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

[the one who mogges]

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.

thx man

 

[walidthelooksmaxxer]

no fasting or calorie restricting? do u want me a 16yo fat bloatcel?

 

[unknownslayer--]

brutal cope, dht has 0 efect on bones

 

[TrveShortcel]

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

I’m a retard and should be skinned alive for being one groyper

 

[testosterone36]

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

so eat clean carbs and boost igf
what if i just sprint 3 times a week

 

[kukkeli1234]

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

Is there any way to get HGH prescribed

 

[IncelMaxxer]

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

until what age does this work?