How to build facial bone, guide to forward craniofacial growth, and bone remodelling. My hypothesis.'

[goat2x]

HGH after puberty is COPE:

Read this:


Growth hormone effects on cortical bone dimensions in young adults with childhood-onset growth hormone deficiency

tldr:
-growth hormone deficient adults (fused growth plates) have taken gh for 2 years (daily injections and increasing dose, at the end of the two years the does was 4-5iu for someone weighing 80kg ca)
-bone width did NOT change significantly
-bone thickness increased, but the bone grew inward and the bone marrow space got smaller
Now those were deficient adults, and pharmagrade gh (100percent real) was not able to give them visibly bigger bones.



The only thing that can obviously be changed compared to that study is the dose, (which prolly was quite low in the beginning) and time of use.


The first graph (solid line) shows the bone width versus time. You can see how the bone width is almost linearly increasing after one year use, where the non treated group (dotted line) shows almost no growth in width anymore after one year use.

So by naively extrapolating, I could see that with very long and constant gh use one could achieve significant change in the appearence, but keep in mind the scale. The bones did grow about 0.1mm !! compared to the non treated group.

So I personally don't think without gh deficiency you can really achieve any significant changes in the face and skull by using external gh.






Acromegaly is unusal growth in bone thickness, mostly in chin, browridge, hands and feets and it is solely due to gh overproduction.

Now the question is, when did those acromegalic patients develop their tumors that lead to gh secretion? And I personally think the ones that are not especially tall (gigantism) had that tumor in their late puberty (just my guess), where the face and skull still can change.
That's how I could explain why acromegaly exists (people that have abnormally thick skulls, hands and feet due to gh overproduction, BUT their bones did not grow in length more than normal)

Hopefully I'm wrong and there is evidence that some people grew their bones significantly long after their puberty ended.


There was a baseball player that appearently grew foot and cap sizes in his 20s and 30s and people accused him of gh abuse.

Could steroids have made Barry Bonds' head grow in size?

Following the federal indictment of Barry Bonds for perjury and obstruction of justice last week, media reports cited the baseball player's refusal to...

slate.com

even if ur bones grow there is a high change that you will look ogre as fuck
since your nose and ear will most likely to grow first

 

[GigaMogger]

Damn this post is high IQ

 

[hairyballscel]

If you look at the diseases where sclerostin is inhibited

examples?

 

[GigaMogger]

 

[Oueyy]

Hard mewing + MEGA dosing Vit K2 mk4 + MK677 + Vit D3 + Boron + Calcium + Magnesium + Incisor chewing and bonesmashing is the ultimate bone remodelling stack

Megadosing like how much ?

 

[AscendingHero]

even if ur bones grow there is a high change that you will look ogre as fuck
since your nose and ear will most likely to grow first

this is if you inject after puberty right?

 

[AscendingHero]

Bumping this masterpiece of a thread

@WadlowMaxxing @Henry_Gandy @TeenAscender
@

@ht-normie-ascending @

@OldVirgin @

@PubertyMaxxer @

@ItisOver @

@AscendingHero @

@Henry_Gandy @

@johnpop @

@Alibaba69 @

@nelson @TeenagePharmacy

Thoughts?

Anything to add, takeway? any legit methods itt?

 

[AscendingHero]

for a protocol, I'd suggest either 5-7.5iu of growth hormone daily, along with IGF-1 Lr3 50-100mcg daily, add in some Mk4 at 100-200mg daily (you can buy pure powder and just wing the dosage, mk4 isn't toxic, just don't go over 500mg). IGF-1 Lr3 would work great, it has a low affinity to bind to IGFBP3 and a higher affinity to the IGFR1-2, it's basically IGF-1 on roids. Most importantly, eat. Leptin and Insulin are the most important hormones for growth, keep that in mind.

So HGH/IGF-1 (Specifically GH with IGF-1 lr3)

HCG (if take high doses of dht)

vitamin k2 mk4 (megadose but not higher than 500 mg)

DSIP

DHT is very important (not so much testosterone)

No AI, we need estrogen and osteoclat/bat to be at en equilibrium and dht does a good job a nuking it. High doses f it up so HCG.

LASTLY AND MOST IMPORTANTLY: NUTRITION! EAT NUTRIENT PROFUSE CALORIE DENSE FOODS (mostly pastured raw animal products) plenty of good carb sources needed.

Anything to add fellow forum members?

 

[Deleted member 4946]

Bumping this masterpiece of a thread

@WadlowMaxxing @Henry_Gandy @TeenAscender
@

@ht-normie-ascending @

@OldVirgin @

@PubertyMaxxer @

@ItisOver @

@AscendingHero @

@Henry_Gandy @

@johnpop @

@Alibaba69 @

@nelson @TeenagePharmacy

Thoughts?

Anything to add, takeway? any legit methods itt?

the creator of this thread is long gone after he ascended to 6psl

 

[Alibaba69]

dn rd + hgh + ur black

 

[FinallyAscended]

Only testosterone works

 

[TeenAscender]

the greatest pubertymaxxer of all time really ascended w hgh to leave us in the dust @Henry_Gandy @AscendingHero

 

[user47283]

here's my hypothesis for inducing forward craniofacial growth. Not a single soul will read though

first, we need to understand the process of bone metabolism. Bone remodeling (or bone metabolism) is a lifelong process where the mature bone tissue is removed from the skeleton (a process called bone resorption) and new bone tissue is formed. these processes also control the reshaping or replacement of bone following injuries like fractures but also micro-damage, which occurs during normal activity. Remodeling responds also to the functional demands of mechanical loading. Two main cells are responsible for bone remodeling, osteoblasts, and osteoclasts. Osteoblasts secrete new bone, osteoclasts break down old bone.

Our goal is to enhance the process of bone remodeling by altering the osteoblast and osteoclast function, this will only work during puberty, whilst the body is in a state of susceptibility to growth factors. This guide is gonna basically me regurgitating all of my research into one thread, it won't be structured well but take what you can from it.

Okay, firstly, don't fast, restrict caloric intake or eat a shit diet whilst in the midst of pubertal growth. You want to follow a diet high in cholesterol, saturated fats, moderate amounts of protein (animal sourced), and most importantly, high carbohydrate. Eat well above 2500kcal daily, you want to be in a constant state of anabolism, you want your metabolism to be firing, without a functioning thyroid none of what I'm about to tell you will work. you'll need to be constantly eating, specifically carbohydrates like potatoes, tubers, and white rice, don't eat any other source of carbohydrates, stick to tubers and vegetables, involve high amounts of cholesterol from eggs and butter, don't consume polyunsaturated fats at all, they will oxidize in the blood and become free radicals, damaging the Leydig cells and lowering steroid hormone levels within the body. Consume fruits like apples and oranges, eat red meats, specifically beef, some fish here and there. Mainly focus on eating as much cholesterol from eggs and consuming large amounts of carbohydrates from the correct sources before you sleep, don't pig out on high-glycemic carbs, that isn't what I'm suggesting, I'll go into more detail later.

don't restrict calories or fast, this will lower the activity of the mTOR/pi3k/ATK pathways as insulin is vital for the activation of these pathways, fasting and lowering caloric intake will also decrease both insulin and leptin within the body, leptin is the hormone that is released when you have eaten past the point of satiation, my findings suggest that leptin is a potent agonist to osteogenic genotypes, essentially it induces bone formation, remodeling, and mineral disposition, it also increases IGF-1 levels, which is what we want. I can't stress how much eating is necessary for bone remodeling. Correcting your diet is step one, following the diet that I have written above will guarantee that you're inducing a constant state of anabolism, insulin will be released when you consume food, your metabolism with increase, in turn producing t3 and t4, both these thyroid hormones will convert somatropin into IGF-1, IGF-1 and insulin will then stimulate the mTOR1-2/pi3k/ATK pathways, in turn inducing hyperplasia, cell proliferation, hypertrophy and increased level of protein synthesis. Basically through the activation of these pathways, your body will be in a constant state of anabolism.

Pi3k is necessary to promote growth and proliferation over the differentiation of adult stem cells It is the difficulty in finding an appropriate amount of proliferation versus differentiation that researchers are trying to determine in order to utilize this balance in the development of various therapies. The constant spike of insulin and IGF-1 is what keeps these pathways active during adolescence, specifically insulin. To keep it simple, I'd say using exogenous forms of either GH or IGF-1 is enough to enhance the mTOR/pi3k pathways, but if you really want to induce growth. Your best bet is to use experimental chemicals that are known as pi3k agonists/activators. Agonists such as 740-Y-P can be used, these will have a potent stimulatory effect on the anabolic pathways, in combination with constant insulin secretion and high IGF-1, and GH levels, you will experience growth like none other, although I don't recommend the usage of these experimental 'pathway agonists' as they are not researched extensively and can possibly cause cancer due to chronic cell proliferation.

constantly activating the mTOR/pi3k/ATK pathways is vital, keeping these anabolic pathways firing during puberty is important for growth, don't fast and don't restrict calories, keep insulin up, keep metabolism firing and get plenty of deep sleep with the correct circadian rhythms, after puberty you can focus on autophagy and anti-aging protocols.

cortisol is a negative hormone, we don't want it. Glucocorticoids will suppress bone formation via the inhibition of osteoclasts, meaning it'll stop the process of the bone breaking down. We want osteoblasts and osteoclasts to be in a state of equilibrium or homeostasis for better words, we want them to be functioning together, but we want them to be functioning at a higher rate than the normal person. the usage of delta sleep-inducing peptide will block corticotropin from synthesizing cortisol, DSIP will also block somatostatin and upregulate the release of gonadotropin, in turn amplifying the release of luteinizing hormone. This peptide is a must in any protocol, due to the blockage of somatostatin and corticotropin.

dihydrotestosterone and E2 are both needed for bone remodeling, testosterone not so much. Estrogen maintains adult bone mass by inhibiting bone resorption and osteoclast activity, which in theory isn't what we want, again we want homeostasis between osteoblast and osteoclast, both estrogen and cortisol block osteoclast activity and bone resorption from occurring, this is the reason estrogen is promoted as necessary for bone health, if you can't make up for the bone resorption with sufficient bone formation than problems occur. Theoretically, if you wanted to reshape your bones, the best method would be to nuke your estrogen with letrozole, this would decrease osteoclast activity substantially, to the point where bone resorption would be almost impossible, it would also exasperate the effects of osteoblast activity, again we don't want this, we want equilibrium between the two, estrogen is needed in keeping homeostasis between the osteoblasts and osteoclasts, dihydrotestosterone increases osteocalcin activity, in turn inducing bone formation and increasing bone mineral deposition, dihydrotestosterone and estrogen together synergize nicely, DHT will decrease the level of estrogen within the body, but not enough to the point where osteoclast activity is altered, we want bone resorption to occur, so that dht can begin the formation of new bone cells. The problem with administrating DHT alone is that at the dosages that we need to be working with in order to increase osteocalcin and osteoblast activity would nuke our estradiol, so the usage of human-chorionic-gonadotropin should be used in order to increase intra-testicular estrogen and aromatase activity. Keep in mind this is all theoretical, but I'm sure that estrogen and dht synergize when it comes to bone metabolism and remodeling.

again, let me just explain, osteoblasts promote the proliferation of bone cells and the growth of bone, whereas osteoclasts promote resorption of the bone cells, essentially osteoclasts are there to renew the bone by metabolizing bone cells, allowing for new bone to form via osteocytes, osteocalcin, and osteoblast activity. Estrogen effectively inhibits osteoclast activity from occurring, this is why post-menopausal women experience BMD issues as osteoclast activity is at an all-time high due to the lack of estrogen in the women's bodies, osteoclasts are high and osteoblasts are low, meaning constant bone metabolism and no new bone cell proliferation and growth. We don't want to nuke our estrogen as we need it to keep homeostasis

I hypothesize that we need high activity of both osteoclast and osteoblast for bone substantial bone growth, others debate that reshaping the bone requires an overabundance of osteoclast activity and less osteoblast, others debate that osteoblasts should be promoted and osteoclasts should be inhibited. Vitamin K2 has agonistic properties on the nuclear factor-kB signaling pathway. Nf-kB agonists have potent pro-anabolic and anti-catabolic effects on bone cells, essentially when this pathway is activated it decreases bone resorption and upregulates osteoblast activity. vitamin K2 action on osteoblast and osteoclast formation and activity is accomplished by down-regulating basal and cytokine-induced NF-kB activation, by increasing IkB mRNA, Furthermore, vitamin K2 prevents repression by tumor necrosis factor-a (TNFa) of SMAD signaling induced by either transforming growth factor B (TGFB) or bone morphogenetic protein-2 (BMP-2). This is why menopausal women who take vitamin K2 experience great results when it comes to BMD, due to there lowered estrogen activity osteoclasts are high, when MK4 is introduced osteoclast are somewhat inhibited and osteoblast activity is increased, countering the effects of low estradiol.

for a protocol, I'd suggest either 5-7.5iu of growth hormone daily, along with IGF-1 Lr3 50-100mcg daily, add in some Mk4 at 100-200mg daily (you can buy pure powder and just wing the dosage, mk4 isn't toxic, just don't go over 500mg). IGF-1 Lr3 would work great, it has a low affinity to bind to IGFBP3 and a higher affinity to the IGFR1-2, it's basically IGF-1 on roids. Most importantly, eat. Leptin and Insulin are the most important hormones for growth, keep that in mind.

again, this is all hypothetical, so take what you can from it. Also for those wanting sources, I have a couple of HGH sources, but I don't have sources for IGF-1LR3. I'd LIKE SOME HIGH IQCELLS TO DISCUSS THIS WITH ME.

@JustTrynaGrow @Slyfex8 @draco @Don't Forget to mew @Tom2004 @Crazzen8 @ht-normie-ascending @Dr Shekelberg @forwardgrowth @maxmendietta @PubertyMaxxer @apollothegun @KKK @EthnicelAscension @PrettyBoyMaxxing @Goblin @Alexanderr @Test @RAITEIII @Mateusz74 @DianabolDownie

great post op, I read every word

 

[TeenAscender]

has anyone here ever actually megadosed mk4?

 

[Laikyn]

has anyone here ever actually megadosed mk4?

yes
did nothing

 

[hallo]

the creator of this thread is long gone after he ascended to 6psl

That's beautiful ngl. He's walking on a beach during sunset as we speak...

 

[Deleted member 17429]

Hard mewing + MEGA dosing Vit K2 mk4 + MK677 + Vit D3 + Boron + Calcium + Magnesium + Incisor chewing and bonesmashing is the ultimate bone remodelling stack

how much would be considered a megadose?

 

[Deleted member 17027]

oh yes goy, mew and chew.

mewing doesn't do fuck all, it's utter cope.

even if mewing was legit, your results would be dependent on the plasticity of your bones, which is regulated via osteoclasts.

i thought that shit depended on the muscles attached to ur palate and those muscles brought that shit upward or smthn
chewing real tho prob the best looksmax method specially for people in puberty

 

[the_nextDavidLaid]

here's my hypothesis for inducing forward craniofacial growth. Not a single soul will read though

first, we need to understand the process of bone metabolism. Bone remodeling (or bone metabolism) is a lifelong process where the mature bone tissue is removed from the skeleton (a process called bone resorption) and new bone tissue is formed. these processes also control the reshaping or replacement of bone following injuries like fractures but also micro-damage, which occurs during normal activity. Remodeling responds also to the functional demands of mechanical loading. Two main cells are responsible for bone remodeling, osteoblasts, and osteoclasts. Osteoblasts secrete new bone, osteoclasts break down old bone.

Our goal is to enhance the process of bone remodeling by altering the osteoblast and osteoclast function, this will only work during puberty, whilst the body is in a state of susceptibility to growth factors. This guide is gonna basically me regurgitating all of my research into one thread, it won't be structured well but take what you can from it.

Okay, firstly, don't fast, restrict caloric intake or eat a shit diet whilst in the midst of pubertal growth. You want to follow a diet high in cholesterol, saturated fats, moderate amounts of protein (animal sourced), and most importantly, high carbohydrate. Eat well above 2500kcal daily, you want to be in a constant state of anabolism, you want your metabolism to be firing, without a functioning thyroid none of what I'm about to tell you will work. you'll need to be constantly eating, specifically carbohydrates like potatoes, tubers, and white rice, don't eat any other source of carbohydrates, stick to tubers and vegetables, involve high amounts of cholesterol from eggs and butter, don't consume polyunsaturated fats at all, they will oxidize in the blood and become free radicals, damaging the Leydig cells and lowering steroid hormone levels within the body. Consume fruits like apples and oranges, eat red meats, specifically beef, some fish here and there. Mainly focus on eating as much cholesterol from eggs and consuming large amounts of carbohydrates from the correct sources before you sleep, don't pig out on high-glycemic carbs, that isn't what I'm suggesting, I'll go into more detail later.

don't restrict calories or fast, this will lower the activity of the mTOR/pi3k/ATK pathways as insulin is vital for the activation of these pathways, fasting and lowering caloric intake will also decrease both insulin and leptin within the body, leptin is the hormone that is released when you have eaten past the point of satiation, my findings suggest that leptin is a potent agonist to osteogenic genotypes, essentially it induces bone formation, remodeling, and mineral disposition, it also increases IGF-1 levels, which is what we want. I can't stress how much eating is necessary for bone remodeling. Correcting your diet is step one, following the diet that I have written above will guarantee that you're inducing a constant state of anabolism, insulin will be released when you consume food, your metabolism with increase, in turn producing t3 and t4, both these thyroid hormones will convert somatropin into IGF-1, IGF-1 and insulin will then stimulate the mTOR1-2/pi3k/ATK pathways, in turn inducing hyperplasia, cell proliferation, hypertrophy and increased level of protein synthesis. Basically through the activation of these pathways, your body will be in a constant state of anabolism.

Pi3k is necessary to promote growth and proliferation over the differentiation of adult stem cells It is the difficulty in finding an appropriate amount of proliferation versus differentiation that researchers are trying to determine in order to utilize this balance in the development of various therapies. The constant spike of insulin and IGF-1 is what keeps these pathways active during adolescence, specifically insulin. To keep it simple, I'd say using exogenous forms of either GH or IGF-1 is enough to enhance the mTOR/pi3k pathways, but if you really want to induce growth. Your best bet is to use experimental chemicals that are known as pi3k agonists/activators. Agonists such as 740-Y-P can be used, these will have a potent stimulatory effect on the anabolic pathways, in combination with constant insulin secretion and high IGF-1, and GH levels, you will experience growth like none other, although I don't recommend the usage of these experimental 'pathway agonists' as they are not researched extensively and can possibly cause cancer due to chronic cell proliferation.

constantly activating the mTOR/pi3k/ATK pathways is vital, keeping these anabolic pathways firing during puberty is important for growth, don't fast and don't restrict calories, keep insulin up, keep metabolism firing and get plenty of deep sleep with the correct circadian rhythms, after puberty you can focus on autophagy and anti-aging protocols.

cortisol is a negative hormone, we don't want it. Glucocorticoids will suppress bone formation via the inhibition of osteoclasts, meaning it'll stop the process of the bone breaking down. We want osteoblasts and osteoclasts to be in a state of equilibrium or homeostasis for better words, we want them to be functioning together, but we want them to be functioning at a higher rate than the normal person. the usage of delta sleep-inducing peptide will block corticotropin from synthesizing cortisol, DSIP will also block somatostatin and upregulate the release of gonadotropin, in turn amplifying the release of luteinizing hormone. This peptide is a must in any protocol, due to the blockage of somatostatin and corticotropin.

dihydrotestosterone and E2 are both needed for bone remodeling, testosterone not so much. Estrogen maintains adult bone mass by inhibiting bone resorption and osteoclast activity, which in theory isn't what we want, again we want homeostasis between osteoblast and osteoclast, both estrogen and cortisol block osteoclast activity and bone resorption from occurring, this is the reason estrogen is promoted as necessary for bone health, if you can't make up for the bone resorption with sufficient bone formation than problems occur. Theoretically, if you wanted to reshape your bones, the best method would be to nuke your estrogen with letrozole, this would decrease osteoclast activity substantially, to the point where bone resorption would be almost impossible, it would also exasperate the effects of osteoblast activity, again we don't want this, we want equilibrium between the two, estrogen is needed in keeping homeostasis between the osteoblasts and osteoclasts, dihydrotestosterone increases osteocalcin activity, in turn inducing bone formation and increasing bone mineral deposition, dihydrotestosterone and estrogen together synergize nicely, DHT will decrease the level of estrogen within the body, but not enough to the point where osteoclast activity is altered, we want bone resorption to occur, so that dht can begin the formation of new bone cells. The problem with administrating DHT alone is that at the dosages that we need to be working with in order to increase osteocalcin and osteoblast activity would nuke our estradiol, so the usage of human-chorionic-gonadotropin should be used in order to increase intra-testicular estrogen and aromatase activity. Keep in mind this is all theoretical, but I'm sure that estrogen and dht synergize when it comes to bone metabolism and remodeling.

again, let me just explain, osteoblasts promote the proliferation of bone cells and the growth of bone, whereas osteoclasts promote resorption of the bone cells, essentially osteoclasts are there to renew the bone by metabolizing bone cells, allowing for new bone to form via osteocytes, osteocalcin, and osteoblast activity. Estrogen effectively inhibits osteoclast activity from occurring, this is why post-menopausal women experience BMD issues as osteoclast activity is at an all-time high due to the lack of estrogen in the women's bodies, osteoclasts are high and osteoblasts are low, meaning constant bone metabolism and no new bone cell proliferation and growth. We don't want to nuke our estrogen as we need it to keep homeostasis

I hypothesize that we need high activity of both osteoclast and osteoblast for bone substantial bone growth, others debate that reshaping the bone requires an overabundance of osteoclast activity and less osteoblast, others debate that osteoblasts should be promoted and osteoclasts should be inhibited. Vitamin K2 has agonistic properties on the nuclear factor-kB signaling pathway. Nf-kB agonists have potent pro-anabolic and anti-catabolic effects on bone cells, essentially when this pathway is activated it decreases bone resorption and upregulates osteoblast activity. vitamin K2 action on osteoblast and osteoclast formation and activity is accomplished by down-regulating basal and cytokine-induced NF-kB activation, by increasing IkB mRNA, Furthermore, vitamin K2 prevents repression by tumor necrosis factor-a (TNFa) of SMAD signaling induced by either transforming growth factor B (TGFB) or bone morphogenetic protein-2 (BMP-2). This is why menopausal women who take vitamin K2 experience great results when it comes to BMD, due to there lowered estrogen activity osteoclasts are high, when MK4 is introduced osteoclast are somewhat inhibited and osteoblast activity is increased, countering the effects of low estradiol.

for a protocol, I'd suggest either 5-7.5iu of growth hormone daily, along with IGF-1 Lr3 50-100mcg daily, add in some Mk4 at 100-200mg daily (you can buy pure powder and just wing the dosage, mk4 isn't toxic, just don't go over 500mg). IGF-1 Lr3 would work great, it has a low affinity to bind to IGFBP3 and a higher affinity to the IGFR1-2, it's basically IGF-1 on roids. Most importantly, eat. Leptin and Insulin are the most important hormones for growth, keep that in mind.

again, this is all hypothetical, so take what you can from it. Also for those wanting sources, I have a couple of HGH sources, but I don't have sources for IGF-1LR3. I'd LIKE SOME HIGH IQCELLS TO DISCUSS THIS WITH ME.

@JustTrynaGrow @Slyfex8 @draco @Don't Forget to mew @Tom2004 @Crazzen8 @ht-normie-ascending @Dr Shekelberg @forwardgrowth @maxmendietta @PubertyMaxxer @apollothegun @KKK @EthnicelAscension @PrettyBoyMaxxing @Goblin @Alexanderr @Test @RAITEIII @Mateusz74 @DianabolDownie

Extremely high IQ thread. Too bad I didn’t understand shit.

 

[Skywalker]

how do i get 30 mm of bone expansion, legit? like i wanna do the whole gamut

 

[Striking resemblance]

What a whole bunch of mumbling in that first post. Way to much work put in that wont make a difference for anyone here. On a seroius note, those things mentioned is not for forward growth. But rather maintaining or decrease the loss of bone over time. To get forward growth there must be force applied, that will make bone grow. K2 is good but there must be the right version. Not mk4 like the rec in op but mk7 which studies show make difference.

 

[pumpeduppecs]

Cliffs someone plz

 

[Iblamejordan]

What a whole bunch of mumbling in that first post. Way to much work put in that wont make a difference for anyone here. On a seroius note, those things mentioned is not for forward growth. But rather maintaining or decrease the loss of bone over time. To get forward growth there must be force applied, that will make bone grow. K2 is good but there must be the right version. Not mk4 like the rec in op but mk7 which studies show make difference.

Mewing and chewing is enough to force our facial bone.

 

[Blackgymmax]

Mewing and chewing is enough to force our facial bone.

You mog us all to death jordan. We cant just mew ourselves into being an international supermodel bro

 

[Pei]

You mog us all to death jordan. We cant just mew ourselves into being an international supermodel bro

That’s not his actual account retard

 

[Iblamejordan]

That’s not his actual account retard

You're more retarded

 

[gwiz]

problem with IGF-1 DES is that it only affect a localised area, i don't know how to inject something where my growth plates are, and yes i know IGF-1 LR3 can get desensitised but like anything that will get desensitised, you cycle it, try read this chart if you can (i can't) https://ijpeonline.biomedcentral.com/articles/10.1186/1687-9856-2014-15/figures/1

wouldn’t injecting in the areas close to growth plates work? i was planning on using des and doing it this way but if it doesn’t work that would be a big waste off time any idea if it would work?

 

[spectacularpixlr]

@RealSurgerymax

 

[WishIwasChico]

has anyone here ever actually megadosed mk4?

ye i did for like 4 months but had to stop as i got really ill, i also abused calcium, vit d, magnesium, boron, silica. I need to start again next month when i get paid at the end of the month. Currently taking 60mg of Mk677 with Huperzine A.

 

[Deleted member 21765]

ye i did for like 4 months but had to stop as i got really ill, i also abused calcium, vit d, magnesium, boron, silica. I need to start again next month when i get paid at the end of the month. Currently taking 60mg of Mk677 with Huperzine A.

did you see any difference?

 

[190cm90kg]

endocrinology wordsalad schizorant. if ur reading this because u want to fix a recessed skull its already too late

 

[Iblamejordan]

How can I get 100~200mg of vitamin k2 mk4?

 

[infini]

here's my hypothesis for inducing forward craniofacial growth. Not a single soul will read though

first, we need to understand the process of bone metabolism. Bone remodeling (or bone metabolism) is a lifelong process where the mature bone tissue is removed from the skeleton (a process called bone resorption) and new bone tissue is formed. these processes also control the reshaping or replacement of bone following injuries like fractures but also micro-damage, which occurs during normal activity. Remodeling responds also to the functional demands of mechanical loading. Two main cells are responsible for bone remodeling, osteoblasts, and osteoclasts. Osteoblasts secrete new bone, osteoclasts break down old bone.

Our goal is to enhance the process of bone remodeling by altering the osteoblast and osteoclast function, this will only work during puberty, whilst the body is in a state of susceptibility to growth factors. This guide is gonna basically me regurgitating all of my research into one thread, it won't be structured well but take what you can from it.

Okay, firstly, don't fast, restrict caloric intake or eat a shit diet whilst in the midst of pubertal growth. You want to follow a diet high in cholesterol, saturated fats, moderate amounts of protein (animal sourced), and most importantly, high carbohydrate. Eat well above 2500kcal daily, you want to be in a constant state of anabolism, you want your metabolism to be firing, without a functioning thyroid none of what I'm about to tell you will work. you'll need to be constantly eating, specifically carbohydrates like potatoes, tubers, and white rice, don't eat any other source of carbohydrates, stick to tubers and vegetables, involve high amounts of cholesterol from eggs and butter, don't consume polyunsaturated fats at all, they will oxidize in the blood and become free radicals, damaging the Leydig cells and lowering steroid hormone levels within the body. Consume fruits like apples and oranges, eat red meats, specifically beef, some fish here and there. Mainly focus on eating as much cholesterol from eggs and consuming large amounts of carbohydrates from the correct sources before you sleep, don't pig out on high-glycemic carbs, that isn't what I'm suggesting, I'll go into more detail later.

don't restrict calories or fast, this will lower the activity of the mTOR/pi3k/ATK pathways as insulin is vital for the activation of these pathways, fasting and lowering caloric intake will also decrease both insulin and leptin within the body, leptin is the hormone that is released when you have eaten past the point of satiation, my findings suggest that leptin is a potent agonist to osteogenic genotypes, essentially it induces bone formation, remodeling, and mineral disposition, it also increases IGF-1 levels, which is what we want. I can't stress how much eating is necessary for bone remodeling. Correcting your diet is step one, following the diet that I have written above will guarantee that you're inducing a constant state of anabolism, insulin will be released when you consume food, your metabolism with increase, in turn producing t3 and t4, both these thyroid hormones will convert somatropin into IGF-1, IGF-1 and insulin will then stimulate the mTOR1-2/pi3k/ATK pathways, in turn inducing hyperplasia, cell proliferation, hypertrophy and increased level of protein synthesis. Basically through the activation of these pathways, your body will be in a constant state of anabolism.

Pi3k is necessary to promote growth and proliferation over the differentiation of adult stem cells It is the difficulty in finding an appropriate amount of proliferation versus differentiation that researchers are trying to determine in order to utilize this balance in the development of various therapies. The constant spike of insulin and IGF-1 is what keeps these pathways active during adolescence, specifically insulin. To keep it simple, I'd say using exogenous forms of either GH or IGF-1 is enough to enhance the mTOR/pi3k pathways, but if you really want to induce growth. Your best bet is to use experimental chemicals that are known as pi3k agonists/activators. Agonists such as 740-Y-P can be used, these will have a potent stimulatory effect on the anabolic pathways, in combination with constant insulin secretion and high IGF-1, and GH levels, you will experience growth like none other, although I don't recommend the usage of these experimental 'pathway agonists' as they are not researched extensively and can possibly cause cancer due to chronic cell proliferation.

constantly activating the mTOR/pi3k/ATK pathways is vital, keeping these anabolic pathways firing during puberty is important for growth, don't fast and don't restrict calories, keep insulin up, keep metabolism firing and get plenty of deep sleep with the correct circadian rhythms, after puberty you can focus on autophagy and anti-aging protocols.

cortisol is a negative hormone, we don't want it. Glucocorticoids will suppress bone formation via the inhibition of osteoclasts, meaning it'll stop the process of the bone breaking down. We want osteoblasts and osteoclasts to be in a state of equilibrium or homeostasis for better words, we want them to be functioning together, but we want them to be functioning at a higher rate than the normal person. the usage of delta sleep-inducing peptide will block corticotropin from synthesizing cortisol, DSIP will also block somatostatin and upregulate the release of gonadotropin, in turn amplifying the release of luteinizing hormone. This peptide is a must in any protocol, due to the blockage of somatostatin and corticotropin.

dihydrotestosterone and E2 are both needed for bone remodeling, testosterone not so much. Estrogen maintains adult bone mass by inhibiting bone resorption and osteoclast activity, which in theory isn't what we want, again we want homeostasis between osteoblast and osteoclast, both estrogen and cortisol block osteoclast activity and bone resorption from occurring, this is the reason estrogen is promoted as necessary for bone health, if you can't make up for the bone resorption with sufficient bone formation than problems occur. Theoretically, if you wanted to reshape your bones, the best method would be to nuke your estrogen with letrozole, this would decrease osteoclast activity substantially, to the point where bone resorption would be almost impossible, it would also exasperate the effects of osteoblast activity, again we don't want this, we want equilibrium between the two, estrogen is needed in keeping homeostasis between the osteoblasts and osteoclasts, dihydrotestosterone increases osteocalcin activity, in turn inducing bone formation and increasing bone mineral deposition, dihydrotestosterone and estrogen together synergize nicely, DHT will decrease the level of estrogen within the body, but not enough to the point where osteoclast activity is altered, we want bone resorption to occur, so that dht can begin the formation of new bone cells. The problem with administrating DHT alone is that at the dosages that we need to be working with in order to increase osteocalcin and osteoblast activity would nuke our estradiol, so the usage of human-chorionic-gonadotropin should be used in order to increase intra-testicular estrogen and aromatase activity. Keep in mind this is all theoretical, but I'm sure that estrogen and dht synergize when it comes to bone metabolism and remodeling.

again, let me just explain, osteoblasts promote the proliferation of bone cells and the growth of bone, whereas osteoclasts promote resorption of the bone cells, essentially osteoclasts are there to renew the bone by metabolizing bone cells, allowing for new bone to form via osteocytes, osteocalcin, and osteoblast activity. Estrogen effectively inhibits osteoclast activity from occurring, this is why post-menopausal women experience BMD issues as osteoclast activity is at an all-time high due to the lack of estrogen in the women's bodies, osteoclasts are high and osteoblasts are low, meaning constant bone metabolism and no new bone cell proliferation and growth. We don't want to nuke our estrogen as we need it to keep homeostasis

I hypothesize that we need high activity of both osteoclast and osteoblast for bone substantial bone growth, others debate that reshaping the bone requires an overabundance of osteoclast activity and less osteoblast, others debate that osteoblasts should be promoted and osteoclasts should be inhibited. Vitamin K2 has agonistic properties on the nuclear factor-kB signaling pathway. Nf-kB agonists have potent pro-anabolic and anti-catabolic effects on bone cells, essentially when this pathway is activated it decreases bone resorption and upregulates osteoblast activity. vitamin K2 action on osteoblast and osteoclast formation and activity is accomplished by down-regulating basal and cytokine-induced NF-kB activation, by increasing IkB mRNA, Furthermore, vitamin K2 prevents repression by tumor necrosis factor-a (TNFa) of SMAD signaling induced by either transforming growth factor B (TGFB) or bone morphogenetic protein-2 (BMP-2). This is why menopausal women who take vitamin K2 experience great results when it comes to BMD, due to there lowered estrogen activity osteoclasts are high, when MK4 is introduced osteoclast are somewhat inhibited and osteoblast activity is increased, countering the effects of low estradiol.

for a protocol, I'd suggest either 5-7.5iu of growth hormone daily, along with IGF-1 Lr3 50-100mcg daily, add in some Mk4 at 100-200mg daily (you can buy pure powder and just wing the dosage, mk4 isn't toxic, just don't go over 500mg). IGF-1 Lr3 would work great, it has a low affinity to bind to IGFBP3 and a higher affinity to the IGFR1-2, it's basically IGF-1 on roids. Most importantly, eat. Leptin and Insulin are the most important hormones for growth, keep that in mind.

again, this is all hypothetical, so take what you can from it. Also for those wanting sources, I have a couple of HGH sources, but I don't have sources for IGF-1LR3. I'd LIKE SOME HIGH IQCELLS TO DISCUSS THIS WITH ME.

@JustTrynaGrow @Slyfex8 @draco @Don't Forget to mew @Tom2004 @Crazzen8 @ht-normie-ascending @Dr Shekelberg @forwardgrowth @maxmendietta @PubertyMaxxer @apollothegun @KKK @EthnicelAscension @PrettyBoyMaxxing @Goblin @Alexanderr @Test @RAITEIII @Mateusz74 @DianabolDownie

This thread (and the steroid one) is harder to understand than it is to follow it. One of several best-of-the-best threads that need a condensed version for people reading it as if they're 10. So many users here deserve to get wiped off with their immaturity or their autism and need to find an appropriate balance.

[edit]
I projected a bit, if the second from the last para is the TL: DR then okay. Most of my frustration was at the First Steroid Cycle thread.

 

[Deleted member 23558]

Calcium stimulates the release of PTH which in turn increases number/activity of osteoclasts. (Ideal in growing years)

Another thing is Ghrelin which is a osteoblast mitogen.

Long story short it is released when in a fasted state.
When Ghrelin lvls elevate it can result in higher levels of bone turnover.

Fasting is key. A fasted state in combination with exercise....I wonder if you can artificially increase Ghrelin lvls
@Dyorotic2

dietary calcium inhibits PTH.

 

[IhateDentists]

Cope

Hgh and steroids might grow your bones

But its more about positioning of the bones,
And harmony

The only way youll position your bones forward and upward is via mewing, chewing, appliances, and osteotomies. Everything else is cope.

If you have the perfect positioning of your facial bones, have a straight nose and wide palate, youre set. Just hghmax and take roids and train your neck, do some bonesmashing on chin and zygos, and get some implants.

Exactly this if they’re already perfectly positioned you just need to hgh max and add some test btw fuck implants let’s reach perfection real human perfection

 

[IhateDentists]

HGH after puberty is COPE:

Read this:


Growth hormone effects on cortical bone dimensions in young adults with childhood-onset growth hormone deficiency

tldr:
-growth hormone deficient adults (fused growth plates) have taken gh for 2 years (daily injections and increasing dose, at the end of the two years the does was 4-5iu for someone weighing 80kg ca)
-bone width did NOT change significantly
-bone thickness increased, but the bone grew inward and the bone marrow space got smaller
Now those were deficient adults, and pharmagrade gh (100percent real) was not able to give them visibly bigger bones.



The only thing that can obviously be changed compared to that study is the dose, (which prolly was quite low in the beginning) and time of use.


The first graph (solid line) shows the bone width versus time. You can see how the bone width is almost linearly increasing after one year use, where the non treated group (dotted line) shows almost no growth in width anymore after one year use.

So by naively extrapolating, I could see that with very long and constant gh use one could achieve significant change in the appearence, but keep in mind the scale. The bones did grow about 0.1mm !! compared to the non treated group.

So I personally don't think without gh deficiency you can really achieve any significant changes in the face and skull by using external gh.






Acromegaly is unusal growth in bone thickness, mostly in chin, browridge, hands and feets and it is solely due to gh overproduction.

Now the question is, when did those acromegalic patients develop their tumors that lead to gh secretion? And I personally think the ones that are not especially tall (gigantism) had that tumor in their late puberty (just my guess), where the face and skull still can change.
That's how I could explain why acromegaly exists (people that have abnormally thick skulls, hands and feet due to gh overproduction, BUT their bones did not grow in length more than normal)

Hopefully I'm wrong and there is evidence that some people grew their bones significantly long after their puberty ended.


There was a baseball player that appearently grew foot and cap sizes in his 20s and 30s and people accused him of gh abuse.

Could steroids have made Barry Bonds' head grow in size?

Following the federal indictment of Barry Bonds for perjury and obstruction of justice last week, media reports cited the baseball player's refusal to...

slate.com

Fuck off retarded kike

 

[futureashtray]

Cope

Hgh and steroids might grow your bones

But its more about positioning of the bones,
And harmony

The only way youll position your bones forward and upward is via mewing, chewing, appliances, and osteotomies. Everything else is cope.

If you have the perfect positioning of your facial bones, have a straight nose and wide palate, youre set. Just hghmax and take roids and train your neck, do some bonesmashing on chin and zygos, and get some implants.

idiot we want to enhance growth and movement, we cant make or move bone when we dont have enough nutrients and its even harder when youre in your late teens because now igf1/hgh levels will decrease dramatically

 

[futureashtray]

here's my hypothesis for inducing forward craniofacial growth. Not a single soul will read though

first, we need to understand the process of bone metabolism. Bone remodeling (or bone metabolism) is a lifelong process where the mature bone tissue is removed from the skeleton (a process called bone resorption) and new bone tissue is formed. these processes also control the reshaping or replacement of bone following injuries like fractures but also micro-damage, which occurs during normal activity. Remodeling responds also to the functional demands of mechanical loading. Two main cells are responsible for bone remodeling, osteoblasts, and osteoclasts. Osteoblasts secrete new bone, osteoclasts break down old bone.

Our goal is to enhance the process of bone remodeling by altering the osteoblast and osteoclast function, this will only work during puberty, whilst the body is in a state of susceptibility to growth factors. This guide is gonna basically me regurgitating all of my research into one thread, it won't be structured well but take what you can from it.

Okay, firstly, don't fast, restrict caloric intake or eat a shit diet whilst in the midst of pubertal growth. You want to follow a diet high in cholesterol, saturated fats, moderate amounts of protein (animal sourced), and most importantly, high carbohydrate. Eat well above 2500kcal daily, you want to be in a constant state of anabolism, you want your metabolism to be firing, without a functioning thyroid none of what I'm about to tell you will work. you'll need to be constantly eating, specifically carbohydrates like potatoes, tubers, and white rice, don't eat any other source of carbohydrates, stick to tubers and vegetables, involve high amounts of cholesterol from eggs and butter, don't consume polyunsaturated fats at all, they will oxidize in the blood and become free radicals, damaging the Leydig cells and lowering steroid hormone levels within the body. Consume fruits like apples and oranges, eat red meats, specifically beef, some fish here and there. Mainly focus on eating as much cholesterol from eggs and consuming large amounts of carbohydrates from the correct sources before you sleep, don't pig out on high-glycemic carbs, that isn't what I'm suggesting, I'll go into more detail later.

don't restrict calories or fast, this will lower the activity of the mTOR/pi3k/ATK pathways as insulin is vital for the activation of these pathways, fasting and lowering caloric intake will also decrease both insulin and leptin within the body, leptin is the hormone that is released when you have eaten past the point of satiation, my findings suggest that leptin is a potent agonist to osteogenic genotypes, essentially it induces bone formation, remodeling, and mineral disposition, it also increases IGF-1 levels, which is what we want. I can't stress how much eating is necessary for bone remodeling. Correcting your diet is step one, following the diet that I have written above will guarantee that you're inducing a constant state of anabolism, insulin will be released when you consume food, your metabolism with increase, in turn producing t3 and t4, both these thyroid hormones will convert somatropin into IGF-1, IGF-1 and insulin will then stimulate the mTOR1-2/pi3k/ATK pathways, in turn inducing hyperplasia, cell proliferation, hypertrophy and increased level of protein synthesis. Basically through the activation of these pathways, your body will be in a constant state of anabolism.

Pi3k is necessary to promote growth and proliferation over the differentiation of adult stem cells It is the difficulty in finding an appropriate amount of proliferation versus differentiation that researchers are trying to determine in order to utilize this balance in the development of various therapies. The constant spike of insulin and IGF-1 is what keeps these pathways active during adolescence, specifically insulin. To keep it simple, I'd say using exogenous forms of either GH or IGF-1 is enough to enhance the mTOR/pi3k pathways, but if you really want to induce growth. Your best bet is to use experimental chemicals that are known as pi3k agonists/activators. Agonists such as 740-Y-P can be used, these will have a potent stimulatory effect on the anabolic pathways, in combination with constant insulin secretion and high IGF-1, and GH levels, you will experience growth like none other, although I don't recommend the usage of these experimental 'pathway agonists' as they are not researched extensively and can possibly cause cancer due to chronic cell proliferation.

constantly activating the mTOR/pi3k/ATK pathways is vital, keeping these anabolic pathways firing during puberty is important for growth, don't fast and don't restrict calories, keep insulin up, keep metabolism firing and get plenty of deep sleep with the correct circadian rhythms, after puberty you can focus on autophagy and anti-aging protocols.

cortisol is a negative hormone, we don't want it. Glucocorticoids will suppress bone formation via the inhibition of osteoclasts, meaning it'll stop the process of the bone breaking down. We want osteoblasts and osteoclasts to be in a state of equilibrium or homeostasis for better words, we want them to be functioning together, but we want them to be functioning at a higher rate than the normal person. the usage of delta sleep-inducing peptide will block corticotropin from synthesizing cortisol, DSIP will also block somatostatin and upregulate the release of gonadotropin, in turn amplifying the release of luteinizing hormone. This peptide is a must in any protocol, due to the blockage of somatostatin and corticotropin.

dihydrotestosterone and E2 are both needed for bone remodeling, testosterone not so much. Estrogen maintains adult bone mass by inhibiting bone resorption and osteoclast activity, which in theory isn't what we want, again we want homeostasis between osteoblast and osteoclast, both estrogen and cortisol block osteoclast activity and bone resorption from occurring, this is the reason estrogen is promoted as necessary for bone health, if you can't make up for the bone resorption with sufficient bone formation than problems occur. Theoretically, if you wanted to reshape your bones, the best method would be to nuke your estrogen with letrozole, this would decrease osteoclast activity substantially, to the point where bone resorption would be almost impossible, it would also exasperate the effects of osteoblast activity, again we don't want this, we want equilibrium between the two, estrogen is needed in keeping homeostasis between the osteoblasts and osteoclasts, dihydrotestosterone increases osteocalcin activity, in turn inducing bone formation and increasing bone mineral deposition, dihydrotestosterone and estrogen together synergize nicely, DHT will decrease the level of estrogen within the body, but not enough to the point where osteoclast activity is altered, we want bone resorption to occur, so that dht can begin the formation of new bone cells. The problem with administrating DHT alone is that at the dosages that we need to be working with in order to increase osteocalcin and osteoblast activity would nuke our estradiol, so the usage of human-chorionic-gonadotropin should be used in order to increase intra-testicular estrogen and aromatase activity. Keep in mind this is all theoretical, but I'm sure that estrogen and dht synergize when it comes to bone metabolism and remodeling.

again, let me just explain, osteoblasts promote the proliferation of bone cells and the growth of bone, whereas osteoclasts promote resorption of the bone cells, essentially osteoclasts are there to renew the bone by metabolizing bone cells, allowing for new bone to form via osteocytes, osteocalcin, and osteoblast activity. Estrogen effectively inhibits osteoclast activity from occurring, this is why post-menopausal women experience BMD issues as osteoclast activity is at an all-time high due to the lack of estrogen in the women's bodies, osteoclasts are high and osteoblasts are low, meaning constant bone metabolism and no new bone cell proliferation and growth. We don't want to nuke our estrogen as we need it to keep homeostasis

I hypothesize that we need high activity of both osteoclast and osteoblast for bone substantial bone growth, others debate that reshaping the bone requires an overabundance of osteoclast activity and less osteoblast, others debate that osteoblasts should be promoted and osteoclasts should be inhibited. Vitamin K2 has agonistic properties on the nuclear factor-kB signaling pathway. Nf-kB agonists have potent pro-anabolic and anti-catabolic effects on bone cells, essentially when this pathway is activated it decreases bone resorption and upregulates osteoblast activity. vitamin K2 action on osteoblast and osteoclast formation and activity is accomplished by down-regulating basal and cytokine-induced NF-kB activation, by increasing IkB mRNA, Furthermore, vitamin K2 prevents repression by tumor necrosis factor-a (TNFa) of SMAD signaling induced by either transforming growth factor B (TGFB) or bone morphogenetic protein-2 (BMP-2). This is why menopausal women who take vitamin K2 experience great results when it comes to BMD, due to there lowered estrogen activity osteoclasts are high, when MK4 is introduced osteoclast are somewhat inhibited and osteoblast activity is increased, countering the effects of low estradiol.

for a protocol, I'd suggest either 5-7.5iu of growth hormone daily, along with IGF-1 Lr3 50-100mcg daily, add in some Mk4 at 100-200mg daily (you can buy pure powder and just wing the dosage, mk4 isn't toxic, just don't go over 500mg). IGF-1 Lr3 would work great, it has a low affinity to bind to IGFBP3 and a higher affinity to the IGFR1-2, it's basically IGF-1 on roids. Most importantly, eat. Leptin and Insulin are the most important hormones for growth, keep that in mind.

again, this is all hypothetical, so take what you can from it. Also for those wanting sources, I have a couple of HGH sources, but I don't have sources for IGF-1LR3. I'd LIKE SOME HIGH IQCELLS TO DISCUSS THIS WITH ME.

@JustTrynaGrow @Slyfex8 @draco @Don't Forget to mew @Tom2004 @Crazzen8 @ht-normie-ascending @Dr Shekelberg @forwardgrowth @maxmendietta @PubertyMaxxer @apollothegun @KKK @EthnicelAscension @PrettyBoyMaxxing @Goblin @Alexanderr @Test @RAITEIII @Mateusz74 @DianabolDownie

basically just use aromasin and igf1 lr3 and youre good

 

[Deleted member 26824]

formatting is crazy shitty but will read later

 

[jojo!·"]

esus christ did I hit a nerve or some shit?

mewing is the biggest lookism cope to ever surface, your face is the same from birth, the only difference is it grows, you were recessed from birth if you are recessed in adulthood. Plenty of the most forward grown chad's I know mouth breathe 24/7 with there jaws dropped to the floor
and it doesn't prevent a recession, you were born to be recessed.

not tryna argue but if

your face is the same from birth

then why did michael ceras jaw dissapear into his adulthood

 

[Deleted member 46941]

not reading this gay shit

Just stole 200 $, should I just take 600 mg test weekly and expect more forward growth?

 

[dsheppa]

not reading this gay shit

Just stole 200 $, should I just take 600 mg test weekly and expect more forward growth?

600 a week is insane you’re gonna end up dying bro. But all this shit depends on age tbh. If your under 25 maybe, under 18 probably, if you’re under 15 taking test and/or hgh will definitely improve masculine facial development

 

[Deleted member 46941]

600 a week is insane you’re gonna end up dying bro. But all this shit depends on age tbh. If your under 25 maybe, under 18 probably, if you’re under 15 taking test and/or hgh will definitely improve masculine facial development

No man I was stressed when I wrote this, me and my mom made a deal where she gives me 250 a week. Im 22

 

[letsdoit]

Thoughts @Osie

 

[trueceI]

if you're going to do MSDO, than I'd suggest taking Mk4 and growth hormone.

@9898 do you still suggest this after osteotomies

 

[angrl_r]

Cope

Hgh and steroids might grow your bones

But its more about positioning of the bones,
And harmony

The only way youll position your bones forward and upward is via mewing, chewing, appliances, and osteotomies. Everything else is cope.

If you have the perfect positioning of your facial bones, have a straight nose and wide palate, youre set. Just hghmax and take roids and train your neck, do some bonesmashing on chin and zygos, and get some implants.

Do u have any good cycle recommendation for bone mass?

 

[Deleted member 60453]

Nigger

Even if it doesnt do anything

It doesnt make you more recessed
What dont you understand

Are you utterly thick or disabled?

Mewing is the natural human posture, without it at any age youre going to get recessed, even its by 1mm

Not having posture = recessed face

Fucking hope you die faggot such a low iq

"yeah yeah uh even tho it doesnt do anything it doesnt make you more reccessed lolll" i doubt your above the age of 13 to think that proves anything you just said jfl

 

[ducksoover]

here's my hypothesis for inducing forward craniofacial growth. Not a single soul will read though

first, we need to understand the process of bone metabolism. Bone remodeling (or bone metabolism) is a lifelong process where the mature bone tissue is removed from the skeleton (a process called bone resorption) and new bone tissue is formed. these processes also control the reshaping or replacement of bone following injuries like fractures but also micro-damage, which occurs during normal activity. Remodeling responds also to the functional demands of mechanical loading. Two main cells are responsible for bone remodeling, osteoblasts, and osteoclasts. Osteoblasts secrete new bone, osteoclasts break down old bone.

Our goal is to enhance the process of bone remodeling by altering the osteoblast and osteoclast function, this will only work during puberty, whilst the body is in a state of susceptibility to growth factors. This guide is gonna basically me regurgitating all of my research into one thread, it won't be structured well but take what you can from it.

Okay, firstly, don't fast, restrict caloric intake or eat a shit diet whilst in the midst of pubertal growth. You want to follow a diet high in cholesterol, saturated fats, moderate amounts of protein (animal sourced), and most importantly, high carbohydrate. Eat well above 2500kcal daily, you want to be in a constant state of anabolism, you want your metabolism to be firing, without a functioning thyroid none of what I'm about to tell you will work. you'll need to be constantly eating, specifically carbohydrates like potatoes, tubers, and white rice, don't eat any other source of carbohydrates, stick to tubers and vegetables, involve high amounts of cholesterol from eggs and butter, don't consume polyunsaturated fats at all, they will oxidize in the blood and become free radicals, damaging the Leydig cells and lowering steroid hormone levels within the body. Consume fruits like apples and oranges, eat red meats, specifically beef, some fish here and there. Mainly focus on eating as much cholesterol from eggs and consuming large amounts of carbohydrates from the correct sources before you sleep, don't pig out on high-glycemic carbs, that isn't what I'm suggesting, I'll go into more detail later.

don't restrict calories or fast, this will lower the activity of the mTOR/pi3k/ATK pathways as insulin is vital for the activation of these pathways, fasting and lowering caloric intake will also decrease both insulin and leptin within the body, leptin is the hormone that is released when you have eaten past the point of satiation, my findings suggest that leptin is a potent agonist to osteogenic genotypes, essentially it induces bone formation, remodeling, and mineral disposition, it also increases IGF-1 levels, which is what we want. I can't stress how much eating is necessary for bone remodeling. Correcting your diet is step one, following the diet that I have written above will guarantee that you're inducing a constant state of anabolism, insulin will be released when you consume food, your metabolism with increase, in turn producing t3 and t4, both these thyroid hormones will convert somatropin into IGF-1, IGF-1 and insulin will then stimulate the mTOR1-2/pi3k/ATK pathways, in turn inducing hyperplasia, cell proliferation, hypertrophy and increased level of protein synthesis. Basically through the activation of these pathways, your body will be in a constant state of anabolism.

Pi3k is necessary to promote growth and proliferation over the differentiation of adult stem cells It is the difficulty in finding an appropriate amount of proliferation versus differentiation that researchers are trying to determine in order to utilize this balance in the development of various therapies. The constant spike of insulin and IGF-1 is what keeps these pathways active during adolescence, specifically insulin. To keep it simple, I'd say using exogenous forms of either GH or IGF-1 is enough to enhance the mTOR/pi3k pathways, but if you really want to induce growth. Your best bet is to use experimental chemicals that are known as pi3k agonists/activators. Agonists such as 740-Y-P can be used, these will have a potent stimulatory effect on the anabolic pathways, in combination with constant insulin secretion and high IGF-1, and GH levels, you will experience growth like none other, although I don't recommend the usage of these experimental 'pathway agonists' as they are not researched extensively and can possibly cause cancer due to chronic cell proliferation.

constantly activating the mTOR/pi3k/ATK pathways is vital, keeping these anabolic pathways firing during puberty is important for growth, don't fast and don't restrict calories, keep insulin up, keep metabolism firing and get plenty of deep sleep with the correct circadian rhythms, after puberty you can focus on autophagy and anti-aging protocols.

cortisol is a negative hormone, we don't want it. Glucocorticoids will suppress bone formation via the inhibition of osteoclasts, meaning it'll stop the process of the bone breaking down. We want osteoblasts and osteoclasts to be in a state of equilibrium or homeostasis for better words, we want them to be functioning together, but we want them to be functioning at a higher rate than the normal person. the usage of delta sleep-inducing peptide will block corticotropin from synthesizing cortisol, DSIP will also block somatostatin and upregulate the release of gonadotropin, in turn amplifying the release of luteinizing hormone. This peptide is a must in any protocol, due to the blockage of somatostatin and corticotropin.

dihydrotestosterone and E2 are both needed for bone remodeling, testosterone not so much. Estrogen maintains adult bone mass by inhibiting bone resorption and osteoclast activity, which in theory isn't what we want, again we want homeostasis between osteoblast and osteoclast, both estrogen and cortisol block osteoclast activity and bone resorption from occurring, this is the reason estrogen is promoted as necessary for bone health, if you can't make up for the bone resorption with sufficient bone formation than problems occur. Theoretically, if you wanted to reshape your bones, the best method would be to nuke your estrogen with letrozole, this would decrease osteoclast activity substantially, to the point where bone resorption would be almost impossible, it would also exasperate the effects of osteoblast activity, again we don't want this, we want equilibrium between the two, estrogen is needed in keeping homeostasis between the osteoblasts and osteoclasts, dihydrotestosterone increases osteocalcin activity, in turn inducing bone formation and increasing bone mineral deposition, dihydrotestosterone and estrogen together synergize nicely, DHT will decrease the level of estrogen within the body, but not enough to the point where osteoclast activity is altered, we want bone resorption to occur, so that dht can begin the formation of new bone cells. The problem with administrating DHT alone is that at the dosages that we need to be working with in order to increase osteocalcin and osteoblast activity would nuke our estradiol, so the usage of human-chorionic-gonadotropin should be used in order to increase intra-testicular estrogen and aromatase activity. Keep in mind this is all theoretical, but I'm sure that estrogen and dht synergize when it comes to bone metabolism and remodeling.

again, let me just explain, osteoblasts promote the proliferation of bone cells and the growth of bone, whereas osteoclasts promote resorption of the bone cells, essentially osteoclasts are there to renew the bone by metabolizing bone cells, allowing for new bone to form via osteocytes, osteocalcin, and osteoblast activity. Estrogen effectively inhibits osteoclast activity from occurring, this is why post-menopausal women experience BMD issues as osteoclast activity is at an all-time high due to the lack of estrogen in the women's bodies, osteoclasts are high and osteoblasts are low, meaning constant bone metabolism and no new bone cell proliferation and growth. We don't want to nuke our estrogen as we need it to keep homeostasis

I hypothesize that we need high activity of both osteoclast and osteoblast for bone substantial bone growth, others debate that reshaping the bone requires an overabundance of osteoclast activity and less osteoblast, others debate that osteoblasts should be promoted and osteoclasts should be inhibited. Vitamin K2 has agonistic properties on the nuclear factor-kB signaling pathway. Nf-kB agonists have potent pro-anabolic and anti-catabolic effects on bone cells, essentially when this pathway is activated it decreases bone resorption and upregulates osteoblast activity. vitamin K2 action on osteoblast and osteoclast formation and activity is accomplished by down-regulating basal and cytokine-induced NF-kB activation, by increasing IkB mRNA, Furthermore, vitamin K2 prevents repression by tumor necrosis factor-a (TNFa) of SMAD signaling induced by either transforming growth factor B (TGFB) or bone morphogenetic protein-2 (BMP-2). This is why menopausal women who take vitamin K2 experience great results when it comes to BMD, due to there lowered estrogen activity osteoclasts are high, when MK4 is introduced osteoclast are somewhat inhibited and osteoblast activity is increased, countering the effects of low estradiol.

for a protocol, I'd suggest either 5-7.5iu of growth hormone daily, along with IGF-1 Lr3 50-100mcg daily, add in some Mk4 at 100-200mg daily (you can buy pure powder and just wing the dosage, mk4 isn't toxic, just don't go over 500mg). IGF-1 Lr3 would work great, it has a low affinity to bind to IGFBP3 and a higher affinity to the IGFR1-2, it's basically IGF-1 on roids. Most importantly, eat. Leptin and Insulin are the most important hormones for growth, keep that in mind.

again, this is all hypothetical, so take what you can from it. Also for those wanting sources, I have a couple of HGH sources, but I don't have sources for IGF-1LR3. I'd LIKE SOME HIGH IQCELLS TO DISCUSS THIS WITH ME.

@JustTrynaGrow @Slyfex8 @draco @Don't Forget to mew @Tom2004 @Crazzen8 @ht-normie-ascending @Dr Shekelberg @forwardgrowth @maxmendietta @PubertyMaxxer @apollothegun @KKK @EthnicelAscension @PrettyBoyMaxxing @Goblin @Alexanderr @Test @RAITEIII @Mateusz74 @DianabolDownie

stopped reading when you mentioned to eat high amount of carbs. you are ignorant as fuck.

The human body DOES NOT NEED CARBS. Neither do we need fibre.

Cite any study showing a cause and effect relationship with the positive impact/need for carbohydrates. There isn't any.

Throughout history the groups of people who ate a mostly carbohydrate diet are the ones who lacked forward growth on the face the most, ie indians (high veg diet and some ate 0 meat due to religion) and east asians who have the flattest faces due to the high consumption of RICE and VEGGIES.

Due to these soft foods (carbs) being present in the diet, it meant that the jaw muscles don't have to work as hard, therefore causing recessed facial features. Poor maxillary growth leads to poor undereye support too, it fucks the whole face up.


TLDR: you don't know shit and your input is ruining this forum among with many others.

 

[bobsmith03]

here's my hypothesis for inducing forward craniofacial growth. Not a single soul will read though

first, we need to understand the process of bone metabolism. Bone remodeling (or bone metabolism) is a lifelong process where the mature bone tissue is removed from the skeleton (a process called bone resorption) and new bone tissue is formed. these processes also control the reshaping or replacement of bone following injuries like fractures but also micro-damage, which occurs during normal activity. Remodeling responds also to the functional demands of mechanical loading. Two main cells are responsible for bone remodeling, osteoblasts, and osteoclasts. Osteoblasts secrete new bone, osteoclasts break down old bone.

Our goal is to enhance the process of bone remodeling by altering the osteoblast and osteoclast function, this will only work during puberty, whilst the body is in a state of susceptibility to growth factors. This guide is gonna basically me regurgitating all of my research into one thread, it won't be structured well but take what you can from it.

Okay, firstly, don't fast, restrict caloric intake or eat a shit diet whilst in the midst of pubertal growth. You want to follow a diet high in cholesterol, saturated fats, moderate amounts of protein (animal sourced), and most importantly, high carbohydrate. Eat well above 2500kcal daily, you want to be in a constant state of anabolism, you want your metabolism to be firing, without a functioning thyroid none of what I'm about to tell you will work. you'll need to be constantly eating, specifically carbohydrates like potatoes, tubers, and white rice, don't eat any other source of carbohydrates, stick to tubers and vegetables, involve high amounts of cholesterol from eggs and butter, don't consume polyunsaturated fats at all, they will oxidize in the blood and become free radicals, damaging the Leydig cells and lowering steroid hormone levels within the body. Consume fruits like apples and oranges, eat red meats, specifically beef, some fish here and there. Mainly focus on eating as much cholesterol from eggs and consuming large amounts of carbohydrates from the correct sources before you sleep, don't pig out on high-glycemic carbs, that isn't what I'm suggesting, I'll go into more detail later.

don't restrict calories or fast, this will lower the activity of the mTOR/pi3k/ATK pathways as insulin is vital for the activation of these pathways, fasting and lowering caloric intake will also decrease both insulin and leptin within the body, leptin is the hormone that is released when you have eaten past the point of satiation, my findings suggest that leptin is a potent agonist to osteogenic genotypes, essentially it induces bone formation, remodeling, and mineral disposition, it also increases IGF-1 levels, which is what we want. I can't stress how much eating is necessary for bone remodeling. Correcting your diet is step one, following the diet that I have written above will guarantee that you're inducing a constant state of anabolism, insulin will be released when you consume food, your metabolism with increase, in turn producing t3 and t4, both these thyroid hormones will convert somatropin into IGF-1, IGF-1 and insulin will then stimulate the mTOR1-2/pi3k/ATK pathways, in turn inducing hyperplasia, cell proliferation, hypertrophy and increased level of protein synthesis. Basically through the activation of these pathways, your body will be in a constant state of anabolism.

Pi3k is necessary to promote growth and proliferation over the differentiation of adult stem cells It is the difficulty in finding an appropriate amount of proliferation versus differentiation that researchers are trying to determine in order to utilize this balance in the development of various therapies. The constant spike of insulin and IGF-1 is what keeps these pathways active during adolescence, specifically insulin. To keep it simple, I'd say using exogenous forms of either GH or IGF-1 is enough to enhance the mTOR/pi3k pathways, but if you really want to induce growth. Your best bet is to use experimental chemicals that are known as pi3k agonists/activators. Agonists such as 740-Y-P can be used, these will have a potent stimulatory effect on the anabolic pathways, in combination with constant insulin secretion and high IGF-1, and GH levels, you will experience growth like none other, although I don't recommend the usage of these experimental 'pathway agonists' as they are not researched extensively and can possibly cause cancer due to chronic cell proliferation.

constantly activating the mTOR/pi3k/ATK pathways is vital, keeping these anabolic pathways firing during puberty is important for growth, don't fast and don't restrict calories, keep insulin up, keep metabolism firing and get plenty of deep sleep with the correct circadian rhythms, after puberty you can focus on autophagy and anti-aging protocols.

cortisol is a negative hormone, we don't want it. Glucocorticoids will suppress bone formation via the inhibition of osteoclasts, meaning it'll stop the process of the bone breaking down. We want osteoblasts and osteoclasts to be in a state of equilibrium or homeostasis for better words, we want them to be functioning together, but we want them to be functioning at a higher rate than the normal person. the usage of delta sleep-inducing peptide will block corticotropin from synthesizing cortisol, DSIP will also block somatostatin and upregulate the release of gonadotropin, in turn amplifying the release of luteinizing hormone. This peptide is a must in any protocol, due to the blockage of somatostatin and corticotropin.

dihydrotestosterone and E2 are both needed for bone remodeling, testosterone not so much. Estrogen maintains adult bone mass by inhibiting bone resorption and osteoclast activity, which in theory isn't what we want, again we want homeostasis between osteoblast and osteoclast, both estrogen and cortisol block osteoclast activity and bone resorption from occurring, this is the reason estrogen is promoted as necessary for bone health, if you can't make up for the bone resorption with sufficient bone formation than problems occur. Theoretically, if you wanted to reshape your bones, the best method would be to nuke your estrogen with letrozole, this would decrease osteoclast activity substantially, to the point where bone resorption would be almost impossible, it would also exasperate the effects of osteoblast activity, again we don't want this, we want equilibrium between the two, estrogen is needed in keeping homeostasis between the osteoblasts and osteoclasts, dihydrotestosterone increases osteocalcin activity, in turn inducing bone formation and increasing bone mineral deposition, dihydrotestosterone and estrogen together synergize nicely, DHT will decrease the level of estrogen within the body, but not enough to the point where osteoclast activity is altered, we want bone resorption to occur, so that dht can begin the formation of new bone cells. The problem with administrating DHT alone is that at the dosages that we need to be working with in order to increase osteocalcin and osteoblast activity would nuke our estradiol, so the usage of human-chorionic-gonadotropin should be used in order to increase intra-testicular estrogen and aromatase activity. Keep in mind this is all theoretical, but I'm sure that estrogen and dht synergize when it comes to bone metabolism and remodeling.

again, let me just explain, osteoblasts promote the proliferation of bone cells and the growth of bone, whereas osteoclasts promote resorption of the bone cells, essentially osteoclasts are there to renew the bone by metabolizing bone cells, allowing for new bone to form via osteocytes, osteocalcin, and osteoblast activity. Estrogen effectively inhibits osteoclast activity from occurring, this is why post-menopausal women experience BMD issues as osteoclast activity is at an all-time high due to the lack of estrogen in the women's bodies, osteoclasts are high and osteoblasts are low, meaning constant bone metabolism and no new bone cell proliferation and growth. We don't want to nuke our estrogen as we need it to keep homeostasis

I hypothesize that we need high activity of both osteoclast and osteoblast for bone substantial bone growth, others debate that reshaping the bone requires an overabundance of osteoclast activity and less osteoblast, others debate that osteoblasts should be promoted and osteoclasts should be inhibited. Vitamin K2 has agonistic properties on the nuclear factor-kB signaling pathway. Nf-kB agonists have potent pro-anabolic and anti-catabolic effects on bone cells, essentially when this pathway is activated it decreases bone resorption and upregulates osteoblast activity. vitamin K2 action on osteoblast and osteoclast formation and activity is accomplished by down-regulating basal and cytokine-induced NF-kB activation, by increasing IkB mRNA, Furthermore, vitamin K2 prevents repression by tumor necrosis factor-a (TNFa) of SMAD signaling induced by either transforming growth factor B (TGFB) or bone morphogenetic protein-2 (BMP-2). This is why menopausal women who take vitamin K2 experience great results when it comes to BMD, due to there lowered estrogen activity osteoclasts are high, when MK4 is introduced osteoclast are somewhat inhibited and osteoblast activity is increased, countering the effects of low estradiol.

for a protocol, I'd suggest either 5-7.5iu of growth hormone daily, along with IGF-1 Lr3 50-100mcg daily, add in some Mk4 at 100-200mg daily (you can buy pure powder and just wing the dosage, mk4 isn't toxic, just don't go over 500mg). IGF-1 Lr3 would work great, it has a low affinity to bind to IGFBP3 and a higher affinity to the IGFR1-2, it's basically IGF-1 on roids. Most importantly, eat. Leptin and Insulin are the most important hormones for growth, keep that in mind.

again, this is all hypothetical, so take what you can from it. Also for those wanting sources, I have a couple of HGH sources, but I don't have sources for IGF-1LR3. I'd LIKE SOME HIGH IQCELLS TO DISCUSS THIS WITH ME.

@JustTrynaGrow @Slyfex8 @draco @Don't Forget to mew @Tom2004 @Crazzen8 @ht-normie-ascending @Dr Shekelberg @forwardgrowth @maxmendietta @PubertyMaxxer @apollothegun @KKK @EthnicelAscension @PrettyBoyMaxxing @Goblin @Alexanderr @Test @RAITEIII @Mateusz74 @DianabolDownie

does this work for ppl over 18?

 

[EsteMog]

here's my hypothesis for inducing forward craniofacial growth. Not a single soul will read though

first, we need to understand the process of bone metabolism. Bone remodeling (or bone metabolism) is a lifelong process where the mature bone tissue is removed from the skeleton (a process called bone resorption) and new bone tissue is formed. these processes also control the reshaping or replacement of bone following injuries like fractures but also micro-damage, which occurs during normal activity. Remodeling responds also to the functional demands of mechanical loading. Two main cells are responsible for bone remodeling, osteoblasts, and osteoclasts. Osteoblasts secrete new bone, osteoclasts break down old bone.

Our goal is to enhance the process of bone remodeling by altering the osteoblast and osteoclast function, this will only work during puberty, whilst the body is in a state of susceptibility to growth factors. This guide is gonna basically me regurgitating all of my research into one thread, it won't be structured well but take what you can from it.

Okay, firstly, don't fast, restrict caloric intake or eat a shit diet whilst in the midst of pubertal growth. You want to follow a diet high in cholesterol, saturated fats, moderate amounts of protein (animal sourced), and most importantly, high carbohydrate. Eat well above 2500kcal daily, you want to be in a constant state of anabolism, you want your metabolism to be firing, without a functioning thyroid none of what I'm about to tell you will work. you'll need to be constantly eating, specifically carbohydrates like potatoes, tubers, and white rice, don't eat any other source of carbohydrates, stick to tubers and vegetables, involve high amounts of cholesterol from eggs and butter, don't consume polyunsaturated fats at all, they will oxidize in the blood and become free radicals, damaging the Leydig cells and lowering steroid hormone levels within the body. Consume fruits like apples and oranges, eat red meats, specifically beef, some fish here and there. Mainly focus on eating as much cholesterol from eggs and consuming large amounts of carbohydrates from the correct sources before you sleep, don't pig out on high-glycemic carbs, that isn't what I'm suggesting, I'll go into more detail later.

don't restrict calories or fast, this will lower the activity of the mTOR/pi3k/ATK pathways as insulin is vital for the activation of these pathways, fasting and lowering caloric intake will also decrease both insulin and leptin within the body, leptin is the hormone that is released when you have eaten past the point of satiation, my findings suggest that leptin is a potent agonist to osteogenic genotypes, essentially it induces bone formation, remodeling, and mineral disposition, it also increases IGF-1 levels, which is what we want. I can't stress how much eating is necessary for bone remodeling. Correcting your diet is step one, following the diet that I have written above will guarantee that you're inducing a constant state of anabolism, insulin will be released when you consume food, your metabolism with increase, in turn producing t3 and t4, both these thyroid hormones will convert somatropin into IGF-1, IGF-1 and insulin will then stimulate the mTOR1-2/pi3k/ATK pathways, in turn inducing hyperplasia, cell proliferation, hypertrophy and increased level of protein synthesis. Basically through the activation of these pathways, your body will be in a constant state of anabolism.

Pi3k is necessary to promote growth and proliferation over the differentiation of adult stem cells It is the difficulty in finding an appropriate amount of proliferation versus differentiation that researchers are trying to determine in order to utilize this balance in the development of various therapies. The constant spike of insulin and IGF-1 is what keeps these pathways active during adolescence, specifically insulin. To keep it simple, I'd say using exogenous forms of either GH or IGF-1 is enough to enhance the mTOR/pi3k pathways, but if you really want to induce growth. Your best bet is to use experimental chemicals that are known as pi3k agonists/activators. Agonists such as 740-Y-P can be used, these will have a potent stimulatory effect on the anabolic pathways, in combination with constant insulin secretion and high IGF-1, and GH levels, you will experience growth like none other, although I don't recommend the usage of these experimental 'pathway agonists' as they are not researched extensively and can possibly cause cancer due to chronic cell proliferation.

constantly activating the mTOR/pi3k/ATK pathways is vital, keeping these anabolic pathways firing during puberty is important for growth, don't fast and don't restrict calories, keep insulin up, keep metabolism firing and get plenty of deep sleep with the correct circadian rhythms, after puberty you can focus on autophagy and anti-aging protocols.

cortisol is a negative hormone, we don't want it. Glucocorticoids will suppress bone formation via the inhibition of osteoclasts, meaning it'll stop the process of the bone breaking down. We want osteoblasts and osteoclasts to be in a state of equilibrium or homeostasis for better words, we want them to be functioning together, but we want them to be functioning at a higher rate than the normal person. the usage of delta sleep-inducing peptide will block corticotropin from synthesizing cortisol, DSIP will also block somatostatin and upregulate the release of gonadotropin, in turn amplifying the release of luteinizing hormone. This peptide is a must in any protocol, due to the blockage of somatostatin and corticotropin.

dihydrotestosterone and E2 are both needed for bone remodeling, testosterone not so much. Estrogen maintains adult bone mass by inhibiting bone resorption and osteoclast activity, which in theory isn't what we want, again we want homeostasis between osteoblast and osteoclast, both estrogen and cortisol block osteoclast activity and bone resorption from occurring, this is the reason estrogen is promoted as necessary for bone health, if you can't make up for the bone resorption with sufficient bone formation than problems occur. Theoretically, if you wanted to reshape your bones, the best method would be to nuke your estrogen with letrozole, this would decrease osteoclast activity substantially, to the point where bone resorption would be almost impossible, it would also exasperate the effects of osteoblast activity, again we don't want this, we want equilibrium between the two, estrogen is needed in keeping homeostasis between the osteoblasts and osteoclasts, dihydrotestosterone increases osteocalcin activity, in turn inducing bone formation and increasing bone mineral deposition, dihydrotestosterone and estrogen together synergize nicely, DHT will decrease the level of estrogen within the body, but not enough to the point where osteoclast activity is altered, we want bone resorption to occur, so that dht can begin the formation of new bone cells. The problem with administrating DHT alone is that at the dosages that we need to be working with in order to increase osteocalcin and osteoblast activity would nuke our estradiol, so the usage of human-chorionic-gonadotropin should be used in order to increase intra-testicular estrogen and aromatase activity. Keep in mind this is all theoretical, but I'm sure that estrogen and dht synergize when it comes to bone metabolism and remodeling.

again, let me just explain, osteoblasts promote the proliferation of bone cells and the growth of bone, whereas osteoclasts promote resorption of the bone cells, essentially osteoclasts are there to renew the bone by metabolizing bone cells, allowing for new bone to form via osteocytes, osteocalcin, and osteoblast activity. Estrogen effectively inhibits osteoclast activity from occurring, this is why post-menopausal women experience BMD issues as osteoclast activity is at an all-time high due to the lack of estrogen in the women's bodies, osteoclasts are high and osteoblasts are low, meaning constant bone metabolism and no new bone cell proliferation and growth. We don't want to nuke our estrogen as we need it to keep homeostasis

I hypothesize that we need high activity of both osteoclast and osteoblast for bone substantial bone growth, others debate that reshaping the bone requires an overabundance of osteoclast activity and less osteoblast, others debate that osteoblasts should be promoted and osteoclasts should be inhibited. Vitamin K2 has agonistic properties on the nuclear factor-kB signaling pathway. Nf-kB agonists have potent pro-anabolic and anti-catabolic effects on bone cells, essentially when this pathway is activated it decreases bone resorption and upregulates osteoblast activity. vitamin K2 action on osteoblast and osteoclast formation and activity is accomplished by down-regulating basal and cytokine-induced NF-kB activation, by increasing IkB mRNA, Furthermore, vitamin K2 prevents repression by tumor necrosis factor-a (TNFa) of SMAD signaling induced by either transforming growth factor B (TGFB) or bone morphogenetic protein-2 (BMP-2). This is why menopausal women who take vitamin K2 experience great results when it comes to BMD, due to there lowered estrogen activity osteoclasts are high, when MK4 is introduced osteoclast are somewhat inhibited and osteoblast activity is increased, countering the effects of low estradiol.

for a protocol, I'd suggest either 5-7.5iu of growth hormone daily, along with IGF-1 Lr3 50-100mcg daily, add in some Mk4 at 100-200mg daily (you can buy pure powder and just wing the dosage, mk4 isn't toxic, just don't go over 500mg). IGF-1 Lr3 would work great, it has a low affinity to bind to IGFBP3 and a higher affinity to the IGFR1-2, it's basically IGF-1 on roids. Most importantly, eat. Leptin and Insulin are the most important hormones for growth, keep that in mind.

again, this is all hypothetical, so take what you can from it. Also for those wanting sources, I have a couple of HGH sources, but I don't have sources for IGF-1LR3. I'd LIKE SOME HIGH IQCELLS TO DISCUSS THIS WITH ME.

@JustTrynaGrow @Slyfex8 @draco @Don't Forget to mew @Tom2004 @Crazzen8 @ht-normie-ascending @Dr Shekelberg @forwardgrowth @maxmendietta @PubertyMaxxer @apollothegun @KKK @EthnicelAscension @PrettyBoyMaxxing @Goblin @Alexanderr @Test @RAITEIII @Mateusz74 @DianabolDownie

https://www.peptidesciences.com/igf-1-lr3-1mg looks like a good source. Im thinking of using a dht derivative and hgh for height and looksmaxxing. would I even need an ai since dot lowers e and should I add igf1 lr3 for this?