got.daim
𝕯𝖝𝕯 𝖈𝖗𝖊𝖜 bio.site/0w0
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Hypothesis: You can increase facial dimorphism and development.
Results:
I've got over 100 studies accumulated on this subject btw.
First of all, we need to know that the face is constituted by trabecular bone, or cancellous bone. NOT the same bone that is in the growth plates.
This is merely the tip of my research but in the end it all added up, it's true steroids will make the face more masculine however they are simply not enough there is SO much more you can do..
Since i'm really fucking sleepy I'll leave you with some links, tomorrow I'll make sense of it.
Keep in mind my primary objective is increasing facial width, lower third and chin size. You can REALLY increase them, a LOT if you know what you're doing.
SOME links which guided me:
Also this: " While failing to replicate associations between testosterone measures and perceived facial masculinity, Pound et al. (2009) observed that reactive, but not baseline, testosterone was positively associated with a global facial masculinity measure.
It is noteworthy that the association between baseline testosterone and facial masculinity also showed a positive trend towards statistical signifcance in this study, suggesting that the relationship between face shape and baseline testosterone might not be completely absent, but instead may reflect a weaker link than the association with reactive testosterone" "If facial bone structure is affected by testosterone levels during puberty it is possible that total tissue exposure to the hormone is more closely aligned with appearance outcomes than baseline measures (see Pound et al., 2009 for a similar argument).
Fuck it i'll just give you a glimpse of what you have to target:
leptin, test, dht, insulin, igf-1 and hgh, dhea, cortisol and oestrogen.
How?
Here's what you have to take (I'll figure out the dosages and timing soon).
Aromatase inhibitors (Alternated, timing is KEY) Will explain more since you should notice that DHT has diminishing effects with time:
"These findings demonstate that androgens stimulate mineralization and that DHT is more active when used for short periods of time and in early stages of bone development in matrix-induced implants."
IGF-1 stimulating supplements and drugs
Vitamin MK 7 (And A LOT of it)
Zync
Alendronic Acid
Vitamin D 1000IU (Need to compensate with much higher MK levels)
Niacin vitamin B3 WITH flush?
Melatonin (Will help you get the sleep and also with some HGH release)
Parathyroid hormone (For no longer than 6 months)
DHEA
Mild cortisol blockers if needed.
Correct nutrition and exercise, NO intermittent fasting, a constant anabolic state.
And of course one of my GREATEST off-label finds, a lipus machine, after seeing this: "It's envisaged that the device could also be deployed to treat microsomia, a congenital underdevelopment of the lower jaw."
You can apply it instead on your zygomatic arches. There is a study I have in which a lipus machine had great success in growing patient's jaws when used specifically for that purpose.
You can also use LSJL for wrist thickness, as it will increase it.
You'll want pubertal levels of those hormones, and you'll see a dramatic increase in face width mostly at the zygomatic arches, don't worry about igf-1 making your face even longer, because I've found that your typical acromegaly long face is actually due to very high igf-1 levels but it's the hypogonadism that makes it that way. Therefore your face will grow a bit in lenght at your lower third but to compensate it will grow even more at the zygomatic arches due to high levels of test/dht compared to oestrogen.
Tomorrow I'll post the complete proof, there is only one problem though. You can really change your face, but it will cost you, probably a lot of money. Still FAR cheaper than surgery though.
When does the "face" stop growing?
Notel: the face is made up of cancellous bone, synonymous with trabecular bone or spongy bone, of which you should know the basic constitution in order to read this article. http://en.wikipedia.org/wiki/Cancellous bone Note2: for purposes of understanding, the end of puberty corresponds to the end of linear growth.
We conclude that growth in the face does not actually STOP after puberty, it merely slows down until it becomes insignificant. This is important because unlike growth plates, this type of bone retains the proliferative potential.
Why is it then that face growth slows down, even when testosterone levels after puberty do not drop?
There are in fact, two MAJOR explanations for this and I'll start with the first one:
After puberty, the pituitary gland stops producing the amounts of HGH it did which leads to decreased cell proliferation due to lowered IGF-1 levels. When it doesn't a condition referred to as acromegaly occurs. That alone is proof enough for growth of the face after puberty. However there are many other hormones involved in the process such as: leptin, IGF-1, testosterone and DHT, DHEA, estrogen and ostrogen, and cortisol.
The second one comes from an endocrinology book I downloaded, which explains the effects of estrogens on cancellous bone:
"Maintenance of a focal balance between formation and resorption (by estrogens), on the other hand, apparently results from opposite effects of estrogens on the life span of osteoclasts and osteoblasts/ osteocytes: a propoptotic effect on osteoclasts and an antiapoptotic effect on osteoblasts and osteocytes" Therefore, the more estrogens, the more bone will tend to maintain a balance between proliferation and resorption of cells, in order to get a healthy balance. Of course, this can easily be altered.
So when does the face stop growing? The answer is simply never.
We now need to grow the face. For aesthetic purposes, I will focus on increasing face width, rather than length, in my next cover all the variables, feel free to ask any questions.
Note3: estrogens are actually needed for bone growth, while too much is bad, they do have an anabolic effect on bone.
Note4: IGF-1 will make overall face size increase, not just length, the reason you might think that is that while people with acromegaly tend to have longer faces, they also suffer from hypogonadism in most cases. In fact cheekbone growth is a reported effect of acromegaly, when coupled with normal to high testosterone levels.
From here on out there wont be any fancy colors because I got lazy and gave up.
For this post I'll describe the various effects of recommended drugs and outline a plan:
We now have confirmation that a process similar to growth plate fusion does not occur for the trabecular bone which make of facial structure, now we need to know how to induce the changes we desire. It is already commonly known that sex hormones influence the development of the face, but what isn't generally known is the they have non genomic effects. This will be very important.
What is really important are these 4 crucial points.
"Proof-of-concept for AR action is demonstrated in androgen-insensitivity models, with production of a nonfunctional AR associated with a dramatic reduction in total bone mass in humans even with excellent estrogen compliance. AR null mice have high turnover osteopenia with increased formation but even stronger enhancement of resorption"
Oestrogen is there to prevent bone resorption. That is it's main function.
"Targeted AR overexpression in the skeleton further supports these findings, as it results in enhanced periosteal formation, reduced endosteal formation, increased trabecular bone formation and a reduction of osteoclast activity, all without changes in circulating steroid levels."
We are aiming for trabecular bone increase. AR signalling does that.
"Estrogens are thought to maintain adult bone mass predominantly through inhibition of bone resorption by osteoclasts (i.e. they act as anti-resorptive agents), which protect the skeleton from further loss of bone. Non-aromatizable androgens such as 5a-dihydrotestosterone (DHT), conversely, are anabolic agents that increase bone mass by stimulation of bone formation, and thus represent an important therapeutic class that has the potential to rebuild lost bone."
Well, there you have it!
On leptin, I'll conclude later on this as I'm still studying it.
On the sex hormones:
"Testosterone can regulate the skeleton through direct activation of androgen receptor (AR), as well as indirect activation of oestrogen receptor (ER) after testosterone is converted to ostrogen in the body. AR seems to play a major part in mediating the effects of testosterone on both trabecular and periosteal bone, although ER contributes to the optimal response to testosterone in periosteal bone growth."
The nitric oxide pathway can be targeted to avoid the bone resportion.
You'll want low cortisol levels:
Cortisol decreases bone formation by inhibiting periosteal cell proliferation. Simple. Same applied to trabecular bone.
However! Estrogen still has an anabolic effect on bone. This is a recent discovery.
Estrogen maintains trabecular bone volume in rats not only by suppression of bone resorption but also by stimulation of bone formation.
I conclude this post by giving you a glimpse of what a "cycle" will be like: Heavy on testosterone, MILD aromatase inhibitor (and will look more into this), let your DHT increase, then use a DHT inhibitor to regain sensitivity. Repeat this cycle for a month. And this is just for the sex hormones.
There will be more drugs required.
You should stack up on anti baldness measures though as it will be a legit concern.
My next post will be a small one about increasing bone formation with lipus, and thickness in the wrists with LSJL.
made by @Ogionth
Results:
I've got over 100 studies accumulated on this subject btw.
First of all, we need to know that the face is constituted by trabecular bone, or cancellous bone. NOT the same bone that is in the growth plates.
This is merely the tip of my research but in the end it all added up, it's true steroids will make the face more masculine however they are simply not enough there is SO much more you can do..
Since i'm really fucking sleepy I'll leave you with some links, tomorrow I'll make sense of it.
Keep in mind my primary objective is increasing facial width, lower third and chin size. You can REALLY increase them, a LOT if you know what you're doing.
SOME links which guided me:
Also this: " While failing to replicate associations between testosterone measures and perceived facial masculinity, Pound et al. (2009) observed that reactive, but not baseline, testosterone was positively associated with a global facial masculinity measure.
It is noteworthy that the association between baseline testosterone and facial masculinity also showed a positive trend towards statistical signifcance in this study, suggesting that the relationship between face shape and baseline testosterone might not be completely absent, but instead may reflect a weaker link than the association with reactive testosterone" "If facial bone structure is affected by testosterone levels during puberty it is possible that total tissue exposure to the hormone is more closely aligned with appearance outcomes than baseline measures (see Pound et al., 2009 for a similar argument).
Fuck it i'll just give you a glimpse of what you have to target:
leptin, test, dht, insulin, igf-1 and hgh, dhea, cortisol and oestrogen.
How?
Here's what you have to take (I'll figure out the dosages and timing soon).
Aromatase inhibitors (Alternated, timing is KEY) Will explain more since you should notice that DHT has diminishing effects with time:
"These findings demonstate that androgens stimulate mineralization and that DHT is more active when used for short periods of time and in early stages of bone development in matrix-induced implants."
IGF-1 stimulating supplements and drugs
Vitamin MK 7 (And A LOT of it)
Zync
Alendronic Acid
Vitamin D 1000IU (Need to compensate with much higher MK levels)
Niacin vitamin B3 WITH flush?
Melatonin (Will help you get the sleep and also with some HGH release)
Parathyroid hormone (For no longer than 6 months)
DHEA
Mild cortisol blockers if needed.
Correct nutrition and exercise, NO intermittent fasting, a constant anabolic state.
And of course one of my GREATEST off-label finds, a lipus machine, after seeing this: "It's envisaged that the device could also be deployed to treat microsomia, a congenital underdevelopment of the lower jaw."
You can apply it instead on your zygomatic arches. There is a study I have in which a lipus machine had great success in growing patient's jaws when used specifically for that purpose.
You can also use LSJL for wrist thickness, as it will increase it.
You'll want pubertal levels of those hormones, and you'll see a dramatic increase in face width mostly at the zygomatic arches, don't worry about igf-1 making your face even longer, because I've found that your typical acromegaly long face is actually due to very high igf-1 levels but it's the hypogonadism that makes it that way. Therefore your face will grow a bit in lenght at your lower third but to compensate it will grow even more at the zygomatic arches due to high levels of test/dht compared to oestrogen.
Tomorrow I'll post the complete proof, there is only one problem though. You can really change your face, but it will cost you, probably a lot of money. Still FAR cheaper than surgery though.
When does the "face" stop growing?
Notel: the face is made up of cancellous bone, synonymous with trabecular bone or spongy bone, of which you should know the basic constitution in order to read this article. http://en.wikipedia.org/wiki/Cancellous bone Note2: for purposes of understanding, the end of puberty corresponds to the end of linear growth.
We conclude that growth in the face does not actually STOP after puberty, it merely slows down until it becomes insignificant. This is important because unlike growth plates, this type of bone retains the proliferative potential.
Why is it then that face growth slows down, even when testosterone levels after puberty do not drop?
There are in fact, two MAJOR explanations for this and I'll start with the first one:
After puberty, the pituitary gland stops producing the amounts of HGH it did which leads to decreased cell proliferation due to lowered IGF-1 levels. When it doesn't a condition referred to as acromegaly occurs. That alone is proof enough for growth of the face after puberty. However there are many other hormones involved in the process such as: leptin, IGF-1, testosterone and DHT, DHEA, estrogen and ostrogen, and cortisol.
The second one comes from an endocrinology book I downloaded, which explains the effects of estrogens on cancellous bone:
"Maintenance of a focal balance between formation and resorption (by estrogens), on the other hand, apparently results from opposite effects of estrogens on the life span of osteoclasts and osteoblasts/ osteocytes: a propoptotic effect on osteoclasts and an antiapoptotic effect on osteoblasts and osteocytes" Therefore, the more estrogens, the more bone will tend to maintain a balance between proliferation and resorption of cells, in order to get a healthy balance. Of course, this can easily be altered.
So when does the face stop growing? The answer is simply never.
We now need to grow the face. For aesthetic purposes, I will focus on increasing face width, rather than length, in my next cover all the variables, feel free to ask any questions.
Note3: estrogens are actually needed for bone growth, while too much is bad, they do have an anabolic effect on bone.
Note4: IGF-1 will make overall face size increase, not just length, the reason you might think that is that while people with acromegaly tend to have longer faces, they also suffer from hypogonadism in most cases. In fact cheekbone growth is a reported effect of acromegaly, when coupled with normal to high testosterone levels.
From here on out there wont be any fancy colors because I got lazy and gave up.
For this post I'll describe the various effects of recommended drugs and outline a plan:
We now have confirmation that a process similar to growth plate fusion does not occur for the trabecular bone which make of facial structure, now we need to know how to induce the changes we desire. It is already commonly known that sex hormones influence the development of the face, but what isn't generally known is the they have non genomic effects. This will be very important.
What is really important are these 4 crucial points.
"Proof-of-concept for AR action is demonstrated in androgen-insensitivity models, with production of a nonfunctional AR associated with a dramatic reduction in total bone mass in humans even with excellent estrogen compliance. AR null mice have high turnover osteopenia with increased formation but even stronger enhancement of resorption"
Oestrogen is there to prevent bone resorption. That is it's main function.
"Targeted AR overexpression in the skeleton further supports these findings, as it results in enhanced periosteal formation, reduced endosteal formation, increased trabecular bone formation and a reduction of osteoclast activity, all without changes in circulating steroid levels."
We are aiming for trabecular bone increase. AR signalling does that.
"Estrogens are thought to maintain adult bone mass predominantly through inhibition of bone resorption by osteoclasts (i.e. they act as anti-resorptive agents), which protect the skeleton from further loss of bone. Non-aromatizable androgens such as 5a-dihydrotestosterone (DHT), conversely, are anabolic agents that increase bone mass by stimulation of bone formation, and thus represent an important therapeutic class that has the potential to rebuild lost bone."
Well, there you have it!
On leptin, I'll conclude later on this as I'm still studying it.
On the sex hormones:
"Testosterone can regulate the skeleton through direct activation of androgen receptor (AR), as well as indirect activation of oestrogen receptor (ER) after testosterone is converted to ostrogen in the body. AR seems to play a major part in mediating the effects of testosterone on both trabecular and periosteal bone, although ER contributes to the optimal response to testosterone in periosteal bone growth."
The nitric oxide pathway can be targeted to avoid the bone resportion.
You'll want low cortisol levels:
Cortisol decreases bone formation by inhibiting periosteal cell proliferation. Simple. Same applied to trabecular bone.
However! Estrogen still has an anabolic effect on bone. This is a recent discovery.
Estrogen maintains trabecular bone volume in rats not only by suppression of bone resorption but also by stimulation of bone formation.
I conclude this post by giving you a glimpse of what a "cycle" will be like: Heavy on testosterone, MILD aromatase inhibitor (and will look more into this), let your DHT increase, then use a DHT inhibitor to regain sensitivity. Repeat this cycle for a month. And this is just for the sex hormones.
There will be more drugs required.
You should stack up on anti baldness measures though as it will be a legit concern.
My next post will be a small one about increasing bone formation with lipus, and thickness in the wrists with LSJL.
made by @Ogionth
@Gengar
@xnj
@imontheloose
@Hernan
@Volksstaffel
@xnj
@imontheloose
@Hernan
@Volksstaffel
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