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

[Deleted member 4946]

Very intriguing, I did not know you got that dosage from xcrunner. I've been skimming through old heightmaxing forums looking for people who had this stack or a similar one blow up in their face, but have not found one. Have you found anything pertaining to failed heightmaxing that consequentially lead to further health issues? The whole thought of hypermethylation does intimadte me, a kid at my school had cancer and it was really sad to see how it just completely broke him.

lol, the only side effects i am getting is more acne, red spots thanks to hormonal increases, feel younger and my stomach pains sometimes, fell like Diarrhoea lmfao as well as growth pains

 

[Deleted member 1849]

lol, the only side effects i am getting is more acne, red spots thanks to hormonal increases, feel younger and my stomach pains sometimes, fell like Diarrhoea lmfao as well as growth pains

6"3 gang im coming for you

 

[Deleted member 4946]

Very intriguing, I did not know you got that dosage from xcrunner. I've been skimming through old heightmaxing forums looking for people who had this stack or a similar one blow up in their face, but have not found one. Have you found anything pertaining to failed heightmaxing that consequentially lead to further health issues? The whole thought of hypermethylation does intimadte me, a kid at my school had cancer and it was really sad to see how it just completely broke him.

also yes, there was a man named Jacob walker who injected methylprotodioscin which increases CNP into his leg, he developed severe tendonitis and he couldn't walk literally had to crawl to acupuncture... They treated him but now he is fucked for life because when he walks or sprints he feels pain in his knees whenever he sprints or walks (this man quit heightmaxxing and went on with his life), however meclizine I'm sure won't do this because all it does is inhibit FGFR3 signalling and it has been tested for it's safety.

 

[Deleted member 1849]

also yes, there was a man named Jacob walker who injected methylprotodioscin which increases CNP into his leg, he developed severe tendonitis and he couldn't walk literally had to crawl to acupuncture... They treated him but now he is fucked for life because when he walks or sprints he feels pain in his knees whenever he sprints or walks (this man quit heightmaxxing and went on with his life), however meclizine I'm sure won't do this because all it does is inhibit FGFR3 signalling and it has been tested for it's safety.

melclozine is completely safe. Used with kids too, there may be sides but at least there are no serious health sides or death tbh. it has been studied for years.

 

[Deleted member 4946]

melclozine is completely safe. Used with kids too, there may be sides but at least there are no serious health sides or death tbh. it has been studied for years.

yes btw he did get that methylprotodioscin off Alibaba, so that may say something

 

[Deleted member 3635]

yeah it's not enough to crash E,

my homemade gel has a higher concentration of DHT, i overdid it an crashed e.

Take pregnolone and it shouldn't crash

 

[RecessedPrettyboy]

Told this to my parents and now my mom wants me to explain this to a doctor to see if he approves
Theres no way a doctor would approve of this right?

 

[TheEndHasNoEnd]

Told this to my parents and now my mom wants me to explain this to a doctor to see if he approves
Theres no way a doctor would approve of this right?

no, this shit is kept secret for a reason. theres a reason why doctors charge thousands for hgh which is less effective rather than this much cheaper stack. get a job and buy it yourself. why the fuck would you tell your parents about this lmao, good luck ascending now that they know jfl.

 

[RecessedPrettyboy]

no, this shit is kept secret for a reason. theres a reason why doctors charge thousands for hgh which is less effective rather than this much cheaper stack. get a job and buy it yourself.

I turned 18 one month ago there is no time for a job
I just have to convince my parents I guess

 

[TheEndHasNoEnd]

I turned 18 one month ago there is no time for a job
I just have to convince my parents I guess

im 18 too and theres certainly plenty of time to get a job (once corona ends). u cant convince ur parents with this, this sort of info is kept for like nba players to get artificially insane growth spurts. if u explain this to a doctor the doctor will say youll get acromegaly (even though there is no risk of it with the follic acid and shit) and there goes ur path to ascension. pharma is fucking dirty man, why would they lose so much money when they can simply overcharge hgh alone which will do much less changes? btw are u talking about poseidons stack or something else

 

[BasedSpinelet257]

S-adenosylmethionine blocks osteosarcoma cells proliferation and invasion in vitro and tumor metastasis in vivo: therapeutic and diagnostic clinical applications - PubMed

Osteosarcoma (OS) is an aggressive and highly metastatic form of primary bone cancer affecting young children and adults. Previous studies have shown that hypomethylation of critical genes is driving metastasis. Here, we examine whether hypermethylation treatment can block OS growth and...

www.ncbi.nlm.nih.gov

"Real-time polymerase chain reaction (qPCR) analysis confirmed that SAM treatment blocked the expression of several prometastatic genes and additional genes identified by EWAS analysis. Immunohistochemical analysis of normal human bone and tissue array from OS patients showed significantly high levels of expression of one of the identified gene platelet-derived growth factor alpha (PDGFA). These studies provide a possible mechanism for the role of DNA demethylation in the development and metastasis of OS to provide a rationale for the use of hypermethylation therapy for OS patients and identify new targets for monitoring OS development and progression."

Potential role of S-adenosylmethionine in osteosarcoma development

''The role of methylation especially in the promoter region was thought to repress gene expression based on the specific cell type15 and in some cases methylation-mediated gene expression, but still the more precise role of methylation in gene expression remains unclear. Similarly, there is no report that associates SAM with osteosarcoma stem cells."

"As evidence of tumor suppression, the SAM-treated mouse tissue was analyzed histologically, which exemplifies the control that SAM has over abnormal cell proliferation, especially on primary osteosarcoma, but it lacks positive effects on metastatic osteosarcoma. At the molecular level, the successful inhibition of primary osteosarcoma was found to be associated with a lower expression of Sox2, a protein highly expressed in osteosarcoma stem cells, along with an upregulated expression of TCTP. The data suggest that the administration of SAM has a positive role in treating primary osteosarcoma, but it has no role in suppressing metastatic osteosarcoma. "

I read another paper that was explaining that the way SAM prevents the spread of cancer is my upregulating and downregulating genes in cancer cells so that they more closely resemble normal cells and in this way metastasis is prevented, but the paper above seems to say that the exact mechanism is not clear. Also thought it was interesting that SAM could prevent primary osteosarcoma (tumors), but had no effect on ones that had already metastasized.

TL;DR I'm not sure how much of a risk SAM itself is in causing cancer. The pi3k pathway induction by Hexarelin is more concerning, but the fact that it's been used in human trials relatively safely makes me scratch my head.

 

[Tom2004]

S-adenosylmethionine blocks osteosarcoma cells proliferation and invasion in vitro and tumor metastasis in vivo: therapeutic and diagnostic clinical applications - PubMed

Osteosarcoma (OS) is an aggressive and highly metastatic form of primary bone cancer affecting young children and adults. Previous studies have shown that hypomethylation of critical genes is driving metastasis. Here, we examine whether hypermethylation treatment can block OS growth and...

www.ncbi.nlm.nih.gov

"Real-time polymerase chain reaction (qPCR) analysis confirmed that SAM treatment blocked the expression of several prometastatic genes and additional genes identified by EWAS analysis. Immunohistochemical analysis of normal human bone and tissue array from OS patients showed significantly high levels of expression of one of the identified gene platelet-derived growth factor alpha (PDGFA). These studies provide a possible mechanism for the role of DNA demethylation in the development and metastasis of OS to provide a rationale for the use of hypermethylation therapy for OS patients and identify new targets for monitoring OS development and progression."

Potential role of S-adenosylmethionine in osteosarcoma development

''The role of methylation especially in the promoter region was thought to repress gene expression based on the specific cell type15 and in some cases methylation-mediated gene expression, but still the more precise role of methylation in gene expression remains unclear. Similarly, there is no report that associates SAM with osteosarcoma stem cells."

"As evidence of tumor suppression, the SAM-treated mouse tissue was analyzed histologically, which exemplifies the control that SAM has over abnormal cell proliferation, especially on primary osteosarcoma, but it lacks positive effects on metastatic osteosarcoma. At the molecular level, the successful inhibition of primary osteosarcoma was found to be associated with a lower expression of Sox2, a protein highly expressed in osteosarcoma stem cells, along with an upregulated expression of TCTP. The data suggest that the administration of SAM has a positive role in treating primary osteosarcoma, but it has no role in suppressing metastatic osteosarcoma. "

I read another paper that was explaining that the way SAM prevents the spread of cancer is my upregulating and downregulating genes in cancer cells so that they more closely resemble normal cells and in this way metastasis is prevented, but the paper above seems to say that the exact mechanism is not clear. Also thought it was interesting that SAM could prevent primary osteosarcoma (tumors), but had no effect on ones that had already metastasized.

TL;DR I'm not sure how much of a risk SAM itself is in causing cancer. The pi3k pathway induction by Hexarelin is more concerning, but the fact that it's been used in human trials relatively safely makes me scratch my head.

Cancer is risk i’m willing to take for even 2” of height

 

[BasedSpinelet257]

Cancer is risk i’m willing to take for even 2” of height

I feel that tbh.

 

[Lev Peshkov]

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

​

This is amazing. Just gotta ask. If I do the GH peptides will it make my face significantly different? I wouldn't want that becuase as Is I am allowed to get lefort 2 + bsso etc. And I want to get gigachad implants too, would this disqualify me from getting these or are face changes minimal if your over 15 I'm 16 lol

 

[Deleted member 4946]

S-adenosylmethionine blocks osteosarcoma cells proliferation and invasion in vitro and tumor metastasis in vivo: therapeutic and diagnostic clinical applications - PubMed

Osteosarcoma (OS) is an aggressive and highly metastatic form of primary bone cancer affecting young children and adults. Previous studies have shown that hypomethylation of critical genes is driving metastasis. Here, we examine whether hypermethylation treatment can block OS growth and...

www.ncbi.nlm.nih.gov

"Real-time polymerase chain reaction (qPCR) analysis confirmed that SAM treatment blocked the expression of several prometastatic genes and additional genes identified by EWAS analysis. Immunohistochemical analysis of normal human bone and tissue array from OS patients showed significantly high levels of expression of one of the identified gene platelet-derived growth factor alpha (PDGFA). These studies provide a possible mechanism for the role of DNA demethylation in the development and metastasis of OS to provide a rationale for the use of hypermethylation therapy for OS patients and identify new targets for monitoring OS development and progression."

Potential role of S-adenosylmethionine in osteosarcoma development

''The role of methylation especially in the promoter region was thought to repress gene expression based on the specific cell type15 and in some cases methylation-mediated gene expression, but still the more precise role of methylation in gene expression remains unclear. Similarly, there is no report that associates SAM with osteosarcoma stem cells."

"As evidence of tumor suppression, the SAM-treated mouse tissue was analyzed histologically, which exemplifies the control that SAM has over abnormal cell proliferation, especially on primary osteosarcoma, but it lacks positive effects on metastatic osteosarcoma. At the molecular level, the successful inhibition of primary osteosarcoma was found to be associated with a lower expression of Sox2, a protein highly expressed in osteosarcoma stem cells, along with an upregulated expression of TCTP. The data suggest that the administration of SAM has a positive role in treating primary osteosarcoma, but it has no role in suppressing metastatic osteosarcoma. "

I read another paper that was explaining that the way SAM prevents the spread of cancer is my upregulating and downregulating genes in cancer cells so that they more closely resemble normal cells and in this way metastasis is prevented, but the paper above seems to say that the exact mechanism is not clear. Also thought it was interesting that SAM could prevent primary osteosarcoma (tumors), but had no effect on ones that had already metastasized.

TL;DR I'm not sure how much of a risk SAM itself is in causing cancer. The pi3k pathway induction by Hexarelin is more concerning, but the fact that it's been used in human trials relatively safely makes me scratch my head.

https://www.sciencedirect.com/science/article/pii/B9780123808660600022?via=ihub

https://molecular-cancer.biomedcentral.com/articles/10.1186/s12943-019-0954-x

DNA Methylation: An Alternative Pathway to Cancer

To provide an introduction to the concept of DNA methylation and its function in normal cells, and to explain the possible mechanisms as to how abnormalities in this phenomenon can relate to carcinogenesis. The clinical implications with reference to ...

www.ncbi.nlm.nih.gov

 

[BasedSpinelet257]

https://www.sciencedirect.com/science/article/pii/B9780123808660600022?via=ihub

https://molecular-cancer.biomedcentral.com/articles/10.1186/s12943-019-0954-x

DNA Methylation: An Alternative Pathway to Cancer

To provide an introduction to the concept of DNA methylation and its function in normal cells, and to explain the possible mechanisms as to how abnormalities in this phenomenon can relate to carcinogenesis. The clinical implications with reference to ...

www.ncbi.nlm.nih.gov

Not at all denying that DNA methylation CAN lead to cancer, but I’m not convinced that all methylation is equal. For example, hypermethylation based on certain genetic factors or poor lifestyle choices likely doesn’t have the exact same effect on DNA methylation in terms of what is upregulated or down regulated as does supplementation SAM-e alone.

I realize that it is hypermethylating and also hypomethylation gets certain genes, but it seems a bit more selective than having certain genes hypomethylated because a person is smoking all the time.

 

[Deleted member 4946]

Not at all denying that DNA methylation CAN lead to cancer, but I’m not convinced that all methylation is equal. For example, hypermethylation based on certain genetic factors or poor lifestyle choices likely doesn’t have the exact same effect on DNA methylation in terms of what is upregulated or down regulated as does supplementation SAM-e alone.

I realize that it is hypermethylating and also hypomethylation gets certain genes, but it seems a bit more selective than having certain genes hypomethylated because a person is smoking all the time.

yes the association between hypomethylation and growth plate senescence has been associated already as well as it maintaining chondrocyte phenotype, I finally got folic acid today, also I found out my wingspan is almost 6'2 while my height is 5'10 what does that mean for me? I get wingspan can be a bit more or less than height but almost 4 inches! Man...

 

[BasedSpinelet257]

yes the association between hypomethylation and growth plate senescence has been associated already as well as it maintaining chondrocyte phenotype, I finally got folic acid today, also I found out my wingspan is almost 6'2 while my height is 5'10 what does that mean for me? I get wingspan can be a bit more or less than height but almost 4 inches! Man...

Ascension is near.

 

[John McCormick]

May I have everyone's attention please!

Strike, if your wingspan is 6'2" and your height right now is 5'10", then that means your potential height would be 6'2". The reason why you did not reach your potential height of 6'2" is perhaps you have had poor posture, poor diet, masturbated too much, didn't sleep early, ate junk food, etc.

If you lived healthy lifestyle without (too much weight lifting) or jerking off too much or hurting your growth plate when you were young then you could have reached 6'2" easily and earlier without much hassle.

My wingspan is 6'0" and I'm only 5'9" and I jacked off when I was young. I jerked off like there was no tomorrow and I practice riding a bike at early age and hurt my knee and back a lot. Growth potential stunted that way and I used to jump from top roof and playgrounds with other kids to try to see who can jump high and this retarded actions stunted my growth development.

 

[Bruh567]

May I have everyone's attention please!

Strike, if your wingspan is 6'2" and your height right now is 5'10", then that means your potential height would be 6'2". The reason why you did not reach your potential height of 6'2" is perhaps you have had poor posture, poor diet, masturbated too much, didn't sleep early, ate junk food, etc.

If you lived healthy lifestyle without (too much weight lifting) or jerking off too much or hurting your growth plate when you were young then you could have reached 6'2" easily and earlier without much hassle.

My wingspan is 6'0" and I'm only 5'9" and I jacked off when I was young. I jerked off like there was no tomorrow and I practice riding a bike at early age and hurt my knee and back a lot. Growth potential stunted that way and I used to jump from top roof and playgrounds with other kids to try to see who can jump high and this retarded actions stunted my growth development.

Since when did frame have to do with height? JFL

 

[John McCormick]

Since when did frame have to do with height? JFL

May I have your attention please?

Wingspan should equal to height. That is normal proportion as defined by Da Vinci. It's a human form. If one is off then there is something wrong you did.

 

[Bromose]

May I have your attention please?

Wingspan should equal to height. That is normal proportion as defined by Da Vinci. It's a human form. If one is off then there is something wrong you did.

It’s suppose to be more than your fuking height, on average 2-3 inches more , higher wingspan = more broad shoulders and longer arms = higher fighting success = more alpha. Wingspan similar to height is a beta cuck trait and makes you look sht.
Swallow the reach pill

 

[Bruh567]

May I have your attention please?

Wingspan should equal to height. That is normal proportion as defined by Da Vinci. It's a human form. If one is off then there is something wrong you did.

Da Vinci did t have anything to prove shot most of is “invention” aren’t real. Just look at all tall basket ball players. Height and frame are totally seperate

 

[416_Wavy]

yeah i guess you can gain in those areas, but longitudinal bone growth especially growing beyond your restrictive genes like gigantism people do, NEEDS hypermethylation remember epigenetics don't change anything in your genes, it can just change which genes at specific sites or all over global hypermethylation are expressed

what is more of a softer stack I want an affordable stack with minimal side effects and maximize the benefits I don't want to take a lot of supplements

no you don't need to run Hex consistently, im sure u can take it constantly for 2 weeks and then wait for just one week, addition of methyl groups doesn't inhibit tolerance

https://www.ebay.com/itm/162097709959 it's really quite cheap for the amount u can buy.

yeah ik it is super expensive but it still less than what you spend on peptides and HGH is it not? Especially if you buy off this: https://au.iherb.com/pr/Lake-Avenue-Nutrition-SAMe-S-Adenosyl-L-Methionine-400-mg-60-Tablets/96277
If u buy off here you would pay 113 AUD for 24 day supply of running 2g SAM-e ENTERIC COATED TABLET, every day. But you guys can spend more than double that for 500 IU of GH lmfao also if u take it eod for a 24 day supply it would cost you 56.5 AUD, if you can't even be bothered to spend that much but able to spend like 300 dollars for HGH just don't bother heightmaxxing, you will waste your money.

There is no lowest dose u can take eod to see results even taking 2g eod won't give u as good results as taking it every day, if u can't afford taking it every day then i said take 2g eod but you won't have good results, if you are thinking of compromising on even 2g eod then just don't heightmaxx then. You guys can spend hundreds of dollars on GH making you grow to your genetic potential faster but you can't spend it on what will keep you growing beyond your genetic potential smh...

can you explain to me how SAMe is related to DNA methylation and height maxing with links to studies and a safer dosage with some increase in height?

 

[Deleted member 4053]

what is more of a softer stack I want an affordable stack with minimal side effects and maximize the benefits I don't want to take a lot of supplements

Do you want results or not? There is no magical stack without side effects, and it is already relatively affordable. You have to make sacrifices, and if taking too many supplements concerns you, then this is not something you want.

 

[Bruh567]

what is more of a softer stack I want an affordable stack with minimal side effects and maximize the benefits I don't want to take a lot of supplements

can you explain to me how SAMe is related to DNA methylation and height maxing with links to studies and a safer dosage with some increase in height?

Higher Risk=Higher Reward tale as old as time

 

[416_Wavy]

Can someone send me a link or the forum strike used that shows SAMe is related to DNA methylation and height maxing

 

[Deleted member 4053]

Can someone send me a link or the forum strike used that shows SAMe is related to DNA methylation and height maxing

Here you go buddy boyo
https://web.archive.org/web/2010102...FFICIAL-THREAD-(info-on-1st-page)-t-8822.html

 

[Deleted member 4946]

Time to achieve the higher sample size straight at the naturalheightgrowth.com site

 

[MentalistKebab]

no you don't need to run Hex consistently, im sure u can take it constantly for 2 weeks and then wait for just one week, addition of methyl groups doesn't inhibit tolerance

https://www.ebay.com/itm/162097709959 it's really quite cheap for the amount u can buy.

yeah ik it is super expensive but it still less than what you spend on peptides and HGH is it not? Especially if you buy off this: https://au.iherb.com/pr/Lake-Avenue-Nutrition-SAMe-S-Adenosyl-L-Methionine-400-mg-60-Tablets/96277
If u buy off here you would pay 113 AUD for 24 day supply of running 2g SAM-e ENTERIC COATED TABLET, every day. But you guys can spend more than double that for 500 IU of GH lmfao also if u take it eod for a 24 day supply it would cost you 56.5 AUD, if you can't even be bothered to spend that much but able to spend like 300 dollars for HGH just don't bother heightmaxxing, you will waste your money.

There is no lowest dose u can take eod to see results even taking 2g eod won't give u as good results as taking it every day, if u can't afford taking it every day then i said take 2g eod but you won't have good results, if you are thinking of compromising on even 2g eod then just don't heightmaxx then. You guys can spend hundreds of dollars on GH making you grow to your genetic potential faster but you can't spend it on what will keep you growing beyond your genetic potential smh...

Bro I dont get why you think people here even have the money for pharma grade HGH ?

So many heightmaxxer who use the classic method (HGH +AI) are trying to replicate HGH with mk 677 and/or peptides because they dont have so much money.

 

[Deleted member 4946]

Bro I dont get why you think people here even have the money for pharma grade HGH ?

So many heightmaxxer who use the classic method (HGH +AI) are trying to replicate HGH with mk 677 and/or peptides because they dont have so much money.

pubertymaxxer spent a lot of money, seriously STOP complaining about the cost it only cost like 300 bucks a month

 

[Madness]

pubertymaxxer spent a lot of money, seriously STOP complaining about the cost it only cost like 300 bucks a month

It’s not about the cost, obtaining Pharma grade hgh is ridiculously hard.

 

[Deleted member 1560]

Cardiovascular impact of GH deficiency and of acromegaly. ... Moreover, GH excess and/or deficiency have been shown to include in their advanced clinical manifestations almost always an impaired cardiac function, which may reduce life expectancy

No thanks, I love my life

 

[Deleted member 4946]

It’s not about the cost, obtaining Pharma grade hgh is ridiculously hard.

im not talking about obtaining pharma HGH

 

[MentalistKebab]

pubertymaxxer spent a lot of money, seriously STOP complaining about the cost it only cost like 300 bucks a month

First of all even if I had the money pubertymaxxers have I would still follow peptide version to increase hgh, there is no reason to overspend.

Secondly in where I live, with 300 bucks a month I can see a prostitute 8 times a month and have still money left. Which makes all the heightmaxxing journey pointless here.

I guess I will cope with folic acid for a while until I win the lottery.

 

[Deleted member 4946]

First of all even if I had the money pubertymaxxers have I would still follow peptide version to increase hgh, there is no reason to overspend.

Secondly in where I live, with 300 bucks a month I can see a prostitute 8 times a month and have still money left. Which makes all the heightmaxxing journey pointless here.

I guess I will cope with folic acid for a while until I win the lottery.

ok keep coping

 

[Chad69]

ok keep coping

Man Iam really scared of the tumor
Yeah I know that you need to stick with right dosages to avoid that...also my frame wouldn’t change right?

 

[Deleted member 4946]

Man Iam really scared of the tumor
Yeah I know that you need to stick with right dosages to avoid that...also my frame wouldn’t change right?

it may change, i do not know about that bro, reversing your growth plate age has already been shown to slow down overall biological aging significantly so i dont know what else it can reverse

 

[Chad69]

it may change, i do not know about that bro, reversing your growth plate age has already been shown to slow down overall biological aging significantly so i dont know what else it can reverse

So if you take it in a long run you will basically stay younger and you won’t age at all?

 

[Deleted member 4946]

So if you take it in a long run you will basically stay younger and you won’t age at all?

no you will age but you will age very slow compare to regular people

 

[Chad69]

no you will age but you will age very slow compare to regular people

Amazing ngl
How did you even found this?
I dont trust xcrunner
He made few scamms in before claiming to gain few inches in a week for large amounts of money

 

[Deleted member 4946]

Credits to @JohnRea for bringing this to my attention in addition to hypermethylation the growth plate area there is more evidence combined with the articles, clinical trials, and anecdotes of hypermethylation resulting in height growth beyond genetic potential

Take a look at this: https://www.mcgill.ca/newsroom/chan...unk-ants-how-environment-controls-size-243448 and https://www.whatisepigenetics.com/d...nces-continuous-variation-in-ant-worker-size/

Mainly hypermethylation specifically the EGFr gene which encodes for the epidermal growth factor receptor

"It's a discovery that completely changes our understanding of how human variation comes to be," said one of the lead researchers, professor Ehab Abouheif of the McGill University.

Many human traits, whether they are intelligence, height, or vulnerability to diseases such as cancer, exist along a continuum.

A McGill University team led by professors Moshe Szyf and Ehab Abouheif arrived at this conclusion by conducting epigenetic experiments on Florida carpenter ants.

"By increasing the degree of DNA methylation of a gene called Egfr - gene involved in controlling growth - they were able to create a spectrum of ants of different sizes. Methylation is a biochemical process that controls the expression of certain genes. Essentially, the researchers found that the more methylated the gene, the larger the size of the ants.

"By modifying the methylation of one particular gene, that affects others, in this case the Egfr gene, we could affect all the other genes involved in cellular growth," said study co-author Sebastian Alvarado from the McGill. "We were working with ants, but it was a bit like discovering that we could create shorter or taller human beings," Alvarado said.

The findings were published today in Nature Communications."

No need to modify the methylation for one specific gene, all over hypermethylation will reverse your growth plate senescence either way and upregulate many different genes for height growth.

Combine this with examples of DMNT3A overgrowth syndrome, weaver syndrome and sotos syndrome, it seems all cases like this with some form of hypermethylation resulted in tall stature.

Amazing ngl
How did you even found this?
I dont trust xcrunner
He made few scamms in before claiming to gain few inches in a week for large amounts of money

im not even going to respond to that bullshit

 

[Traxanas]

Credits to @JohnRea for bringing this to my attention in addition to hypermethylation the growth plate area there is more evidence combined with the articles, clinical trials, and anecdotes of hypermethylation resulting in height growth beyond genetic potential

Take a look at this: https://www.mcgill.ca/newsroom/chan...unk-ants-how-environment-controls-size-243448 and https://www.whatisepigenetics.com/d...nces-continuous-variation-in-ant-worker-size/

Mainly hypermethylation specifically the EGFr gene which encodes for the epidermal growth factor receptor

"It's a discovery that completely changes our understanding of how human variation comes to be," said one of the lead researchers, professor Ehab Abouheif of the McGill University.

Many human traits, whether they are intelligence, height, or vulnerability to diseases such as cancer, exist along a continuum.

A McGill University team led by professors Moshe Szyf and Ehab Abouheif arrived at this conclusion by conducting epigenetic experiments on Florida carpenter ants.

"By increasing the degree of DNA methylation of a gene called Egfr - gene involved in controlling growth - they were able to create a spectrum of ants of different sizes. Methylation is a biochemical process that controls the expression of certain genes. Essentially, the researchers found that the more methylated the gene, the larger the size of the ants.

"By modifying the methylation of one particular gene, that affects others, in this case the Egfr gene, we could affect all the other genes involved in cellular growth," said study co-author Sebastian Alvarado from the McGill. "We were working with ants, but it was a bit like discovering that we could create shorter or taller human beings," Alvarado said.

The findings were published today in Nature Communications."

No need to modify the methylation for one specific gene, all over hypermethylation will reverse your growth plate senescence either way and upregulate many different genes for height growth.

Combine this with examples of DMNT3A overgrowth syndrome, weaver syndrome and sotos syndrome, it seems all cases like this with some form of hypermethylation resulted in tall stature.

im not even going to respond to that bullshit

No need to modify the methylation for one specific gene, all over hypermethylation will reverse your growth plate senescence either way and upregulate many different genes for height growth.

That's nice to hear since targeting a specific gene seems impossible naturally JFL + humans don't only have 1 gene or so that determines size.

Overall, the more methylated the growth-related gene, the larger the ants were.

I've read the article before but this other one I haven't and it dives deeper into it mentioning DNA methylation, that is indeed lifefuel.

Anyway, they should further research with mammals instead like rats that are more close to humans. I feel like that would be even better. Although what I want to know is if this can truly apply to humans this easily with over-the-counter pills as I don't think they're that reliable in specifically inducing hypermethylation, inducing it seems like no joke hence my skepticism which makes me question whether if 2g of SAM-E is enough, the highest dosage recommendation is 1600mg. At the same time drugs like panadol require no prescription yet when overdosed can be fatal and is still available for purchase, they don't give a shit so I guess why would they with methylation.

Maybe asking someone legit that knows more about this stuff can help us. I remember you saying your dad is a biochemist, what are his thoughts?

 

[Deleted member 4946]

That's nice to hear since targeting a specific gene seems impossible naturally JFL + humans don't only have 1 gene or so that determines size.


I've read the article before but this other one I haven't and it dives deeper into it mentioning DNA methylation, that is indeed lifefuel.

Anyway, they should further research with mammals instead like rats that are more close to humans. I feel like that would be even better. Although what I want to know is if this can truly apply to humans this easily with over-the-counter pills as I don't think they're that reliable in specifically inducing hypermethylation, inducing it seems like no joke hence my skepticism which makes me question whether if 2g of SAM-E is enough, the highest dosage recommendation is 1600mg. At the same time drugs like panadol require no prescription yet when overdosed can be fatal and is still available for purchase, they don't give a shit so I guess why would they with methylation.

Maybe asking someone legit that knows more about this stuff can help us. I remember you saying your dad is a biochemist, what are his thoughts?

he was an ex biochemist he agress that taking higher doses of methionine and folate will force more methyl groups to be added to all parts of the body, it can't be excreted until the full methylation process is over so yes he agrees that sam-e folic acid and folinic acid at those dosages work

 

[RAITEIII]

he was an ex biochemist he agress that taking higher doses of methionine and folate will force more methyl groups to be added to all parts of the body, it can't be excreted until the full methylation process is over so yes he agrees that sam-e folic acid and folinic acid at those dosages work

You're very lucky with a dad like thst ngl. Mine sucked.

 

[BasedSpinelet257]

Credits to @JohnRea for bringing this to my attention in addition to hypermethylation the growth plate area there is more evidence combined with the articles, clinical trials, and anecdotes of hypermethylation resulting in height growth beyond genetic potential

Take a look at this: https://www.mcgill.ca/newsroom/chan...unk-ants-how-environment-controls-size-243448 and https://www.whatisepigenetics.com/d...nces-continuous-variation-in-ant-worker-size/

Mainly hypermethylation specifically the EGFr gene which encodes for the epidermal growth factor receptor

"It's a discovery that completely changes our understanding of how human variation comes to be," said one of the lead researchers, professor Ehab Abouheif of the McGill University.

Many human traits, whether they are intelligence, height, or vulnerability to diseases such as cancer, exist along a continuum.

A McGill University team led by professors Moshe Szyf and Ehab Abouheif arrived at this conclusion by conducting epigenetic experiments on Florida carpenter ants.

"By increasing the degree of DNA methylation of a gene called Egfr - gene involved in controlling growth - they were able to create a spectrum of ants of different sizes. Methylation is a biochemical process that controls the expression of certain genes. Essentially, the researchers found that the more methylated the gene, the larger the size of the ants.

"By modifying the methylation of one particular gene, that affects others, in this case the Egfr gene, we could affect all the other genes involved in cellular growth," said study co-author Sebastian Alvarado from the McGill. "We were working with ants, but it was a bit like discovering that we could create shorter or taller human beings," Alvarado said.

The findings were published today in Nature Communications."

No need to modify the methylation for one specific gene, all over hypermethylation will reverse your growth plate senescence either way and upregulate many different genes for height growth.

Combine this with examples of DMNT3A overgrowth syndrome, weaver syndrome and sotos syndrome, it seems all cases like this with some form of hypermethylation resulted in tall stature.

I mentioned this study in a paper I wrote on the effects of SAM-e on psychological well being last semester. It’s interesting that you say that all hypermethylation reverses growth plate senescence because I always thought it was key that we find a map detailing which genes SAM can and cannot effect.

 

[Solidcoin]

I mentioned this study in a paper I wrote on the effects of SAM-e on psychological well being last semester. It’s interesting that you say that all hypermethylation reverses growth plate senescence because I always thought it was key that we find a map detailing which genes SAM can and cannot effect.

This is amazing and all but, don't you worry about why these genetic limits were put in place? why would our bodies not grow bigger if adequate nutrition was available? it's hard to ignore the fact that what's been coded for to limit growth is done on the premise of survival, having bodily process being incompatible with the rest of your body just because you influenced a single part will make the entire system crumble and pose serious health risks.

 

[BasedSpinelet257]

This is amazing and all but, don't you worry about why these genetic limits were put in place? why would our bodies not grow bigger if adequate nutrition was available? it's hard to ignore the fact that what's been coded for to limit growth is done on the premise of survival, having bodily process being incompatible with the rest of your body just because you influenced a single part will make the entire system crumble and pose serious health risks.

I get that in the general sense, but the limit for human body size is much higher than what we’re hoping to achieve through these methods.

As for why we even have to override these mechanisms to begin with, there could be any number of factors from simply having disadvantageous methylation patterns as a result of variable development and letting nature take its course or having legitimate hormone/nutrient/environmental deficiency.

What I’m trying to say is that there are many roads that lead to the end result of lesser body size, and I feel like it’s a misnomer to assume that you were SUPPOSED to end up that rather rather than that just being how it turned out.

 

[Mayorga]

you need things that silence tumor suppressor genes and turn on oncogenes

Hope it works as intended and without any ill-effects, although going for hypermethilation all over and crossing your fingers that it "hits" the right genes sounds like trying to kill a fly in a kindergarten with a nuclear bomb without frying any kids.

 

[Deleted member 4946]

You're very lucky with a dad like thst ngl. Mine sucked.

what? Dad's don't suck man, just cause mine was specialised in an area that by some coincidence became useful for me doesn't mean anything, I'm sure your dad can help you with something