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

if you're going to do MSDO, than I'd suggest taking Mk4 and growth hormone.
What will the effects be? Will it speed the process? Or it’ll promote new bone growth. I honestly believe if you cut the mandible in half and the suture is split then it is a great time to supplement and hard Mew as if your life depended on it and to top it with FacePulling
 
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What will the effects be? Will it speed the process? Or it’ll promote new bone growth. I honestly believe if you cut the mandible in half and the suture is split then it is a great time to supplement and hard Mew as if your life depended on it and to top it with FacePulling
MK4 will inhibit the osteoclasts from metabolizing bone, it'll also upregulate osteoblast activity, meaning more bone is being created than it is being metabolized and broken down, adding in some growth hormone will basically exasperate the cell proliferative effects of MK4.
 
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MK4 will inhibit the osteoclasts from metabolizing bone, it'll also upregulate osteoblast activity, meaning more bone is being created than it is being metabolized and broken down, adding in some growth hormone will basically exasperate the cell proliferative effects of MK4.
Why take MK4 if it’s an inhibitor unless I didn’t understand this well so MK4 in conjunction with Growth hormone will have crazy bone regenerative benefits?
 
Why take MK4 if it’s an inhibitor unless I didn’t understand this well so MK4 in conjunction with Growth hormone will have crazy bone regenerative benefits?
no, here me out.

the activation of the nuclear factor-kB (NF-kB) signal transduction pathway is essential for osteoclast formation and bone resorption, mk4 downregulates cytokine-induced NF-kB activation, by increasing IkB mRNA, in a y-carboxylation-independent manner, through this process mk4 has pro-anabolic anti-catabolic properties, again, osteoblasts promote bone cell proliferation, whereas osteoclasts promote the metabolism of current bone cells, mk4 effectively inhibits an essential pathway that is vital for osteoclast activity.

if you were to get MSDO, your best bet would be to inhibit osteoclasts and upregulate osteoblasts, IGF-1 has cell proliferative effects in every single part of the body, including bone, in combination with Mk4 you'd reap very positive results.
 
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here's my hypothesis for inducing forward craniofacial growth. Not a single soul will read though :feelswhy:

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
Interesting, so how would you counteract the damage you are doing to your body during this process? That's why people go bald, there organs can't operate well enough to satisfy bloods requirements.
 
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Interesting, so how would you counteract the damage you are doing to your body during this process? That's why people go bald, there organs can't operate well enough to satisfy bloods requirements.
chad > some small damage to your body.
 
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chad > some small damage to your body.
Think about that a little more. Chad is the perfect being right? would the perfect being be damaged?

It's also important to keep in mind how easy it is to fuck up your hair. Theirs around 30 different causes it's not just genetic.
 
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Ban this faggot

Thinks mouthbreathing doesnt affect facial growth

Even if you think mewing is cope, thinking mouth breathing doesnt effect facial growth makes me want to beat the shit out of you
Yh lol mewing makes a difference for teenagers

no one is “recessed” from birth you just can’t be lol

ever race has forward grown faces from mewing at birth
That site isnt even secure lol jfl

how can someone spend hundreds on a site that Doesn’t even have basic security

and that isn’t your source either ik that for sure
 
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Aren't bones in the face supposed to never fuse ?
 
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No one here from 2016 lookism? I remember there was the user Lono who did research and found out that all this bone remodeling stuff is cope, its mainly determined by the protein sclerostin. There are sclerostin inhibitor drugs on the market now but there like $120 a month, and obviously thats via prescription for osteoporosis. If you look at the diseases where sclerostin is inhibited, they're terrible disfigured but they have an extremely high amount of bone mass and volume in certain areas.

In theory, a sclerostin inhibitor + bonesmashing may work for bone growth.
 
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No one here from 2016 lookism? I remember there was the user Lono who did research and found out that all this bone remodeling stuff is cope, its mainly determined by the protein sclerostin. There are sclerostin inhibitor drugs on the market now but there like $120 a month, and obviously thats via prescription for osteoporosis. If you look at the diseases where sclerostin is inhibited, they're terrible disfigured but they have an extremely high amount of bone mass and volume in certain areas.

In theory, a sclerostin inhibitor + bonesmashing may work for bone growth.
not bonesmashing.

but a sclerostin inhibitor in combination with everything I've written in the thread.
 
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dn read
 
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Excellent info. Posts like these inspire to take action and further research

The thing about endocrinology is that, it's a complex clockwork in the body where altering a thing has many other affects.

Because of this the learning curve is fucked up and a ton of information is needed before experimenting. This stops majority of normal people from trying this stuff out for aesthetic gains.

I hope in future, when we understand the human biology to the core... Going hormones way for aesthetics would be as common as implants and fillers.
 
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not bonesmashing.

but a sclerostin inhibitor in combination with everything I've written in the thread.

You wouldnt need the other stuff from what I understand. Bone smashing as well as heavy lifting has been shown to increase the density of bone, its possible that with a sclerostin inhibitor this would translate to essentially bone scabs being formed.
not bonesmashing.

but a sclerostin inhibitor in combination with everything I've written in the thread.

I think a sclerostin inhibito may be adequate, but the stuff you added would speed up the process. And bone smashing may work, seeing as heavy lifting or even playing tennis has been shown to increase bone density with the bones involved. Also, martial artists have higher bone densities on their hand, so this would support bone smashing: https://www.hindawi.com/journals/isrn/2013/185090/
 
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sorry for being offtopic but who is that guy from your avi?
 
here's my hypothesis for inducing forward craniofacial growth. Not a single soul will read though :feelswhy:

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
Read every word, great thread.




Although, Im one of the people who say activate osteoblasts, inhibit osteoclasts.

Its safer, although I get your take. More bone mass is very important for facial aesthetics imo
 
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Read every word, great thread.




Although, Im one of the people who say activate osteoblasts, inhibit osteoclasts.

Its safer, although I get your take. More bone mass is very important for facial aesthetics imo
thanks, and yeah, i've come to that conclusion aswell.
sorry for being offtopic but who is that guy from your avi?
I don't actually know, sorry mate.
 
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Bookmarked, will read everything with your pubertymaxxing thread after work
 
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As a birdcel suffering from no browridge and no forward growth,did read
 
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Why does your protocol not include DSIP peptide?

Would you recommend me the flowing Chemical Protocol? @Dyorotic2

7.5-10 iu Puretropin HGH ed
12.5mg Aromasin e2d
250mcg DSIP ed
1-2 Drops Titan DHT Gel on Dick ed
 
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well considering mk677 is a ghrelin agonist, it does make sense.

but you're going to get far better results by just injecting growth hormone and IGF-1.
Why though, why would the results be different when it's not exogenous.
 
here's my hypothesis for inducing forward craniofacial growth. Not a single soul will read though :feelswhy:

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 post, I wish I wasnt retarded in biolgoy
Can't the staff make it so unregistered users can't see threads? I bet AstroSky is reading this as we breath.
For real
Would k2 mk7 work as well? Cause mk4 cant be found where I live
 
Why does your protocol not include DSIP peptide?

Would you recommend me the flowing Chemical Protocol? @Dyorotic2

7.5-10 iu Puretropin HGH ed
12.5mg Aromasin e2d
250mcg DSIP ed
1-2 Drops Titan DHT Gel on Dick ed
@KKK @BackFromTheMogging @karbo @Slyfex8 @GarixTheChad pls answer
 
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I guess you're dying then.

and now this isn't really coping. An ugly kid can go through puberty and come out 6.5psl.
So true lmao, people used to run away from my ugly ass a kid, but after puberty all of a sudden I became a popular kid. that is what blackpilled me
@KKK @BackFromTheMogging @karbo @Slyfex8 @GarixTheChad pls answer
I am not high IQ chemcel but it looks good to me. I would run that
 
I read through all your shit but u never fucking respond to questions lol
 
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I have neglected my k2 consumption in the last 6 months. And I still haven't done anything about growth hormone substitutes in my laziness.

But just as confident as I have been back then, so am I now that they are going to assist me greatly in my chewing ascencion.
 
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Very good post imo (did read). I've been looking into this quite a bit since I am cursed with the long face death sentence. I remember reading a few papers on pathways of bone remodeling and how to augment them. I'll try to look for them again but your post seems to be in line in what I was reading previously (roles of igf1, E2, etc). I think one thing you should mention is that you should be including a fairly high amount of bone comprising minerals (basically calcium, boron, etc) that are incorporated into the "newly-formed" bone. When you have a large amount of osteoclast activity, increasing the amount of ingredients which are used to remake new bone is probably good (harmless either way).

Btw tag me when u make threads like this, I'm very interested in modifying craniofacial growth.
From what I remember when I rated you, midface wasn't the main issue, it was having a narrow face/skull.
 
From what I remember when I rated you, midface wasn't the main issue, it was having a narrow face/skull.

Yea it is for sure. My midface isn’t particularly long (and LeFort would shorten it bc I have maxillary excess). I’m not sure what can even be done about having a narrow face tho?
 
so for facepulling since im trying to pull the bone forward and not really create new bone is increasing GH/igf-1 and taking calcium mk4 and d3 the right play? @Dyorotic2
 
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@Dyorotic2 are there any sides to taking this stuff or major health risks? You seem to of researched tf out of this and it reaped the benefits at a young age . Being the only youngin to take gh and dht u gotta share some experience like what exactly happend for you I know you grew but like facial bone wise did u ascend
 
Where can u buy k2 mk4 in powder form?
Ive not seen any which is more than 15mg capsules
 
Did ur face change?
You are doing it for like 4 months now
 
Mk4 seems to be quite expensive if you take above 40 mg. Most of the supplies don't intend on people chewing through it so quickly so maybe we gotta buy it directly from the lab.

On another note, if I take mk4 at that dose WITHOUT vitamin D I feel aches in my jaw and joints. Not a good sign, so be careful. It's probably needed along with all the other fat solubles in order for it to be utilized by the body
 
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Yea it is for sure. My midface isn’t particularly long (and LeFort would shorten it bc I have maxillary excess). I’m not sure what can even be done about having a narrow face tho?
MSE
 
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Haven't read yet, but being the high iqcel I am, I think that by increasing GH and DHT, bone plasticity definitely increases, but this by itself isn't going to do shit. If you have high HGH and DHT levels and have high K2 levels , bonesmashing will give visible results. Practically unsound, but theoretically sound notion.
 
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hey bro, do you got a source for dht and HGH? i'd like a source bro, can i also pm you for that source, thanks bro.

hey also, a couple questions, is there any side effects from taking dht and HGH? will i bald if i take it? also i'm scared that im gonna stop my natural hormones from working and my balls will shrink, is that true? i don't want my hormones to stop, also am i going to bald ? thanks bro i can pm you for sources
 
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damn im always late to the party, so hgh+igf-1 lr3 can induce growth in facebones but not in spine or leg bones, interesting..
 
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here's my hypothesis for inducing forward craniofacial growth. Not a single soul will read though :feelswhy:

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
what age puberty stop?
 
what age puberty stop?
like 18-20, but thanks to my new stack i am going to give myself induced delayed puberty even if i am at tanner stage 4, so for me my puberty will only be completed at like my very late 20's like 27-28 if i decide to take it that long (which i definitely won't lol)
I now have access to 25 mcg of synethic t3 thyroid, one of dr sam robbins video on how to grow mentions that you need small amounts of t3 and t4 thyroid plus AI and HGH and IGF-1 to yield best growth results, (side note: t4 is unnecessary as it converts to t3 anyway and IGF-1 LR3 is IGF-1 on roids) and I get it, high thyroid will cause hyperthyroidism while low will cause hypothyroidism, how much would i need to help my body support all this supra physiological levels of HGH
 
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like 18-20, but thanks to my new stack i am going to give myself induced delayed puberty even if i am at tanner stage 4, so for me my puberty will only be completed at like my very late 20's like 27-28 if i decide to take it that long (which i definitely won't lol)
I now have access to 25 mcg of synethic t3 thyroid, one of dr sam robbins video on how to grow mentions that you need small amounts of t3 and t4 thyroid plus AI and HGH and IGF-1 to yield best growth results, (side note: t4 is unnecessary as it converts to t3 anyway and IGF-1 LR3 is IGF-1 on roids) and I get it, high thyroid will cause hyperthyroidism while low will cause hypothyroidism, how much would i need to help my body support all this supra physiological levels of HGH
So you can make puberty longer
 
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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.
very cool. how about a diet and lifestyle protocol as well? god bless :feelsokman:
 
damn im always late to the party, so hgh+igf-1 lr3 can induce growth in facebones but not in spine or leg bones, interesting..
I don't know whether or not you're just being a cunt, you seem to always try and contradict everything I say.

yes, facial bone never stops growing, the skull can enlargen over time, bone mass can increase. Femur bones cannot once the plates have closed.
 
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My bones are perfectly fine, the problem is the placement of them
 
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I don't know whether or not you're just being a cunt, you seem to always try and contradict everything I say.

yes, facial bone never stops growing, the skull can enlargen over time, bone mass can increase. Femur bones cannot once the plates have closed.
did u take an AI while you were on your stack
 
did u take an AI while you were on your stack
No, Aromatase inhibitors are dangerous and stupid. I use high dosages of dihydrotestosterone, basically antagonizes estrogen in all tissue. My E2 came back in very low, I don't think an Aromatase inhibitor would be needed. I just bought a huge amount of somatropin and gonna be blasting 15IU's daily. Along with an acetylcholinesterase inhibitor and some sort of GHRH analog to further antagonize somatostatin activity. Currently researching a possible somatostatin receptor subtype antagonist, could be big.
 
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No, Aromatase inhibitors are dangerous and stupid. I use high dosages of dihydrotestosterone, basically antagonizes estrogen in all tissue. My E2 came back in very low, I don't think an Aromatase inhibitor would be needed. I just bought a huge amount of somatropin and gonna be blasting 15IU's daily. Along with an acetylcholinesterase inhibitor and some sort of GHRH analog to further antagonize somatostatin activity. Currently researching a possible somatostatin receptor subtype antagonist, could be big.
just inject BMP-7, research this noggin/ osteogenic protein, it inhibits BMP-7, research how the genetics regulate it so it can control your growth, and research to what extent it can control your long bone growth (with open growth plates) of course, There's far more to this that you haven't researched yet, somatropin IGF-1 and thyroid is all you need to control, those are the only factors the gigantism mutation affects
 
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just inject BMP-7, research this noggin/ osteogenic protein, it inhibits BMP-7, research how the genetics regulate it so it can control your growth, and research to what extent it can control your long bone growth (with open growth plates) of course, There's far more to this that you haven't researched yet, somatropin IGF-1 and thyroid is all you need to control, those are the only factors the gigantism mutation affects
Oh yes, just inject rBMP-7.

are you retarded, that shit is insanely expensive and you'll never be able to get your hands on pharmaceutical grade.
 
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Oh yes, just inject rBMP-7.

are you retarded, that shit is insanely expensive and you'll never be able to get your hands on pharmaceutical grade.
russian star peptides used to sell it and it worked
 
russian star peptides used to sell it and it worked
nope, Russian star peptides is a total and utter scam, they've shilled their products on a multitude of forum's particularly forums revolving around maximizing height.

Also what's your current stack?
 

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