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

[Deleted member 4946]

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?

m8 loads of people have put their reviews in and all of them grew from it, there is a limit to skepticism but you my friend have gone well over the top: http://russianstarpeptides.com/product/bmp-7-height-formula/#reviews even if there is small height increase it doesnt mean it doesnt exist Im going to take spironolactone, Aromasin, GHRP-2, MOD-GRF 1-29, Hexarelin, T3 thyroid, IGF-1 LR3, SAM-E Glucosamine Chondroitin MSM.

Don't underestimate DNA methylation promotion from SAM-E when the BMP-7 is inserted and it can go through the cell membrane via Type 1 and Type II pathway and TGF-Beta pathway is also stimulated simultaneously without inhibitors of BMP (like noggin) and inhibitors of TGF (like chordin) doesn't block the proteins. And as soon as it enters the cytoplasm, it also has to go through another hurdle and hope that I-Smad like Smad-6 and Smad-7 doesn't interrupt R-smads and Co-Smads. The Smurf1 is another smad signaling inhibitor that has to be dealt with.

As soon as Smad 4 who acts upon binding R-Smads and C-Smads enter into the nucleus and transcription of DNA occurs, that's when DNA methylation CAN occur. That's when "OFF" can turn into "ON" and "ON" can even turn off to "OFF". But TGF-Beta isn't the only pathway. There is also have MAPK pathway signaling that can also aid in proteins to reach the nucleus. This is IF all the inhibitors don't bind into any of the protein AND if inflammation does NOT occur. Let's hope for that.

The Smad 4 that binds with R-smads and Co-smads must enter the nubles. That's where the DNA IS located at. That's when DNA methylation occurs. That's also when cells communicate to other cells to transdifferentiate and then go through mitosis eventually.
Then mesenchymal stem cells within the bone marrow can differentiate into chondroctyes or osteoblasts depending on which gene receptor acts upon when protein binds into the adaptor.
When mesenchymal stem cells proliferate into chondrocytes and it starts to divide you will grow taller so this has to occur properly in cellular levels.

The E coli bacterial plasmid is a good vector that can rapidly multiply the source of your body's own BMP-7 so we can induce more growth from stacks.

I believe instead of looking for somatostatin receptor antagonists you should be looking for noggin, chordin, I-smad, Smurf1 inhibitors, growth will happen beyond genetic regulation if a stack can be found for this

I suggest you look up a picture chart of bmp2 and its SMAD-dependent pathway AND Smad-Independent pathway.

Smad-dependent pathway signaling uses Cbfa1 as transcription factors and this brings the result of Osteogenesis. If you want to experience interstitial height growth, you want the Chondrogenesis which uses the transcription factor of Sox9 and it's from Smad-independent pathway such as MAPK-signaling and this occurs from possibly downregulating FGFR3 and upregulating FGFR2 from BMPR-IA receptor.

This is only for BMP-2 btw, for BMP-7 it might be a little different that is why you also need to study the DNA structure of different BMP's this goes into epigentics this will give you more info: https://media.nature.com/w582/natur...boneres20155/images_hires/boneres20155-f4.jpg (BMP-7 and OP-1 are interchangeable btw)

DNA methylation silences the gene and it can work towards the CpG height increase inhibiting genes. Basically the role of DNA methylation would be to silence the inhibiting height increase genes. That is why I take it. I'll wait for your take on this instead of you saying there is nothing you can do for how specific height inhibition or promoting genes can be manipulated with the right choice of chemicals. According to Vsauce( yes really), the genetic limit for humans to grow who don't have a condition is 7 foot 3. So if you want to make the excuse of 'genetic potential' then the potential can extend that far.

 

[TURBO]

If you're taking Vitamin k2 on an empty stomach is pretty much all going to waste. It needs to be taken with a high fat meal.

Vitamin A, D, E & K - How Much and What Type of Fat Do You Need to Absorb These Fat Soluble Vitamins?

There are a handful of very basic questions in nutrition science, no one appears to have an answer to. One of these questions, which is directly related to the well-known fact that the vitamins A, D, E & K are "lipid soluble". This means that they are "solved" and thus made absorbable by fats...

suppversity.blogspot.com

 

[reptiles]

If you're taking Vitamin k2 on an empty stomach is pretty much all going to waste. It needs to be taken with a high fat meal.

Vitamin A, D, E & K - How Much and What Type of Fat Do You Need to Absorb These Fat Soluble Vitamins?

There are a handful of very basic questions in nutrition science, no one appears to have an answer to. One of these questions, which is directly related to the well-known fact that the vitamins A, D, E & K are "lipid soluble". This means that they are "solved" and thus made absorbable by fats...

suppversity.blogspot.com

View attachment 303527

Would this work at 18? I'm 18 currently and I wanna know if this might work

 

[Deleted member 4946]

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?

so what is your opinion on my stack?

 

[Deleted member 2756]

so what is your opinion on my stack?

explain it to me?

 

[ChaddeusPeuterschmit]

dn read

 

[Deleted member 4946]

explain it to me?

I gave you all the other growth factors and shit i am taking, DNA methylation is important for the transcription factor (epigetics) of genes upregulating the chondrogenesis, this is why 2000 mg (enteric coated) of SAM-E and folic+folnic acid IS NECESSARY. To summarise how important the DNA methylation is, DNA methylation is to silence the inhibiting height increase genes, you said there are a million different growth factors and proteins and shit that are stimulated with growth occurs well DNA methylation will always keep them 'ON' till of course the receptors in the growth plates are no more (plate fusion). Then again there is intra-articular cartilage you can use to keep growing after plate fusion, but there are far too many factors that i have not researched fully yet for that to happen.

spironolactone, Aromasin, GHRP-2, MOD-GRF 1-29, Hexarelin, T3 thyroid, IGF-1 LR3, SAM-E Glucosamine Chondroitin MSM, this stack should keep all pathways going normally (give me your take on how we can find noggin, chordin, I-smad, Smurf1 inhibitors) IGF-1 will already stimulate all other growth factors to be stimulated at once. https://www.ncbi.nlm.nih.gov/pubmed/25627998

MSM Enhances GH Signaling via the Jak2/STAT5b Pathway in Osteoblast-Like Cells and Osteoblast Differentiation through the Activation of STAT5b in MSCs

Methylsulfonylmethane (MSM) is a naturally occurring sulfur compound with well-known anti-oxidant properties and anti-inflammatory activities. But, its effects on bone are unknown. Growth hormone (GH) is regulator of bone growth and bone metabolism. GH ...

www.ncbi.nlm.nih.gov

Why tf do i bother writing this shit, none ya cunts even ask me questions are give me anymore retarded skepticism

 

[Deleted member 2756]

spironolactone, Aromasin, GHRP-2, MOD-GRF 1-29, Hexarelin, T3 thyroid, IGF-1 LR3, SAM-E Glucosamine Chondroitin MSM, this stack should keep all pathways going normally (give me your take on how we can find noggin, chordin, I-smad, Smurf1 inhibitors) IGF-1 will already stimulate all other growth factors to be stimulated at once,

don't take spironolactone, that is so fucking idiotic and retarded, could cause permanent hypogonadism. Also, you need an acetylcholinesterase inhibitor, to keep somatostatin under cholinergic suppression, for the time that mod-grf isn't agonizing the GHRHR. Keeping somatostatin permanently inhibited is key. Somatostatin doesn't just have an effect on the pituitary gland, it is anti-proliferative and pro-apoptosis, there are Somatostatin receptor sites in the majority of our tissue, meaning it'll exert hormone regulatory functions outside of the hypothalamic/pituitary axis.

The reason why I think the majority of these kid's with idiopathic short stature don't grow when administrated GH is that somatostatin upregulates because exogenous GHRH doesn't get secreted from the hypothalamus, somatostatin actually inhibits the release of thyrotropin-releasing-hormone (TRH), TRH is what signals the thyrotrope cells to synthesize TSH, therefore somatostatin being upregulated due to the negative feedback loop that is interfering with GHRH is causing a decrease in thyroid stimulation, thus, a lack of T3 and T4 are being produced.

using a long-acting synthetic GHRH analog like CJC-1295 would prevent the upregulation of somatostatin, along with an acetylcholinesterase inhibitor.

I don't know much about noggin, I know that the actual protein itself plays a key role in the development of your skull in the womb, hence the creative name.

 

[Deleted member 4946]

don't take spironolactone, that is so fucking idiotic and retarded, could cause permanent hypogonadism. Also, you need an acetylcholinesterase inhibitor, to keep somatostatin under cholinergic suppression, for the time that mod-grf isn't agonizing the GHRHR. Keeping somatostatin permanently inhibited is key. Somatostatin doesn't just have an effect on the pituitary gland, it is anti-proliferative and pro-apoptosis, there are Somatostatin receptor sites in the majority of our tissue, meaning it'll exert hormone regulatory functions outside of the hypothalamic/pituitary axis.

The reason why I think the majority of these kid's with idiopathic short stature don't grow when administrated GH is that somatostatin upregulates because exogenous GHRH doesn't get secreted from the hypothalamus, somatostatin actually inhibits the release of thyrotropin-releasing-hormone (TRH), TRH is what signals the thyrotrope cells to synthesize TSH, therefore somatostatin being upregulated due to the negative feedback loop that is interfering with GHRH is causing a decrease in thyroid stimulation, thus, a lack of T3 and T4 are being produced.

using a long-acting synthetic GHRH analog like CJC-1295 would prevent the upregulation of somatostatin, along with an acetylcholinesterase inhibitor.

I don't know much about noggin, I know that the actual protein itself plays a key role in the development of your skull in the womb, hence the creative name.

just with GH treatment the males grew an average of 9.5cm over the untreated controls, no somatostatin inhibitor included, if these weak stacks can yield such high growth results then my stack can yield more https://ijpeonline.biomedcentral.com/articles/10.1186/1687-9856-2014-15 and they only took 0.16 to 0.28 mg/kg/week, so the ones who took the higher dose (12 IU per day) were the ones who grew 11.6 cm over the control, this is all without inhibiting somatostatin, no low estrogen, no glucosamine and chondroitin to increase the number of proliferative chondrocytes by two-fold percentage of remaining cartilage increase four-fold and the percentage of trabecular bone increase three-fold in comparison to the control group: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4286662/ no MSM to promote osteogenic differentiation of MSCs through activation of STAT5b: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3469535/ and no SAM-E for the most important factor of DNA methylation so the transcription factors from your genes to bind to bone protein receptors (induced epigenetics): https://www.ncbi.nlm.nih.gov/pubmed/8647346 and no IGF-1 LR3 (IGF-1 on roids, won't bind to any IGF-1 binding proteins and is like 3 times more potent) no hexarelin to stimulate pi3k pathway (which induces mass proliferation): https://www.ncbi.nlm.nih.gov/pubmed/18218693, no anti-androgens to slow down tanner stage and therefore give you a lot more time to grow you can take HCG even if you do get hypogonadism, no aromasin to delay your bone age even further and no GHRP-2 and MOD-GRF 3 times a day to stimulate a very powerful (and very natural response so that your body won't shut off it's own endogenous production) and it inhibits somatostatin while the HGH is being released, no small amounts of t3 thryoid to help my body synthesize more IGF-1 from all that elevated HGH, if those ISS kids saw almost 5 inches of growth with 12 IU of GH a day (only) compared to the untreated control, then Im quite sure I can get those 9 inches with this obviously superior stack, it is even easier for me to say it as my height prediction is 6'2 anyway, so even without taking drugs and going full natural ill reach that height, im aiming 5 inches over that which by the culmination of studies is very much possible

 

[Deleted member 2756]

just with GH treatment the males grew an average of 9.5cm over the untreated controls, no somatostatin inhibitor included, if these weak stacks can yield such high growth results then my stack can yield more https://ijpeonline.biomedcentral.com/articles/10.1186/1687-9856-2014-15 and they only took 0.16 to 0.28 mg/kg/week, so the ones who took the higher dose (12 IU per day) were the ones who grew 11.6 cm over the control, this is all without inhibiting somatostatin, no low estrogen, no glucosamine and chondroitin to increase the number of proliferative chondrocytes by two-fold percentage of remaining cartilage increase four-fold and the percentage of trabecular bone increase three-fold in comparison to the control group: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4286662/ no MSM to promote osteogenic differentiation of MSCs through activation of STAT5b: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3469535/ and no SAM-E for the most important factor of DNA methylation so the transcription factors from your genes to bind to bone protein receptors (induced epigenetics): https://www.ncbi.nlm.nih.gov/pubmed/8647346 and no IGF-1 LR3 (IGF-1 on roids, won't bind to any IGF-1 binding proteins and is like 3 times more potent) no hexarelin to stimulate pi3k pathway (which induces mass proliferation): https://www.ncbi.nlm.nih.gov/pubmed/18218693, no anti-androgens to slow down tanner stage and therefore give you a lot more time to grow you can take HCG even if you do get hypogonadism, no aromasin to delay your bone age even further and no GHRP-2 and MOD-GRF 3 times a day to stimulate a very powerful (and very natural response so that your body won't shut off it's own endogenous production) and it inhibits somatostatin while the HGH is being released, no small amounts of t3 thryoid to help my body synthesize more IGF-1 from all that elevated HGH, if those ISS kids saw almost 5 inches of growth with 12 IU of GH a day (only) compared to the untreated control, then Im quite sure I can get those 9 inches with this obviously superior stack, it is even easier for me to say it as my height prediction is 6'2 anyway, so even without taking drugs and going full natural ill reach that height, im aiming 5 inches over that which by the culmination of studies is very much possible

wow great, I actually learned something from your posts for once. 11.6cm is insane, but keep in mind we aren't children anymore, I'm 17 and you're 15, children have a higher susceptibility to growth hormone-related stimuli.

Even then, exogenous GH is always going to be better than synthetic GHRH analogs Ghrelin receptor agonists and GHS agonists. Injecting the recombinant growth hormone ensures that you bypass somatostatin. Good stuff though, keep the discussion going.

also, by the way, the body desensitizes to IGF-1LR3, I'd suggest taking IGF-1DES as it's actually 10fold more potent than endogenous IGF-1 and has a short half-life, around 30 minutes, which means the body doesn't build a tolerance as it's in and out fast.

 

[Deleted member 4946]

wow great, I actually learned something from your posts for once. 11.6cm is insane, but keep in mind we aren't children anymore, I'm 17 and you're 15, children have a higher susceptibility to growth hormone-related stimuli.

Even then, exogenous GH is always going to be better than synthetic GHRH analogs Ghrelin receptor agonists and GHS agonists. Injecting the recombinant growth hormone ensures that you bypass somatostatin. Good stuff though, keep the discussion going.

also, by the way, the body desensitises to IGF-1LR3, I'd suggest taking IGF-1DES as it's actually 10fold more potent than endogenous IGF-1 and has a short half-life, around 30 minutes, which means the body doesn't build a tolerance as it's in and out fast.

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

 

[mattzdeb]

hold up reading this through again I couldn't understand is k2 good for bone remodeling by inhibiting the pathway mentioned? and by MK4 do you mean k2 mk4?

 

[PenileFacialSurgery]

Didn’t read...

But bookmarked, will definitely read later.

 

[Incoming]

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

 

[GarixTheChad]

Will i get bubble gut from HGH and IGF-1 LR3?

 

[Incoming]

You said that nuking estrogen will inhibit osteoclast activity, limiting resorption and remodeling but it seems the opposite is true.
Not to mention resorption rate for cranial bones is really low compared to the rest of the body, you need what osteoclasts you can get

Osteoporosis: Practice Essentials, Background, Pathophysiology

Osteoporosis, a chronic, progressive disease of multifactorial etiology (see Etiology), is the most common metabolic bone disease in the United States. It has been most frequently recognized in elderly white women, although it does occur in both sexes, all races, and all age groups.

emedicine.medscape.com

 

[Deleted member 6400]

over for my 18 year old ass

 

[a1phenohorriblebones]

So high iq that this post is stupid af

 

[JizzFarmer]

Why mk4 over mk7, mk7 has a higher bioavailability?

 

[Deleted member 2756]

Why mk4 over mk7, mk7 has a higher bioavailability?

MK4 is absorbed into the bone at a higher rate. They both have their benefits. MK4 has also been proven to inhibit aromatase and increase testosterone through an unknown mechanism, whereas mk7 doesn't.

using both is beneficial though, again they have their pro's and cons.

 

[JizzFarmer]

MK4 is absorbed into the bone at a higher rate. They both have their benefits. MK4 has also been proven to inhibit aromatase and increase testosterone through an unknown mechanism, whereas mk7 doesn't.

using both is beneficial though, again they have their pro's and cons.

Ok, I will switch to mk4 after my mk7 runs out.

 

[Deleted member 2756]

Ok, I will switch to mk4 after my mk7 runs out.

It's really expensive though, that's the issue. Also, mk7 has a substantially higher half-life, off the top of my head, I think MK4's is 4 hours, so you'd have to dose frequently.

 

[JizzFarmer]

It's really expensive though, that's the issue. Also, mk7 has a substantially higher half-life, off the top of my head, I think MK4's is 4 hours, so you'd have to dose frequently.

Ffs just looked up mk4 and its around $0.10 aud per mg. Fucking oaf these jew scammers

 

[Deleted member 2756]

Fucking oaf these jew scammers

 

[JizzFarmer]

View attachment 573129

Dyosteinic6

 

[SadnessWYJ]

How to leanmaxxing then while doing this diet

 

[bruh3610]

How to leanmaxxing then while doing this diet

Nigga what? Did u just call this a diet?

“What are ur macros?” “Yea bro my macros are 3g of igf1 every day”

 

[bruh3610]

Dyosteinic6

Diuretic6

 

[SadnessWYJ]

Wrong word, i mesnt

Nigga what? Did u just call this a diet?

“What are ur macros?” “Yea bro my macros are 3g of igf1 every day”

meant how to cut or lean maxx while doing this no calories less thing

 

[bruh3610]

Wrong word, i mesnt

meant how to cut or lean maxx while doing this no calories less thing

Just eat your flintstone gummies
Your bones need minerals to grow not calories

 

[Deleted member 3163]

Genetics only tbh

 

[maxmendietta]

damn son i must be my maxilla cuz ion remember projecting

 

[DrOtaku]

oh yes goy, mew and chew.

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

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

Invisalign can move teeth with 0.5-1 newton of force. Tongue exerts between 0.3 to 0.5 newton. A jaw can exert 1,100-1,300 newtons.

 

[Yusu]

is 16 hours a day fast bad for growth if you eat iver 3k calories in the eatinh window

 

[john2]

Thinks mouthbreathing doesnt affect facial growth

@Dyorotic2 he^ is right about this part.

Mouth-breathing will ruin your face further on.
But mewing (after 12 yo) won't fix/improve anything at all.
It's better to nose breath with your mouth shut.

 

[The Bleach Pill]

How tf I'm supposed to leanmaxx while eating a surplus?

I thought u left u fat cunt. All that crying on your last post jfl.

 

[Deleted member 2756]

Ah yes, my original hypothesis.

 

[Deleted member 6892]

Ah yes, my original hypothesis.

Is it wrong

 

[Deleted member 2756]

Is it wrong

not really, my views have changed quite significantly since then however..

 

[hairyballscel]

But mewing (after 12 yo) won't fix/improve anything at all.
It's better to nose breath with your mouth shut.

It can, change is very slow after 12 but its possible, and even if you think it wont work its a good preventive measure

 

[bossman]

not really, my views have changed quite significantly since then however..

would you mind explaining what your views are now then?

 

[Deleted member 5818]

Hahaha ain't I entretaining?
Now I'm not fat anymore jfl

So since joining this website on the 25th (14 days ago) you’re not fat anymore jfl

 

[Deleted member 5818]

I was losing weight before joining btw, also in 14 days you can drop 10kg no prob

The ol just get a knife and chop it off theory?

 

[SteveRogers]

oh yes goy, mew and chew.

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

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

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

 

[SteveRogers]

It can, change is very slow after 12 but its possible, and even if you think it wont work its a good preventive measure

Exactly, mewing reverses the negative effects of gravity on midface, HARD, like VERY HARD mewing is needed in order to create change, which can be achieved at any age, as OP said, facial bones never fully fuse.

 

[SteveRogers]

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.

This why arnold skull mogs everyone?

 

[hairyballscel]

Exactly, mewing reverses the negative effects of gravity on midface, HARD, like VERY HARD mewing is needed in order to create change, which can be achieved at any age, as OP said, facial bones never fully fuse.

Ppl here act like when ur 12 a switch is turned and now mewing will have no effect on you... jfl

 

[ThreadMatters]

why the fuck is this guy banned too? if mods keep doing this shit soon we will only have offtopic section and greycels asking if MEWING works

@ALLTHEFUCKINGMODS

 

[her]

why the fuck is this guy banned too? if mods keep doing this shit soon we will only have offtopic section and greycels asking if MEWING works

@ALLTHEFUCKINGMODS

He requested a ban...

 

[Mouthbreath]

HGH after puberty is COPE:

Read this:


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

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



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


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

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

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






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

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

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


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

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

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

slate.com