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

[Deleted member 2756]

not 6-8 months, teens who used the letrozole had an age of 17.3 but had bone age of 15.4

thanks for the correction.

 

[Deleted member 4946]

thanks for the correction.

bro on that same article it apparently shoes that guys who received AI and GH had even slower bone age compared to those with just AI: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5155684/figure/F1/ and what in the fuck this one shows they grew like 20 cm: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5155684/figure/F2/ but it was higher, just a reminder they started this when they were 14.1 years old, this one shows that the ones who took AI and GH had the highest IGF-1 levels: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5155684/figure/F4/
This one shows that HGH/AI decreased estradiol more than just AI alone
Ok and this one shows GH treatment had the lowest increase in T but AI alone had highest increase (almost 100ng/dl) but AI+Gh had second highest: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5155684/figure/F4/

It's time I'm waiting for more theorising with u man.

 

[Deleted member 2756]

bro on that same article it apparently shoes that guys who received AI and GH had even slower bone age compared to those with just AI: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5155684/figure/F1/

insane statistics. GH rapidly aged the bone, whereas GH and AI didn't. AI's seriously make a difference.

https://academic.oup.com/jcem/article/91/3/799/2843281 give this study a read, 250mcg/kg of CJC-1295 (DAC) administrated once weekly was able to keep IGF-1 elevated beyond 400ng/dl in non-adolescent men for 4 days, peaking on day 7 and then slowly dropping, at 21 days IGF-1 is still higher than the baseline. 12-15mg of CJC-1295 bi-weekly ALONE is enough to reach the 400ng/dl range within non-adolescents, this is without GHSR and Ghrelin receptor agonists like hexarelin and GHRP-2-6.

I'm thinking of running 15mg of CJC-1295 DAC biweekly split into 7.5mg dosages at once. On the days that I inject the CJC i'll also dose Hexarelin alongside it to create insanely high GH pulses as serum CJC-1295 blood levels drop within the first day or so, but the GHF-R agonism continues. Keep in mind I am also using exogenous GH dosed at around 15-17.5IU.

 

[Deleted member 4946]

insane statistics. GH rapidly aged the bone, whereas GH and AI didn't. AI's seriously make a difference.

https://academic.oup.com/jcem/article/91/3/799/2843281 give this study a read, 250mcg/kg of CJC-1295 (DAC) administrated once weekly was able to keep IGF-1 elevated beyond 400ng/dl in non-adolescent men for 4 days, peaking on day 7 and then slowly dropping, at 21 days IGF-1 is still higher than the baseline. 12-15mg of CJC-1295 bi-weekly ALONE is enough to reach the 400ng/dl range within non-adolescents, this is without GHSR and Ghrelin receptor agonists like hexarelin and GHRP-2-6.

I'm thinking of running 15mg of CJC-1295 DAC biweekly split into 7.5mg dosages at once. On the days that I inject the CJC i'll also dose Hexarelin alongside it to create insanely high GH pulses as serum CJC-1295 blood levels drop within the first day or so, but the GHF-R agonism continues. Keep in mind I am also using exogenous GH dosed at around 15-17.5IU.

I never knew there were experiments done with peptides, damn it'll be a good read, yeah and to also answer your top statement, the GH and AI treatment actually slowed down bone age more than actual AI itself how is that possible, we see on the graph GH rapidly ages bone, and AI seriously delays bone age but then AI and GH lower bone age more than AI itself? What kind of trickery is this?

 

[Deleted member 2756]

I never knew there were experiments done with peptides, damn it'll be a good read

there are loads. Hexarelin is used for diseases such as anorexia Nervosa and HIV.

 

[Deleted member 2756]

I never knew there were experiments done with peptides, damn it'll be a good read, yeah and to also answer your top statement, the GH and AI treatment actually slowed down bone age more than actual AI itself how is that possible, we see on the graph GH rapidly ages bone, and AI seriously delays bone age but then AI and GH lower bone age more than AI itself? What kind of trickery is this?

well high amounts of GH cause temporary hypogonadism. Could be it.

I never knew there were experiments done with peptides, damn it'll be a good read, yeah and to also answer your top statement, the GH and AI treatment actually slowed down bone age more than actual AI itself how is that possible, we see on the graph GH rapidly ages bone, and AI seriously delays bone age but then AI and GH lower bone age more than AI itself? What kind of trickery is this?

https://pubmed.ncbi.nlm.nih.gov/2566942/?from_term=somatostatin+pyridostigmine&from_pos=2 @Strike_Poseidon just found something interesting.

regarding the usage of pyridostigmine as an acetylcholinesterase inhibitor, which has potent somatostatin suppressive properties. They tested the response to GHRH with 100g of glucose, GHRH 100mcg/kg along with Pyridostigmine, GHRH 100mcg/kg with pyridostigmine and 100g of glucose all at once. In the first test, the administration of oral glucose inhibited the actions of the GHRH, in the second test the effects of GHRH were exasperated via the usage of 120mg of pyridostigmine, and in the last test, the response of GH secretion from GHRH + pyridostigmine wasn't blunted when the patient was administrated 100g of oral glucose. hyperglycemia was unable to reduce the potentiating effect of pyridostigmine on GH secretion elicited by GHRH. Based on the reported actions of pyridostigmine, acute hyperglycemia might act over GH release by inducing hypothalamic somatostatin release.

this is big, that means eating won't blunt the response to GHRH-R agonists and GHS-R agonists.

 

[Deleted member 4946]

well high amounts of GH cause temporary hypogonadism. Could be it.

https://pubmed.ncbi.nlm.nih.gov/2566942/?from_term=somatostatin+pyridostigmine&from_pos=2 @Strike_Poseidon just found something interesting.

regarding the usage of pyridostigmine as an acetylcholinesterase inhibitor, which has potent somatostatin suppressive properties. They tested the response to GHRH with 100g of glucose, GHRH 100mcg/kg along with Pyridostigmine, GHRH 100mcg/kg with pyridostigmine and 100g of glucose all at once. In the first test, the administration of oral glucose inhibited the actions of the GHRH, in the second test the effects of GHRH were exasperated via the usage of 120mg of pyridostigmine, and in the last test, the response of GH secretion from GHRH + pyridostigmine wasn't blunted when the patient was administrated 100g of oral glucose. hyperglycemia was unable to reduce the potentiating effect of pyridostigmine on GH secretion elicited by GHRH. Based on the reported actions of pyridostigmine, acute hyperglycemia might act over GH release by inducing hypothalamic somatostatin release.

this is big, that means eating won't blunt the response to GHRH-R agonists and GHS-R agonists.

Don't get it, what are you trying to suggest here?

 

[Deleted member 2756]

Don't get it, what are you trying to suggest here?

when you consume food, whether it be protein, fats or carbohydrates GH secretion is suppressed to sub 0.5ng/ml, glucose seems to be the strongest at suppressing the secretion, although fats and protein both still do due to the spike in insulin.

acetylcholinesterase is the enzyme that metabolizes and breaks down acetylcholine. When you inhibit the enzyme, cholinergic activity rises and somatostatin becomes suppressed, the study basically proves that glucose potently upregulates somatostatin activity, therefore abolishing the secretion of GH for a short period of time.

in the study, an acetylcholinesterase inhibitor was used (pyridostigmine), along with 100mcg/kg of recombinant human GHRH. In the first test, they administrated GHRH intramuscularly, with 100g of glucose orally, then tested the blood levels of GH, as you'd expect, the GH response was nearly zero, when GHRH and pyridostigmine were administrated together, the effects of the GHRH were exasperated due to the cholinergic control of somatostatin, they then again administrated GHRH along with 120mg of pyridostigmine, then gave the patient 100g of glucose orally, they tested blood levels and the GH response wasn't suppressed.

meaning the GH secretion response to glucose revolves around the upregulation of somatostatin, acetylcholine activity potently suppresses somatostatin from being released. Inhibiting the enzyme that metabolizes acetylcholine, through the usage of pyridostigmine allows the somatroph cells to constantly secrete GH (of course as long as there is stimuli, either GHR agonist or a GHRH analog).

 

[Deleted member 4946]

when you consume food, whether it be protein, fats or carbohydrates GH secretion is suppressed to sub 0.5ng/ml, glucose seems to be the strongest at suppressing the secretion, although fats and protein both still do due to the spike in insulin.

acetylcholinesterase is the enzyme that metabolizes and breaks down acetylcholine. When you inhibit the enzyme, cholinergic activity rises and somatostatin becomes suppressed, the study basically proves that glucose potently upregulates somatostatin activity, therefore abolishing the secretion of GH for a short period of time.

in the study, an acetylcholinesterase inhibitor was used (pyridostigmine), along with 100mcg/kg of recombinant human GHRH. In the first test, they administrated GHRH intramuscularly, with 100g of glucose orally, then tested the blood levels of GH, as you'd expect, the GH response was nearly zero, when GHRH and pyridostigmine were administrated together, the effects of the GHRH were exasperated due to the cholinergic control of somatostatin, they then again administrated GHRH along with 120mg of pyridostigmine, then gave the patient 100g of glucose orally, they tested blood levels and the GH response wasn't suppressed.

meaning the GH secretion response to glucose revolves around the upregulation of somatostatin, acetylcholine activity potently suppresses somatostatin from being released. Inhibiting the enzyme that metabolizes acetylcholine, through the usage of pyridostigmine allows the somatroph cells to constantly secrete GH (of course as long as there is stimuli, either GHR agonist or a GHRH analog).

ok that's all well and good, now we need to fins sources for mestinon now, also to answer your earlier thing why AI and GH were slowing down bone age very low I don't think it's because GH also induced hypogonadism as well because on this results: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5155684/figure/F4/

The T levels were still between 600-800 ng/dl

 

[Deleted member 3043]

chad thread tbh

 

[Deleted member 4946]

Ok it's official I asked some r/Trans DIY people how to get spironolactone and they sent me sources to shesalady,shop, I have now sent them payment through western union for 60 100 mg tablets of the Aldactone, all this at cost of everyone on there thinking I'm a gender dysphoric abomination

 

[Deleted member 2756]

Ok it's official I asked some r/Trans DIY people how to get spironolactone and they sent me sources to shesalady,shop, I have now sent them payment through western union for 60 100 mg tablets of the Aldactone, all this at cost of everyone on there thinking I'm a gender dysphoric abomination

you're really gonna castrate yourself?

come on...

 

[Alexanderr]

Since I’m on a really tight budget I’ll go with method 3 and either convert to method 1 or 2 when I make enough money.

 

[Alexanderr]

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.

So, is there like one week left where we don’t take anything at all, since there’s no week D? Or do we just start taking ghrp-2 again for the 4th week of the month?

 

[LifeMaxxing]

Diorotic what is your opinion on DHT gel as of now?
Sorry dyorotic

 

[Deleted member 4946]

you're really gonna castrate yourself?

come on...

look man, ill use it responsibly IK all drugs have risks if you abuse them and for this I will sacrifice my masculinity during my teen years, the greatest scientists of our time had to risk many things for their big discoveries' there is no point In me not trying EVERYTHING that I can afford, I won't forgive myself in the future if I did that

 

[Deleted member 2756]

So, is there like one week left where we don’t take anything at all, since there’s no week D? Or do we just start taking ghrp-2 again for the 4th week of the month?

don't take the hexarelin for longer than a week, take GHRP-2 or GHRP-6 for two weeks, than hex for one. Rinse and repeat.

 

[Alexanderr]

don't take the hexarelin for longer than a week, take GHRP-2 or GHRP-6 for two weeks, than hex for one. Rinse and repeat.

Okay, thanks.

 

[Hopeful333]

well high amounts of GH cause temporary hypogonadism. Could be it.

https://pubmed.ncbi.nlm.nih.gov/2566942/?from_term=somatostatin+pyridostigmine&from_pos=2 @Strike_Poseidon just found something interesting.

regarding the usage of pyridostigmine as an acetylcholinesterase inhibitor, which has potent somatostatin suppressive properties. They tested the response to GHRH with 100g of glucose, GHRH 100mcg/kg along with Pyridostigmine, GHRH 100mcg/kg with pyridostigmine and 100g of glucose all at once. In the first test, the administration of oral glucose inhibited the actions of the GHRH, in the second test the effects of GHRH were exasperated via the usage of 120mg of pyridostigmine, and in the last test, the response of GH secretion from GHRH + pyridostigmine wasn't blunted when the patient was administrated 100g of oral glucose. hyperglycemia was unable to reduce the potentiating effect of pyridostigmine on GH secretion elicited by GHRH. Based on the reported actions of pyridostigmine, acute hyperglycemia might act over GH release by inducing hypothalamic somatostatin release.

this is big, that means eating won't blunt the response to GHRH-R agonists and GHS-R agonists.

Does gh and igf-1 rapidly age bone?

I'm thinking of taking mk 677 and huperzine a, for height, frame and muscle growth.

If I don't take an AI could I risk stunting my growth or rapidly increasing my bone age?

Would you recommend me taking mk 677 without an AI at 17?

I understand hgh is optimal but I'm not in the position the pay or use that right now.

Thanks in advance.

 

[Alexanderr]

Does gh and igf-1 rapidly age bone?

I'm thinking of taking mk 677 and huperzine a, for height, frame and muscle growth.

If I don't take an AI could I risk stunting my growth or rapidly increasing my bone age?

Would you recommend me taking mk 677 without an AI at 17?

I understand hgh is optimal but I'm not in the position the pay or use that right now.

Thanks in advance.

GH rapidly aged the bone, whereas GH and AI didn't. AI's seriously make a difference.

If you can’t afford HGH you should go with his third method (which is a lot cheaper) instead of solely Mk-677.

 

[Hopeful333]

If you can’t afford HGH you should go with his third method (which is a lot cheaper) instead of solely Mk-677.

Do you not have to inject peptides like 3 times a day? I just won't be able to do that

 

[Deleted member 2756]

Does gh and igf-1 rapidly age bone?

I'm thinking of taking mk 677 and huperzine a, for height, frame and muscle growth.

If I don't take an AI could I risk stunting my growth or rapidly increasing my bone age?

Would you recommend me taking mk 677 without an AI at 17?

I understand hgh is optimal but I'm not in the position the pay or use that right now.

Thanks in advance.

huperzine A has been found to not impact the cholinergic suppression of somatostatin, as would something like pyridostigmine or other acetylcholinesterase inhibitor classed drugs.

MK677 alone is weak and should be used in conjunction with a GHRH analog or 'receptor agonist', as MK677 has a longer half-life than most Growth hormone-secretagogue-receptor agonists using it with CJC-1295 (DAC) would work well for keeping serum GH elevated. I don't recommend MK677 at all as it interferes with the insulin/GH/IGF-1 axis, it will cause insulin resistance over time, and eventually diabetes if abused.

I'm going to bed, i'll give you some more information in the morning.

 

[Hopeful333]

huperzine A has been found to not impact the cholinergic suppression of somatostatin, as would something like pyridostigmine or other acetylcholinesterase inhibitor classed drugs.

MK677 alone is weak and should be used in conjunction with a GHRH analog or 'receptor agonist', as MK677 has a longer half-life than most Growth hormone-secretagogue-receptor agonists using it with CJC-1295 (DAC) would work well for keeping serum GH elevated. I don't recommend MK677 at all as it interferes with the insulin/GH/IGF-1 axis, it will cause insulin resistance over time, and eventually diabetes if abused.

I'm going to bed, i'll give you some more information in the morning.

Thanks

Thanks

would taking Berberine with mk 677 negate the insulin and blood sugar sides?

 

[Hopeful333]

huperzine A has been found to not impact the cholinergic suppression of somatostatin, as would something like pyridostigmine or other acetylcholinesterase inhibitor classed drugs.

MK677 alone is weak and should be used in conjunction with a GHRH analog or 'receptor agonist', as MK677 has a longer half-life than most Growth hormone-secretagogue-receptor agonists using it with CJC-1295 (DAC) would work well for keeping serum GH elevated. I don't recommend MK677 at all as it interferes with the insulin/GH/IGF-1 axis, it will cause insulin resistance over time, and eventually diabetes if abused.

I'm going to bed, i'll give you some more information in the morning.

Sorry about the spamming.

What do you think of this stack?

With this protocol, IGF-1 levels will exceed, or at least match a HIGH dose of pharma grade GH:

3333.33-5000mcg CJC-1295 DAC subQ inject before bed – Monday, Wednesday, Saturday (10,000-15,000mcg – 10-15mg total per week)

25mg MK-677 before bed every day

With this protocol, you can reach an IGF-1 level close to (or exceed) 700ng/mL.

 

[Alexanderr]

Alright, so, I just ordered everything I need. Lets hope this fucking works out.

 

[Chad69]

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 dont have the time to read....just tell me all the looksmaxes I can about hormones as a teen

 

[Hopeful333]

Alright, so, I just ordered everything I need. Lets hope this fucking works out.

Alright, so, I just ordered everything I need. Lets hope this fucking works out.

What did you order, where from and cost etc? Pm

 

[Alexanderr]

What did you order, where from and cost etc? Pm

All the shit he mentioned in the peptides method, some BAC water, syringes and some alcohol wipes.

 

[Budflog]

I’m 18 5’11 where tf do I buy this/what routine should I do

 

[Alexanderr]

I’m 18 5’11 where tf do I buy this/what routine should I do

Depends, can you afford HGH and IGF-1 LR3? If you can you should run method 2 tbh. If only HGH then method 1 and if you’re really poor then method 3 should be the way to go.
Of course since you’re 18, nothing is guaranteed (nothing ever is with heightmaxxing but you get my point), it depends on your pubertal timing and whether your growth plates have fused or not.
Being blatantly honest I think you might see some gains frame wise but not much height wise but I could be wrong, there’s always exceptions.

 

[Budflog]

Being blatantly honest I think you might see some gains frame wise but not much height wise but I could be wrong, there’s always exceptions.

Hey man thanks for the help. How would I gauge if this is a good investment? Like I understand that I might get no gains or I might get a lot, is there a good way to measure pubertal timing or bone age or whatever tf you should measure. If I was confident I could get an inch or more I’d be willing to drop up to a grand but if all I was gonna get was maybe frame then Idgaf.

 

[Alexanderr]

With this protocol, IGF-1 levels will exceed, or at least match a HIGH dose of pharma grade GH:

3333.33-5000mcg CJC-1295 DAC subQ inject before bed – Monday, Wednesday, Saturday (10,000-15,000mcg – 10-15mg total per week)

Something tells me pharma grade GH wouldn’t be as expensive as it is if you could just inject some peptides and get the same levels of IGF-1 as you would’ve with a high dose of pharma GH.

Hey man thanks for the help. How would I gauge if this is a good investment? Like I understand that I might get no gains or I might get a lot, is there a good way to measure pubertal timing or bone age or whatever tf you should measure. If I was confident I could get an inch or more I’d be willing to drop up to a grand but if all I was gonna get was maybe frame then Idgaf.

I suppose you could try this test out to see which tanner stage you’re on. Might help you gauge whether you still possible have some vertical growth left in you.

Tanner Stage Calculator for Boys: Growing Up in the Lord: A Study for Teenage Boys by Jeffrey W. Hamilton

growingupboys.info

It isn’t terribly accurate nor is it as accurate as what your doctor would tell you regarding your development so don’t rely on the test too much. It’s a decent way to figure out where you currently stand in puberty though. Another thing that might help you figure out whether his whole endeavor might be worth it is noting down whether you’ve experienced any growth recently (as in the last year, for example). If you have then you just might still be able to grow some more but if you’ve stopped growing vertically for several years I wouldn’t count on it. If you wanna be sure if you could still grow then get some x-ray’s done.

All heightmaxxers spend hundreds (if not thousands) of euros on shit that might not give them a single cm, all on the off chance they might grow several cm/inches in the end. Personally, I don’t want to look back a few years later regretting I didn’t do anything while I still potentially could.

 

[Deleted member 4946]

Does gh and igf-1 rapidly age bone?

I'm thinking of taking mk 677 and huperzine a, for height, frame and muscle growth.

If I don't take an AI could I risk stunting my growth or rapidly increasing my bone age?

Would you recommend me taking mk 677 without an AI at 17?

I understand hgh is optimal but I'm not in the position the pay or use that right now.

Thanks in advance.

androgens and estrogen is responsible for again the bone, mainly estrogen

Something tells me pharma grade GH wouldn’t be as expensive as it is if you could just inject some peptides and get the same levels of IGF-1 as you would’ve with a high dose of pharma GH.

I suppose you could try this test out to see which tanner stage you’re on. Might help you gauge whether you still possible have some vertical growth left in you.

Tanner Stage Calculator for Boys: Growing Up in the Lord: A Study for Teenage Boys by Jeffrey W. Hamilton

growingupboys.info

It isn’t terribly accurate nor is it as accurate as what your doctor would tell you regarding your development so don’t rely on the test too much. It’s a decent way to figure out where you currently stand in puberty though. Another thing that might help you figure out whether his whole endeavor might be worth it is noting down whether you’ve experienced any growth recently (as in the last year, for example). If you have then you just might still be able to grow some more but if you’ve stopped growing vertically for several years I wouldn’t count on it. If you wanna be sure if you could still grow then get some x-ray’s done.

All heightmaxxers spend hundreds (if not thousands) of euros on shit that might not give them a single cm, all on the off chance they might grow several cm/inches in the end. Personally, I don’t want to look back a few years later regretting I didn’t do anything while I still potentially could.

no heightmaxxer has actually taken a full stack like the ones i am recommending, the ones that did even one or two of them, like HGH and IGF-1 LR3 one guy on this forum grew 2cm in one month at age 18

 

[Hopeful333]

androgens and estrogen is responsible for again the bone, mainly estrogen

no heightmaxxer has actually taken a full stack like the ones i am recommending, the ones that did even one or two of them, like HGH and IGF-1 LR3 one guy on this forum grew 2cm in one month at age 18

Can you take an ai less regularly and not get as much sides.

 

[Deleted member 4946]

Can you take an ai less regularly and not get as much sides.

yeah
anyway, my hexarelin and ghrp-2 and mod-grf and aromasin are in my house right now well hidden from my parents, next I'm gonna buy igf-1 lr3 and then soon glucosamine, chondroitin,MSM and SAM-E, not starting anything yet until i get my anti-androgen (spironolactone) drug as well

 

[Hopeful333]

yeah
anyway, my hexarelin and ghrp-2 and mod-grf and aromasin are in my house right now well hidden from my parents, next I'm gonna buy igf-1 lr3 and then soon glucosamine, chondroitin,MSM and SAM-E, not starting anything yet until i get my anti-androgen (spironolactone) drug as well

Well done. How the fuck are you hiding this shit from parents. A secret mini fridge? How are you getting the money any tips?

 

[Deleted member 4946]

Well done. How the fuck are you hiding this shit from parents. A secret mini fridge? How are you getting the money any tips?

i am hiding it in my shoebox and dumping icecubes in the shit, I'm getting money by doing paper delivery. This is why 99.5 percent of teens wont heightmaxx, even if they acquire the knowledge and the will to inject themselves with drugs there are other problems like hiding it from parents and getting money for drugs in the first place which is why u don't see many people giving their results for heightmaxxing (teens in puberty of course), also stupid scare techniques for risk of death put most of them off from ever attempting heightmaxx

Also another thing to keep in mind, hexarelin doesn't work unless you are in puberty (for heightmaxx) or post-puberty (for other shit)

 

[Hopeful333]

i am hiding it in my shoebox and dumping icecubes in the shit, I'm getting money by doing paper delivery. This is why 99.5 percent of teens wont heightmaxx, even if they acquire the knowledge and the will to inject themselves with drugs there are other problems like hiding it from parents and getting money for drugs in the first place which is why u don't see many people giving their results for heightmaxxing (teens in puberty of course), also stupid scare techniques for risk of death put most of them off from ever attempting heightmaxx

Also another thing to keep in mind, hexarelin doesn't work unless you are in puberty (for heightmaxx) or post-puberty (for other shit)

Fair play, are you sure the shoebox filled with ice will work?

 

[BasedSpinelet257]

yeah
anyway, my hexarelin and ghrp-2 and mod-grf and aromasin are in my house right now well hidden from my parents, next I'm gonna buy igf-1 lr3 and then soon glucosamine, chondroitin,MSM and SAM-E, not starting anything yet until i get my anti-androgen (spironolactone) drug as well

Can you explain why you recommended 2000mg of Sam-e? Is that just a random number high dose?

 

[Deleted member 4946]

Can you explain why you recommended 2000mg of Sam-e? Is that just a random number high dose?

that is to keep your methylation going, anyway i will combine it with folinic acid and folic acid it's based off xcrunner's research
2000mg SAM-e (enteric tabs only)
800 ug folinic acid
800 ug folic acid

this increases DNA methylation, loss of this occurs with endochondral ossification of the growth plates, this will keep your body in a young state always, therefore constantly in growing state

Fair play, are you sure the shoebox filled with ice will work?

yes it'll work, i insulate it as well a bit just to the right temperature, once it is reconsituted in can last in there for a long time
People here fail to understand how important increasing DNA methylation is for the heightmaxxing stack, all these peptides and shit will exhaust your growth plate cells ability for proliferation because indirect evidence suggests that growth plate senescence occurs because stem-like cells in the growth plate resting zone have a finite proliferative capacity that is gradually exhausted, we can induce epigenetics like by taking things like SAM-E, folic acid and folinic acid: https://joe.bioscientifica.com/view/journals/joe/186/1/1860241.xml

Xcrunner tried this on 2 of his clients in his trials(ages 15 and 17), although they had inactive plates to begin with. He Gave them 2g of sam-e enteric coated tablet form plus about 500-800mcg folic acid and pure puerarin (basically weakened form of hexarelin)..today they are now both 21 and the 17 year old is now 23. The 23 year old is 6ft 3 and still growing!, he still has the same amount of facial hair since he was 17 and no hair on his legs still His plates never became inactive as a result, and the crazy thing is, his mum is 5ft 3 and dad 5ft 6. This suggests that increasing DNA methylation will make the body continue growing as it never gets physically older to realise it's time to stop increasing proliferation so fast, so this could be a way to physical anti-aging for puberty heightmaxxing

that is to keep your methylation going, anyway i will combine it with folinic acid and folic acid it's based off xcrunner's research
2000mg SAM-e (enteric tabs only)
800 ug folinic acid
800 ug folic acid

this increases DNA methylation, loss of this occurs with endochondral ossification of the growth plates, this will keep your body in a young state always, therefore constantly in growing state

yes it'll work, i insulate it as well a bit just to the right temperature, once it is reconsituted in can last in there for a long time
People here fail to understand how important increasing DNA methylation is for the heightmaxxing stack, all these peptides and shit will exhaust your growth plate cells ability for proliferation because indirect evidence suggests that growth plate senescence occurs because stem-like cells in the growth plate resting zone have a finite proliferative capacity that is gradually exhausted, we can induce epigenetics like by taking things like SAM-E, folic acid and folinic acid: https://joe.bioscientifica.com/view/journals/joe/186/1/1860241.xml

Xcrunner tried this on 2 of his clients in his trials(ages 15 and 17), although they had inactive plates to begin with. He Gave them 2g of sam-e enteric coated tablet form plus about 500-800mcg folic acid and pure puerarin (basically weakened form of hexarelin)..today they are now both 21 and the 17 year old is now 23. The 23 year old is 6ft 3 and still growing!, he still has the same amount of facial hair since he was 17 and no hair on his legs still His plates never became inactive as a result, and the crazy thing is, his mum is 5ft 3 and dad 5ft 6. This suggests that increasing DNA methylation will make the body continue growing as it never gets physically older to realise it's time to stop increasing proliferation so fast, so this could be a way to physical anti-aging for puberty heightmaxxing, glucoasmine and chondroitin can increase the amount of proliferative chondrocytes by like 2 fold and 4 fold for free proliferative chondrocytes, MSM induces mass osteoblast differentiation. It is true, taking all of this will have synergistic effect on the open growth plate

glucoasmine and chondroitin can increase the amount of proliferative chondrocytes by like 2 fold and 4 fold for free proliferative chondrocytes, MSM induces mass osteoblast differentiation. It is true, taking all of this will have synergistic effect on the open growth plates, don't just think all of this DNA methylation and chondroitin and stuff is just cope and all you need is just HGH, I am not saying you wont grow with just HGH as the numerous studies of kids with ISS treated with GH show otherwise, but this will improve final height by A LOT

 

[Deleted member 2756]

yeah
anyway, my hexarelin and ghrp-2 and mod-grf and aromasin are in my house right now well hidden from my parents, next I'm gonna buy igf-1 lr3 and then soon glucosamine, chondroitin,MSM and SAM-E, not starting anything yet until i get my anti-androgen (spironolactone) drug as well

add in an acetylcholinesterase inhibitor, the consumption of sugars (glucose) when absorbed by the GI tract potently upregulate somatostatin concentrations, therefore blunting the effects of GHRH (if there is an active GHRH signal attached to the GHRH-R). Somatostatin upregulation is what causes the glucose-related GH release suppression.

 

[Deleted member 4946]

add in an acetylcholinesterase inhibitor, the consumption of sugars (glucose) when absorbed by the GI tract potently upregulate somatostatin concentrations, therefore blunting the effects of GHRH (if there is an active GHRH signal attached to the GHRH-R). Somatostatin upregulation is what causes the glucose-related GH release suppression.

bro, there was a shit incident ,my GHRP-2 while I was taking off the cap, that metal thing around the sterile rubber stopper came off when I put the needle in to put my bac water in, I took out my needle and the rubber stopper came out as well. I put it back in. This peptide was exposed to oxygen for 5 seconds but it was reconstituted. Will this affect my peptide? Should I take it? Btw it was reconsituted no lyphophilized so it already had BAC water in there

 

[Deleted member 2756]

bro, there was a shit incident ,my GHRP-2 while I was in the taking of the cap, that metal thing around the sterile rubber stopper came off when I put the needle in to put my bac water in, I took it out and the rubber stopper came out as well. I put it back in. This peptide was exposed to oxygen for 5 seconds but it was reconstituted. Will this affect my peptide? Should I take it? Btw it was reconsituted no lyphophilized so it already had BAC water in there

yeah, it's fine, exposure to oxygen doesn't mean shit, the factories sell the powder by the KG in tight lock bags.

how much did you spend on GHRP-2? how many vials did you order?

 

[Deleted member 4946]

yeah, it's fine, exposure to oxygen doesn't mean shit, the factories sell the powder by the KG in tight lock bags.

how much did you spend on GHRP-2? how many vials did you order?

only one for now and it cost 55 aud

 

[Deleted member 4946]

yeah, it's fine, exposure to oxygen doesn't mean shit, the factories sell the powder by the KG in tight lock bags.

how much did you spend on GHRP-2? how many vials did you order?

use this resource as a guide: https://education.endocrine.org/system/files/ESAP 2015 Laboratory Reference Ranges.pdf

 

[BasedSpinelet257]

that is to keep your methylation going, anyway i will combine it with folinic acid and folic acid it's based off xcrunner's research
2000mg SAM-e (enteric tabs only)
800 ug folinic acid
800 ug folic acid

this increases DNA methylation, loss of this occurs with endochondral ossification of the growth plates, this will keep your body in a young state always, therefore constantly in growing state

yes it'll work, i insulate it as well a bit just to the right temperature, once it is reconsituted in can last in there for a long time
People here fail to understand how important increasing DNA methylation is for the heightmaxxing stack, all these peptides and shit will exhaust your growth plate cells ability for proliferation because indirect evidence suggests that growth plate senescence occurs because stem-like cells in the growth plate resting zone have a finite proliferative capacity that is gradually exhausted, we can induce epigenetics like by taking things like SAM-E, folic acid and folinic acid: https://joe.bioscientifica.com/view/journals/joe/186/1/1860241.xml

Xcrunner tried this on 2 of his clients in his trials(ages 15 and 17), although they had inactive plates to begin with. He Gave them 2g of sam-e enteric coated tablet form plus about 500-800mcg folic acid and pure puerarin (basically weakened form of hexarelin)..today they are now both 21 and the 17 year old is now 23. The 23 year old is 6ft 3 and still growing!, he still has the same amount of facial hair since he was 17 and no hair on his legs still His plates never became inactive as a result, and the crazy thing is, his mum is 5ft 3 and dad 5ft 6. This suggests that increasing DNA methylation will make the body continue growing as it never gets physically older to realise it's time to stop increasing proliferation so fast, so this could be a way to physical anti-aging for puberty heightmaxxing

glucoasmine and chondroitin can increase the amount of proliferative chondrocytes by like 2 fold and 4 fold for free proliferative chondrocytes, MSM induces mass osteoblast differentiation. It is true, taking all of this will have synergistic effect on the open growth plates, don't just think all of this DNA methylation and chondroitin and stuff is just cope and all you need is just HGH, I am not saying you wont grow with just HGH as the numerous studies of kids with ISS treated with GH show otherwise, but this will improve final height by A LOT

Excellent response. By inactive growth plates, did he specify whether they were completely ossified or just very close to it?Going along with that, does it matter that you take high dose SAM before growth plate closure to ensure that they remain open or is it equally effective on closed plates? Thanks again.

 

[Deleted member 4946]

Excellent response. By inactive growth plates, did he specify whether they were completely ossified or just very close to it?Going along with that, does it matter that you take high dose SAM before growth plate closure to ensure that they remain open or is it equally effective on closed plates? Thanks again.

SAM-E and MSM in some of his trials were able to make the inactive plate people grow, why? Because of articular cartilage. Inactive growth plate means they can't grow anymore unless the pubertal hormone and protein environment is made again, this can be done with the chemicals. Anyway high dose sam-e before growth plate closure is better than after, i don't know how long it'll last but take it folinic acid, folic acid and SAM-E your plates will remain open almost forever

 

[BasedSpinelet257]

Ve

SAM-E and MSM in some of his trials were able to make the inactive plate people grow, why? Because of articular cartilage. Inactive growth plate means they can't grow anymore unless the pubertal hormone and protein environment is made again, this can be done with the chemicals. Anyway high dose sam-e before growth plate closure is better than after, i don't know how long it'll last but take it folinic acid, folic acid and SAM-E your plates will remain open almost forever

Very helpful replies. Thanks. Do you by chance have the links to these studies/anecdotes?

 

[Deleted member 4946]

@Dyorotic2 I found more inhibitors for chondrocyte response to IGF-1: https://www.ncbi.nlm.nih.gov/pubmed/11003576

Nitric oxide inhibits chondrocyte response to IGF-I: inhibition of IGF-IRbeta tyrosine phosphorylation - PubMed

Chondrocytes in arthritic cartilage respond poorly to insulin-like growth factor I (IGF-I). Studies with inducible nitric oxide synthase (iNOS) knockout mice suggest that NO is responsible for part of the cartilage insensitivity to IGF-I. These studies characterize the relationship between NO...

www.ncbi.nlm.nih.gov

Inhibition of transforming growth factor beta production by nitric oxide-treated chondrocytes: implications for matrix synthesis - PubMed

NO can modulate proteoglycan synthesis indirectly by decreasing the production of TGFbeta1 by chondrocytes exposed to IL-1beta. It prevents autocrine-stimulated increases in TGFbeta1, thus potentially diminishing the anabolic effects of this cytokine in chondrocytes.

www.ncbi.nlm.nih.gov

Nitric oxide decreases IGF-1 receptor function in vitro; glutathione depletion enhances this effect in vivo - PubMed

Insulin-like growth factor-1 (IGF) helps maintain healthy articular cartilage; however, arthritic cartilage becomes less responsive to the anabolic actions of IGF. We previously showed that high concentrations of nitric oxide (NO) decrease IGF receptor tyrosine phosphorylation and response to...

www.ncbi.nlm.nih.gov

Nitric Oxide is anti chondrogenic

Ve


Very helpful replies. Thanks. Do you by chance have the links to these studies/anecdotes?

http://www.heightquest.com/2010/09/increase-your-height-with-s-adenosyl.html It is theory right now, but xcrunner has done it and seen the results of it first hand in his word document on how to grow taller as teen he describes all that.

Also, a reason, why growth hormone fails in some people, is because of the bodies mechanisms maintain homeostasis by lowering endogenous growth hormone levels. These attempts can be less or more extreme in different people depending on how restrictive your genetics are

 

[Alexanderr]

i am hiding it in my shoebox and dumping icecubes in the shit, I'm getting money by doing paper delivery. This is why 99.5 percent of teens wont heightmaxx, even if they acquire the knowledge and the will to inject themselves with drugs there are other problems like hiding it from parents and getting money for drugs in the first place which is why u don't see many people giving their results for heightmaxxing (teens in puberty of course), also stupid scare techniques for risk of death put most of them off from ever attempting heightmaxx

I’m putting my shit in our family fridge, a mini fridge was too expensive and would require me to wait until my next paycheck which I have no time for, I made sure to buy a little box with a lock though (in which I can keep my vials), so they can’t see what’s inside or open it.