Theory Mechanotransductio, bonesmashing full science breakdown and theories (7 Viewers)

[Synapse]

This is not true. https://pubmed.ncbi.nlm.nih.gov/20811069/

Wnt/β-catenin activation should actually biased bone homeostasis towards growth through osteoblastogenesis and the expression of BMP-2.

"BMP or Bone Morphogenetic Proteins are a group of proteins that play a crucial role in bone and tissue formation, they are the signals that tell stemcells to become osteoblasts. stem cells are cells that have the ability to turn into multible types of cells, and osteoblasts are the cells in your body that build new bone. unlike GH or other groups that are reliant on growth plates, BMP's can grow new bone tissue from zero. although stem cell get limited to what cells they can become" after puberty, they can always turn to osteoblasts throughout the life."

No, and my previous answer serves as an answer to this conjecture. Have you actually read it all?

i will research more about this, i still have my doubts on this.

 

[surgerymax]

i will research more about this, i still have my doubts on this.

the scar tissue theory seems much more legit imo , much less mental gymnastics and a very simple mechanism that is very plausible

I would post but the formatting is going to be utter garbage

 

[Synapse]

the scar tissue theory seems much more legit imo , much less mental gymnastics and a very simple mechanism that is very plausible

I would post but the formatting is going to be utter garbage

i think the same, seems a more realistic mechanism, i will investigate into this anyways so i don't fall behind the fallacy of dismissing stuff just because i haven't done enough research.

 

[Tabula Rasa]

i will research more about this, i still have my doubts on this.

All you need is in the thread. If you click on the numbers before the quotes you can read the full studies yourself.

the scar tissue theory seems much more legit imo , much less mental gymnastics and a very simple mechanism that is very plausible

I would post but the formatting is going to be utter garbage

There is no mental gymnastics, it's in fact really simple, one axis and a way for the bone to respond to stress or the lack of it. I haven't done a deep dive in scar tissue apposition tho.

 

[IBlameMyDadsHeight]

BONESMASHING
Highest ROI softmax?

After reading several threads of absolute brain rot—especially the horrible and idiotic thread by Jonas, "The truth about steroids and peptides affecting bones and height" (JFL at that bullshit being in BOTB) —along with various opinions from other people lacking any critical thinking skills, I decided to make this thread focusing on the following points:
1-How it works.
2-Subperiosteal hematomas and its impossibility as a consistent theory.
(Suck it seif)
3-Bone homeostasis.


This thread assumes that bonesmashing works, and will focus on explaining how.

THREAD SONG:

How it works:

Bonesmashing works through the Wnt/β-catenin axis and sclerostin

As you may have read, mechanotransduction is essential for regulating bone homeostasis and shifting it toward the growth process rather than the resorption process. Sclerostin, whose expression increases with a lack of mechanical load, that inhibits the Wnt/β-catenin pathway.


The role of the Wnt/β-catenin pathway in mechanotransduction.
The Wnt/β-catenin pathway through the downregulation of sclerostin via mechanotransduction. The Wnt/β-catenin pathway leads to osteoanabolic processes through osteoblastogenesis, promoting mesenchymal stem cells to differentiate into osteoblasts, resulting in their proliferation over osteoclasts.
This pathway also upregulates BMP-2, one of the most potent bone growth factor.



Nitric oxide release and its role in the sclerostin and Wnt/β-catenin axis.
Mechanical bone loading causes osteocytes to release nitric oxide, which rapidly degrades sclerostin which also further increases Wnt/β-catenin.[8]In response to mechanical loading of bone, osteocytes produce nitric oxide (NO) and decrease sclerostin protein expression, leading to an increase in bone mass.

Subperiosteal hematoma theory
I’m not going to spend much time on this point since I developed a fairly detailed response at the time, which I will now quote.


Bone homeostasis and Growth factors

Contrary to my previous belief that the results of bonesmashing were limited without the use of exogenous growth factors such as rHGH, sex hormones or their derivatives, and parathyroid hormone analogs, the Wnt/β-catenin pathway is one of the main regulators of bone homeostasis. By being upregulated through mechanotransduction, this pathway could produce noticeable results solely through proper bonesmashing technique and application, and synergize as well as greatly amplify the aforementioned factors.


Tl;dnr: Start bonesmashing rn!!!!

Tags:
Dexter birthdefect
​

Bone smashing

 

[Tabula Rasa]

Bone smashing

Yes "IBlameMyDadsHeight" bonesmashing and if you please read the thread.

 

[EqBeliever]

BONESMASHING
Highest ROI softmax?

After reading several threads of absolute brain rot—especially the horrible and idiotic thread by Jonas, "The truth about steroids and peptides affecting bones and height" (JFL at that bullshit being in BOTB) —along with various opinions from other people lacking any critical thinking skills, I decided to make this thread focusing on the following points:
1-How it works.
2-Subperiosteal hematomas and its impossibility as a consistent theory.
(Suck it seif)
3-Bone homeostasis.


This thread assumes that bonesmashing works, and will focus on explaining how.

THREAD SONG:

How it works:

Bonesmashing works through the Wnt/β-catenin axis and sclerostin

As you may have read, mechanotransduction is essential for regulating bone homeostasis and shifting it toward the growth process rather than the resorption process. Sclerostin, whose expression increases with a lack of mechanical load, that inhibits the Wnt/β-catenin pathway.


The role of the Wnt/β-catenin pathway in mechanotransduction.
The Wnt/β-catenin pathway through the downregulation of sclerostin via mechanotransduction. The Wnt/β-catenin pathway leads to osteoanabolic processes through osteoblastogenesis, promoting mesenchymal stem cells to differentiate into osteoblasts, resulting in their proliferation over osteoclasts.
This pathway also upregulates BMP-2, one of the most potent bone growth factor.



Nitric oxide release and its role in the sclerostin and Wnt/β-catenin axis.
Mechanical bone loading causes osteocytes to release nitric oxide, which rapidly degrades sclerostin which also further increases Wnt/β-catenin.[8]In response to mechanical loading of bone, osteocytes produce nitric oxide (NO) and decrease sclerostin protein expression, leading to an increase in bone mass.

Subperiosteal hematoma theory
I’m not going to spend much time on this point since I developed a fairly detailed response at the time, which I will now quote.


Bone homeostasis and Growth factors

Contrary to my previous belief that the results of bonesmashing were limited without the use of exogenous growth factors such as rHGH, sex hormones or their derivatives, and parathyroid hormone analogs, the Wnt/β-catenin pathway is one of the main regulators of bone homeostasis. By being upregulated through mechanotransduction, this pathway could produce noticeable results solely through proper bonesmashing technique and application, and synergize as well as greatly amplify the aforementioned factors.


Tl;dnr: Start bonesmashing rn!!!!

Tags:
Dexter birthdefect
​

t2 softmax def

 

[surgerymax]

All you need is in the thread. If you click on the numbers before the quotes you can read the full studies yourself.

There is no mental gymnastics, it's in fact really simple, one axis and a way for the bone to respond to stress or the lack of it. I haven't done a deep dive in scar tissue apposition tho.

both theories seems plausible in a way but my main reason objections with this are the cited studies are often in controlled , nondamaging strain whereas bonesmashing creates acute trauma or microfractures

'Animals—18-week-old C57Bl/6J male mice and 6-month-old virgin female Lewis rats were used for the ulnar loading studies. The unloading studies were performed in 6-week-old male C57Bl/6J mice. The mice were purchased from Jackson Labs, and the rats were purchased from Harlan, Inc. The animals were housed at the Indiana University Animal Care Facility until the proper age for each experiment was reached. Standard rodent chow and water were provided ad libitum. All of the procedures performed in the experiments were in accordance with the Institutional Animal Care and Use Committee guidelines.
In Vivo Ulnar Loading—Under isoflurane-induced anesthesia, the right forearms of mice and rats were loaded for 360 cycles/day (2 Hz). The mice used for immunolocalization of sclerostin were loaded for 2 consecutive days and then sacrificed on day 3. The rats and mice used for RNA analysis (in situ hybridization and quantitative PCR) were loaded for a single session (1 day) and sacrificed 24 h later. Loading was conducted on a customized electromagnetic actuator at peak force of 2.7 newtons for mice and 17 newtons for rats, which generates ∼2200 μϵ at the midshaft ulna (Fig. 1A). Strain magnitudes were determined previously using miniature strain gauges bonded to the midshaft ulnar surface (20, 21). The left forearms were not loaded and served as an internal control for loading effects. All of the mice were allowed normal cage activity between loading bouts. Intraperitoneal injections of calcein and alizarin complexone (22 mg/kg body mass; Sigma) were administered to some of the mice 4 and 10 days after the first load day to monitor regional bone formation rates in the ulnae. To collect adequate amounts of ulnar diaphyseal tissue for gene expression analysis, nine adult female virgin Lewis rats were subjected to a single bout of ulnar loading at 17-newton peak force (∼2200 μϵ; 2 Hz; 360 cycles) using a similar device as described for mice. The rat ulnas were harvested 24 h after loading, snap frozen in liquid N2, and processed for RNA analysis as described below.'



Additionally fracture healing produces a temporary callus that remodels back to normal architecture which is not permanent targeted hypertrophy that is aesthetic. This is the same reason micro fracturing techniques in shit like muay thai are pseudoscience

There are also just massive oversimplifications of these pathways

The core claims that blunt force trauma from bonesmashing reliably triggers targeted facial bone growth through these pathways misapplies legitimate science and ignores alot of limitations


I believe the scar tissue theory to be alot more viable due to its simple and clear mechanism

Blunt trauma = capillary rupture = bleeding = acute inflammation = fibroblast activation = collagen deposition and fibrosis
This is textbook wound healing and with repeated disruption pushing it towards chronic inflammation and excessive fibrous tissue

 

[surgerymax]

both theories seems plausible in a way but my main reason objections with this are the cited studies are often in controlled , nondamaging strain whereas bonesmashing creates acute trauma or microfractures

'Animals—18-week-old C57Bl/6J male mice and 6-month-old virgin female Lewis rats were used for the ulnar loading studies. The unloading studies were performed in 6-week-old male C57Bl/6J mice. The mice were purchased from Jackson Labs, and the rats were purchased from Harlan, Inc. The animals were housed at the Indiana University Animal Care Facility until the proper age for each experiment was reached. Standard rodent chow and water were provided ad libitum. All of the procedures performed in the experiments were in accordance with the Institutional Animal Care and Use Committee guidelines.
In Vivo Ulnar Loading—Under isoflurane-induced anesthesia, the right forearms of mice and rats were loaded for 360 cycles/day (2 Hz). The mice used for immunolocalization of sclerostin were loaded for 2 consecutive days and then sacrificed on day 3. The rats and mice used for RNA analysis (in situ hybridization and quantitative PCR) were loaded for a single session (1 day) and sacrificed 24 h later. Loading was conducted on a customized electromagnetic actuator at peak force of 2.7 newtons for mice and 17 newtons for rats, which generates ∼2200 μϵ at the midshaft ulna (Fig. 1A). Strain magnitudes were determined previously using miniature strain gauges bonded to the midshaft ulnar surface (20, 21). The left forearms were not loaded and served as an internal control for loading effects. All of the mice were allowed normal cage activity between loading bouts. Intraperitoneal injections of calcein and alizarin complexone (22 mg/kg body mass; Sigma) were administered to some of the mice 4 and 10 days after the first load day to monitor regional bone formation rates in the ulnae. To collect adequate amounts of ulnar diaphyseal tissue for gene expression analysis, nine adult female virgin Lewis rats were subjected to a single bout of ulnar loading at 17-newton peak force (∼2200 μϵ; 2 Hz; 360 cycles) using a similar device as described for mice. The rat ulnas were harvested 24 h after loading, snap frozen in liquid N2, and processed for RNA analysis as described below.'



Additionally fracture healing produces a temporary callus that remodels back to normal architecture which is not permanent targeted hypertrophy that is aesthetic. This is the same reason micro fracturing techniques in shit like muay thai are pseudoscience

There are also just massive oversimplifications of these pathways

The core claims that blunt force trauma from bonesmashing reliably triggers targeted facial bone growth through these pathways misapplies legitimate science and ignores alot of limitations


I believe the scar tissue theory to be alot more viable due to its simple and clear mechanism

Blunt trauma = capillary rupture = bleeding = acute inflammation = fibroblast activation = collagen deposition and fibrosis
This is textbook wound healing and with repeated disruption pushing it towards chronic inflammation and excessive fibrous tissue

The scar tissue mechanism also does come with obvious caveats too

 

[Tabula Rasa]

both theories seems plausible in a way but my main reason objections with this are the cited studies are often in controlled , nondamaging strain whereas bonesmashing creates acute trauma or microfractures

'Animals—18-week-old C57Bl/6J male mice and 6-month-old virgin female Lewis rats were used for the ulnar loading studies. The unloading studies were performed in 6-week-old male C57Bl/6J mice. The mice were purchased from Jackson Labs, and the rats were purchased from Harlan, Inc. The animals were housed at the Indiana University Animal Care Facility until the proper age for each experiment was reached. Standard rodent chow and water were provided ad libitum. All of the procedures performed in the experiments were in accordance with the Institutional Animal Care and Use Committee guidelines.
In Vivo Ulnar Loading—Under isoflurane-induced anesthesia, the right forearms of mice and rats were loaded for 360 cycles/day (2 Hz). The mice used for immunolocalization of sclerostin were loaded for 2 consecutive days and then sacrificed on day 3. The rats and mice used for RNA analysis (in situ hybridization and quantitative PCR) were loaded for a single session (1 day) and sacrificed 24 h later. Loading was conducted on a customized electromagnetic actuator at peak force of 2.7 newtons for mice and 17 newtons for rats, which generates ∼2200 μϵ at the midshaft ulna (Fig. 1A). Strain magnitudes were determined previously using miniature strain gauges bonded to the midshaft ulnar surface (20, 21). The left forearms were not loaded and served as an internal control for loading effects. All of the mice were allowed normal cage activity between loading bouts. Intraperitoneal injections of calcein and alizarin complexone (22 mg/kg body mass; Sigma) were administered to some of the mice 4 and 10 days after the first load day to monitor regional bone formation rates in the ulnae. To collect adequate amounts of ulnar diaphyseal tissue for gene expression analysis, nine adult female virgin Lewis rats were subjected to a single bout of ulnar loading at 17-newton peak force (∼2200 μϵ; 2 Hz; 360 cycles) using a similar device as described for mice. The rat ulnas were harvested 24 h after loading, snap frozen in liquid N2, and processed for RNA analysis as described below.'



Additionally fracture healing produces a temporary callus that remodels back to normal architecture which is not permanent targeted hypertrophy that is aesthetic. This is the same reason micro fracturing techniques in shit like muay thai are pseudoscience

There are also just massive oversimplifications of these pathways

The core claims that blunt force trauma from bonesmashing reliably triggers targeted facial bone growth through these pathways misapplies legitimate science and ignores alot of limitations


I believe the scar tissue theory to be alot more viable due to its simple and clear mechanism

Blunt trauma = capillary rupture = bleeding = acute inflammation = fibroblast activation = collagen deposition and fibrosis
This is textbook wound healing and with repeated disruption pushing it towards chronic inflammation and excessive fibrous tissue

I am not an advocate of blunt traumas, that's not mentioned anywhere in my thread. That leads us this study which shows that a low magnitude load with rest periods between loads becomes osteogenic, part of this mechanism could be explained by the presence of lacunocanalicular fluid near the osteocytes which mediates the mechanotransductive effect on bone. That pretty much puts end to the scar depposition theory. https://pmc.ncbi.nlm.nih.gov/articles/PMC1435731/

 

[surgerymax]

I am not an advocate of blunt traumas, that's not mentioned anywhere in my thread. That leads us this study which shows that a low magnitude load with rest periods between loads becomes osteogenic, part of this mechanism could be explained by the presence of lacunocanalicular fluid near the osteocytes which mediates the mechanotransductive effect on bone. That pretty much puts end to the scar depposition theory. https://pmc.ncbi.nlm.nih.gov/articles/PMC1435731/

how does that put an end to the scar deposition theory ?

And the study you’re showing is still done with controlled loading , how exactly do you suggest bone smashing is done then

 

[Tabula Rasa]

how does that put an end to the scar deposition theory ?

And the study you’re showing is still done with controlled loading , how exactly do you suggest bone smashing is done then

The important thing is the load, not that it's controlled at X kHz, any load downregulates SOST and full disload upregulates SOST.

I'm gatekeeping that.

 

[surgerymax]

The important thing is the load, not that it's controlled at X kHz, any load downregulates SOST and full disload upregulates SOST.

I'm gatekeeping that.

in that case this doesn’t seem to be much of a ‘bones smash’ theory more so something entirely different

 

[Tabula Rasa]

in that case this doesn’t seem to be much of a ‘bones smash’ theory more so something entirely different

Relating bonesmashing to just hitting yourself in the face with a hammer seems retarded to me. Still, it would work, tbh.

 

[surgerymax]

Relating bonesmashing to just hitting yourself in the face with a hammer seems retarded to me. Still, it would work, tbh.

my general definition of the concept would be using intentional blunt force trauma for aesthetic benefits facially

Which i do not believe this would work for as again this needs controlled loading

 

[Tabula Rasa]

Which i do not believe this would work for as again this needs controlled loading

Why?

 

[surgerymax]

Why?

bone smash is acute blunt force trauma , everything cited here uses long term loading in a controlled environment

I think the science is legit but bone smash is not the right stimulus

 

[Tabula Rasa]

bone smash is acute blunt force trauma , everything cited here uses long term loading in a controlled environment

No, one of the first things I mention in this thread is the loss of bone mass that astronauts experience due to the lack of stress on their bones. Any stimulus activates osteocytes, even walk, and as long as you're not a complete idiot hitting yourself with all your might, bonesmashing with a hammer or your knuckles is useful.

 

[Synapse]

No, one of the first things I mention in this thread is the loss of bone mass that astronauts experience due to the lack of stress on their bones. Any stimulus activates osteocytes, even walk, and as long as you're not a complete idiot hitting yourself with all your might, bonesmashing with a hammer or your knuckles is useful.

Done my research, it seems like a legit mechanism Aryan Incel, what's your input on this?, not sure how much it can be practically applied tho.

 

[Tabula Rasa]

Done my research, it seems like a legit mechanism Aryan Incel, what's your input on this?, not sure how much it can be practically applied tho.

Boyo how tf have you done a research in less than a day? This threads took me almost a week

 

[Aryan Incel]

BONESMASHING
Highest ROI softmax?

After reading several threads of absolute brain rot—especially the horrible and idiotic thread by Jonas, "The truth about steroids and peptides affecting bones and height" (JFL at that bullshit being in BOTB) —along with various opinions from other people lacking any critical thinking skills, I decided to make this thread focusing on the following points:
1-How it works.
2-Subperiosteal hematomas and its impossibility as a consistent theory.
(Suck it seif)
3-Bone homeostasis.


This thread assumes that bonesmashing works, and will focus on explaining how.

THREAD SONG:

How it works:

Bonesmashing works through the Wnt/β-catenin axis and sclerostin

As you may have read, mechanotransduction is essential for regulating bone homeostasis and shifting it toward the growth process rather than the resorption process. Sclerostin, whose expression increases with a lack of mechanical load, that inhibits the Wnt/β-catenin pathway.


The role of the Wnt/β-catenin pathway in mechanotransduction.
The Wnt/β-catenin pathway through the downregulation of sclerostin via mechanotransduction. The Wnt/β-catenin pathway leads to osteoanabolic processes through osteoblastogenesis, promoting mesenchymal stem cells to differentiate into osteoblasts, resulting in their proliferation over osteoclasts.
This pathway also upregulates BMP-2, one of the most potent bone growth factor.



Nitric oxide release and its role in the sclerostin and Wnt/β-catenin axis.
Mechanical bone loading causes osteocytes to release nitric oxide, which rapidly degrades sclerostin which also further increases Wnt/β-catenin.[8]In response to mechanical loading of bone, osteocytes produce nitric oxide (NO) and decrease sclerostin protein expression, leading to an increase in bone mass.

Subperiosteal hematoma theory
I’m not going to spend much time on this point since I developed a fairly detailed response at the time, which I will now quote.


Bone homeostasis and Growth factors

Contrary to my previous belief that the results of bonesmashing were limited without the use of exogenous growth factors such as rHGH, sex hormones or their derivatives, and parathyroid hormone analogs, the Wnt/β-catenin pathway is one of the main regulators of bone homeostasis. By being upregulated through mechanotransduction, this pathway could produce noticeable results solely through proper bonesmashing technique and application, and synergize as well as greatly amplify the aforementioned factors.


Tl;dnr: Start bonesmashing rn!!!!

Tags:
Dexter birthdefect
​

Well put out thread with real scientific backing. However the thing is we can’t be sure the difference of bone mass it will actually make. Will it be significant or will it be negligible? I’m more in the side of negligible personally as Ive tried it out for a year or two and after the swelling went down I saw no difference bone structure wise personally

 

[Synapse]

Boyo how tf have you done a research in less than a day? This threads took me almost a week

skill issue, basically i just checked and read the studies you provided and some other and cross referenced some info and blah blah, and got to the same conclusion you did, the mechanism is very real and legit, congrats to you for all the investigation, however i don't think it will have a significant impact structure wise, so people need to have realistic expectations about what they can achieve with this, ik a lot of people who have bonesmashed for a good amount of time and they said the impact was almost unnoticeable.

 

[surgerymax]

Done my research, it seems like a legit mechanism Aryan Incel, what's your input on this?, not sure how much it can be practically applied tho.

i agree the mechanism seems legit but its application with 'bone smashing' is not the ideal stimulus
you'd need some other stimulus which hes allegedly gatekeeping

 

[Synapse]

i agree the mechanism seems legit but its application with 'bone smashing' is not the ideal stimulus
you'd need some other stimulus which hes allegedly gatekeeping

we all know its raw milk and ghkcu

 

[surgerymax]

we all know its raw milk and ghkcu

2mg ghk-cu eod and wrap it up