Not a single person in this thread believes that HGH will do anything except a few of us retarded graycels. Also HCG w/o an AI and proper pct is an accident waiting to happen.
Are you retarded boss? Hgh won't do anything
:lul: :lul: @Mohamad @Extra Chromosome @Chad1212

Put this delusional greycel in his place
 
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Are you retarded boss? Hgh won't do anything
:lul: :lul: @Mohamad @Extra Chromosome @Chad1212

Put this delusional greycel in his place
greycels.....
 
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Are you retarded boss? Hgh won't do anything
:lul: :lul: @Mohamad @Extra Chromosome @Chad1212

Put this delusional greycel in his place

@Dyorotic2 and @Strike_Poseidon almost hate each other because of how different their views on heightmaxxing are, yet they both say HGH is a cope unless you’re deficient.
 
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@Dyorotic2 and @Strike_Poseidon almost hate each other because of how different their views on heightmaxxing are, yet they both say HGH is a cope unless you’re deficient.
Oh sure, the primary trigger in growth (growth hormone) doesn't do anything. In the studies it is conducted of deficient people ofc, we know this however they all say that it doesn't mean it won't work in people not deficient. By that logic would Testosterone only work if you are deficient? And does tren only work if your deficient. Mnay studies on this, so rather than listening to incel brainlets do some actual research
 
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Oh sure, the primary trigger in growth (growth hormone) doesn't do anything. In the studies it is conducted of deficient people ofc, we know this however they all say that it doesn't mean it won't work in people not deficient. By that logic would Testosterone only work if you are deficient? And does tren only work if your deficient. Mnay studies on this, so rather than listening to incel brainlets do some actual research
this doesn't work in terms of bone growth, muscle can always grow
 
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While the plates are open you can grow massively. I've studied this a lot.
How many anecdotal cases do you have? Strike and a few other people who focus on DNA methylation have at least 5 of people growing past their parents heights. There are no studies that show children with normal height can grow from HGH. Even if they could, you’d still get a significant HGH boost from Strike's stack. Dyortic and @PubertyMaxxer both used HGH and failed. Pubertymaxxer was 15 at the time, that's the main time for bone growth.
 
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Did I stutter anywhere? I did say you need EVERYTHING, you also need turmeric too as it will have good synergy when used with the bmp formula and u need folinic acid
Is the folic acid and folinic acid dosages the same?
 
That’s not necessarily true lmao
Well ofc it's true. If your plates are open EVERYTHING will grow. Bow ofc if you have manlet parent you have a certain genetic potential. But you ceasily expect 1-2 inches
 
Well ofc it's true. If your plates are open EVERYTHING will grow. Bow ofc if you have manlet parent you have a certain genetic potential. But you ceasily expect 1-2 inches
 
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@Dyorotic2 @Strike_Poseidon. What do you think of justtrynagrow's method? Anything you would change or Improve?
 
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@Strike_Poseidon , can you outline what in this BMP formula which ingredients do what including studies to prove they do what you say?
 
JFL at taking over 5 iu of growth - must be ordering it from China and allowing it degenerate in transit when not stored. I know IFBB pros who don’t take that much growth, why does a skinny fat incel need to?
 
Has anyone got any height gains from your stack strike? @Strike_Poseidon
 
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Has anyone got any height gains from your stack strike? @Strike_Poseidon
people say they do, i call bs. no way fucking tumeric and some shitty anti dopaminergetic antihistamine can induce growth. maybe there is something to methylation but that's yet to be seen.
 
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Boron , calclium , keto dht , k2m4 , d3 3,000 iu , eating in a caloric surplus to boost igf1 also 500mgs of test perweek i am now done with this cycle and saw good gains + facial changes will now do MSE + facepulling
what kind of changes did you see?
 
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@Strike_Poseidon , can you outline what in this BMP formula which ingredients do what including studies to prove they do what you say?




BMP-2 used in a smad independent pathway like MAPK p38 will target chondrogenesis, it is the Runx2 pathway which causes osteogenesis and if done in excess can result in chondrogenic and osteosarcomas, BMP-2 with MAPK signalling and sox9 transcriptional factor can revert dormant MSC's in inactive/closed plates (on the epiphyseal line https://regenexx.com/blog/skeletal-...the-growth-plates-may-one-day-make-us-taller/) basically to dedifferentiate bmp induced chondrocytes into mesenchymal stem cells. Understand this picture to get a just of all of this first:
This same process can be used for OP-1( BMP-7) however the activation may be a little different
 
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people say they do, i call bs. no way fucking tumeric and some shitty anti dopaminergetic antihistamine can induce growth. maybe there is something to methylation but that's yet to be seen.
Even without it mainly targeting chondrogenesis people in their late thirties and forties have seen growth, and no they are not shilling for evomuse, this formula wasn't even made for height growth in the first place! Purely muscle growth
 

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what kind of changes did you see?
I'd love to know as well. Pretty sure Test E was studied to stunt growth at 500mg EOW and worked to the point that it stunted their growth like 2-3 inches. He took twice that. Hopefully he took an AI too.
 
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Even without it mainly targeting chondrogenesis people in their late thirties and forties have seen growth, and no they are not shilling for evomuse, this formula wasn't even made for height growth in the first place! Purely muscle growth
Those are nothing but 2 delusional oldcels.
no way tumeric and some shitty anti dopaminergetic antihistamine can induce growth. methylation
Also this. Even if the theory is correct I (personally) suspect that the current compounds/drugs don't have the level of influence in your body needed for the results we're looking for.

Something else could though.
 
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Even without it mainly targeting chondrogenesis people in their late thirties and forties have seen growth, and no they are not shilling for evomuse, this formula wasn't even made for height growth in the first place! Purely muscle growth
Half of an inch lol. Much more likely just the result of increased intervertebral disc height from glucosamine (due to improved lubrication) than actual longitudinal bone growth
 
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